Home About us Contact
|
Home About us Contact | ||
|
|
||
Mast Cells (mast + cell)
Kinds of Mast Cells Terms modified by Mast Cells Selected AbstractsComparison of Four Staining Methods for Detection of Mast Cells in Equine Bronchoalveolar Lavage FluidJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2006Mathilde Leclere Mast cells normally are present in equine bronchoalveolar lavage fluid (BALF), but usually represent <2% of all cells in healthy horses. An increased percentage of mast cells has been associated with airway hyperactivity and inflammatory airway diseases, but marked differences are reported between studies in normal and diseased horses. Because an abnormal mast cell count may be of clinical relevance, we compared the ability of a fast Romanowsky method to stain mast cell granules with that of 3 metachromatic stains: automated Romanowsky, May-Grünwald Giemsa, and toluidine blue stains. The BALF cells from 24 horses were studied. A differential cell count was performed blindly on 400 cells. The percentages of mast cells obtained were analyzed by means of repeated-measures analysis of variance and Fischer's PLSD test. The Bland and Altman method was used to assess agreement among stains. The mean percentage of mast cells in BALF was significantly lower with the fast Romanowsky than with the automated Romanowsky, May-Grünwald Giemsa, and toluidine blue stains. With the fast Romanowsky stain, the metachromatic granules of mast cells were not stained, and their identification was based on morphologic criteria. Toluidine blue staining allowed detection of the highest mean percentage of mast cells, but was inadequate for performing a differential cell count on other cell types. In conclusion, fast Romanosky stain may be inadequate for detection of mast cells in equine BALF, whereas automated Romanowsky, May-Grünwald Giemsa, and toluidine blue stains provide metachromatic staining of mast cell granules. [source] Effects of Low Power Laser Irradiation on Intracellular Calcium and Histamine Release in RBL-2H3 Mast CellsPHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 4 2007Wen-Zhong Yang Although laser irradiation has been reported to promote skin wound healing, the mechanism is still unclear. As mast cells are found to accumulate at the site of skin wounds we hypothesized that mast cells might be involved in the biological effects of laser irradiation. In this work the mast cells, RBL-2H3, were used in vitro to investigate the effects of laser irradiation on cellular responses. After laser irradiation, the amount of intracellular calcium ([Ca2+]i) was increased, followed by histamine release, as measured by confocal fluorescence microscopy with Fluo-3/AM staining and a fluorescence spectrometer with o -phthalaldehyde staining, respectively. The histamine release was mediated by the increment of [Ca2+]i from the influx of the extracellular buffer solution through the cation channel protein, transient receptor potential vanilloid 4 (TRPV4). The TRPV4 inhibitor, Ruthenium Red (RR) can effectively block such histamine release, indicating that TRPV4 was the key factor responding to laser irradiation. These induced responses of mast cells may provide an explanation for the biological effects of laser irradiation on promoting wound healing, as histamine is known to have multi-functions on accelerating wound healing. [source] Degranulation of Mast Cells Provokes a Massive Inflammatory Reaction in the Tympanic Membrane,THE LARYNGOSCOPE, Issue 7 2001Per Olof Eriksson MD Abstract Objective The pars flaccida is extremely rich in mast cells. On stimulation the mast cells release preformed and de novo synthesized inflammatory substances. The purpose of this study was to examine how these mast cell substances provoke inflammatory changes in the tympanic membrane. Study Design In vivo, murine model. Methods In a rat model, the mast cell secretagogue compound 48/80 was applied locally to the tympanic membrane on 4 consecutive days and the ensuing inflammatory changes were evaluated by otological, light, and electron microscopy 3, 6, 9, 12, 18, 24, 36, and 48 hours and 4, 6, and 8 days later. Results Degranulation of the mast cells occurred within 3 hours of applying compound 48/80. Release of the mast cell substances coincided with an inflammatory event characterized by a two-stage reaction: an edema stage, peaking 6 hours after application, followed by a massive invasion of inflammatory cells, peaking at 24 and 48 hours. Pars flaccida and pars tensa were both involved, pars flaccida showing the earliest changes. Pars tensa exhibited the same biphasic reaction as pars flaccida, but approximately 6 hours later. Conclusions The mast cells of the pars flaccida have the capacity to elicit an intense inflammation of the tympanic membrane. The biphasic reaction pattern resembles that observed in experimental otitis media, suggesting involvement of the mast cells in this inflammatory condition of the middle ear. [source] Morphological and Immunocytochemical Investigations on Mast Cells in Porcine UreterANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 6 2005A. Vodenicharov Summary Morphological, morphometric, histochemical and immunocytochemical investigations on mast cells, located in the wall of ureter of 8 months aged pigs were performed. Mast cells were found in all three layers of ureteral wall, but their distribution was irregular and the number unequal. It was established that alcian blue (AB)-positive mast cells were significantly more than toluidine blue (TB)-positive mast cells. A statistically significant smaller number of both AB and TB-stained mast cells were observed in the tunica mucosa. The largest number of mast cells was found in the tunica muscularis. In the adventitia, mast cells were higher in number in the main connective tissue than in the connective tissue near the blood vessels. Mast cells stained with TB showed variably expressed , -metachromasia, which was best visible in those situated in the lamina propria of the mucosa. The prevailing parts of mast cells, however, were AB-positive after AB-safranin staining. This was mostly found in mast cells of the tunica muscularis and in mast cells of perivascular location in the tunica adventitia. Immunocytochemically, mast cells were found to be positive for histamine and vasoactive intestinal polypeptide in the muscle coat, and to histamine in the adventitia, as well. On the basis of obtained results it was presumed that the mast cells in porcine ureter most probably took part not only in keeping of local homeostasis, but played also an important role of mobility of smooth muscle cells in the middle layer of ureter on one hand, and, on the other, in the adventitial blood vessels. [source] Dynamics of Mast Cells in Lymph Node Following Antigenic StimulationANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 1 2004D. O. Dabak Summary Dynamics of mast cells in rat cervical lymph nodes were examined using conventional histological techniques after injection of Salmonella paratyphi B-H antigen. There was no significant change in the number of mast cells at sixth hour and on the first day of stimulation compared with the controls. The number of mast cells was increased in all lymph node compartments on the second day of stimulation, which continued in the following 3 days. On the eighth day of stimulation, although the mast cell number decreased in the subcapsular area, it was still high in the paracortical area and medullary sinuses of the lymph nodes. On the second day of stimulation, the mast cell number was apparently increased in the subcapsular area than those of the other compartments. In the following days of stimulation, the highest number of mast cells was seen in the medullary sinuses. The highest paracortical mast cell number was determined on the third day of stimulation and some mast cells were observed near the high endothelial venules (HEVs). The changes of mast cell number among the lymph node compartments after antigenic stimulation support the hypothesis that the migration of mast cells occurred. This migration pattern indicates that mast cells enter the lymph node via afferent lymphatics and migrate to the lymph node compartments following antigenic stimulation. [source] Mast cell adhesion to bronchial smooth muscle in asthma specifically depends on CD51 and CD44 variant 6ALLERGY, Issue 8 2010P.-O. Girodet To cite this article: Girodet P-O, Ozier A, Trian T, Begueret H, Ousova O, Vernejoux J-M, Chanez P, Marthan R, Berger P, Tunon de Lara JM. Mast cell adhesion to bronchial smooth muscle in asthma specifically depends on CD51 and CD44 variant 6. Allergy 2010; 65: 1004,1012. Abstract Background:, Mast cells infiltrate the bronchial smooth muscle (BSM) in asthmatic patients, but the mechanism of mast cell adhesion is still unknown. The adhesion molecules CD44 (i.e. hyaluronate receptor) and CD51 (i.e. vitronectin receptor) are widely expressed and bind to many extracellular matrix (ECM) proteins. The aims of the study are (i) to identify the role of ECM in mast cell adhesion to BSM and (ii) to examine the role of CD51 and CD44 in this adhesion. Methods:, Human lung mast cells, human mast cell line (HMC-1), and BSM cells from control donors or asthmatic patients were cultured in the presence/absence of various cytokines. Mast cell,BSM interaction was assessed using 3H-thymidine-pulsed mast cells, confocal immunofluorescence, or electron microscopy. Adhesion molecules expression and collagen production on both cell types were evaluated by quantitative RT-PCR, western blot, and flow cytometry. Results:, Mast cell adhesion to BSM cells mostly involved type I collagen of the ECM. Such an adhesion was increased in normal BSM cells under inflammatory condition, whereas it was maximal in asthmatic BSM cells. Blockade of either CD51 or CD44 significantly decreased mast cell adhesion to BSM. At the molecular level, protein and the transcriptional expression of type I collagen, CD51 or CD44 remained unchanged in asthmatic BSM cells or in mast cells/BSM cells under inflammatory conditions, whereas that of CD44 variant isoform 6 (v6) was increased. Conclusions:, Mast cell,BSM cell adhesion involved collagen, CD44, and CD51, particularly under inflammatory conditions. CD44v6 expression is increased in asthmatic BSM cells. [source] Mast cell,derived tryptase inhibits apoptosis of human rheumatoid synovial fibroblasts via rho-mediated signalingARTHRITIS & RHEUMATISM, Issue 4 2010Norifumi Sawamukai Objective An abundance of mast cells are found in the synovium of patients with rheumatoid arthritis (RA). However, the role of mast cells in the pathogenesis of RA remains unclear. This study was undertaken to elucidate a role for mast cells in RA by investigating the antiapoptotic effects of tryptase, a major product of mast cells, on RA synovial fibroblasts (RASFs). Methods RA synovial tissue was obtained from RA patients during joint replacement surgery, and histologic changes in the tissue were examined. The expression of cell surface molecules and apoptotic markers on RASFs were detected by flow cytometry. Rho activation was determined using a pull-down assay. Results Mast cells, bearing both c-Kit and tryptase, accumulated in the sublining area of proliferating synovial tissue from RA patients. Protease-activated receptor 2 (PAR-2), a receptor for tryptase, was expressed on RASFs in the lining area, close to tryptase-positive mast cells in the RA synovium. Fas-mediated apoptosis of RASFs was significantly inhibited, in a dose-dependent manner, by the addition of tryptase, and this effect correlated with increased activation of Rho kinase. Furthermore, Y27632, a Rho kinase inhibitor, reduced the antiapoptotic effect of tryptase on RASFs, suggesting that Rho was responsible for the antiapoptotic effects of tryptase. Conclusion These results demonstrate that tryptase has a strong antiapoptotic effect on RASFs through the activation of Rho. Thus, we propose that the release of tryptase by mast cells leads to the binding of tryptase to PAR-2 on RASFs and inhibits the apoptosis of RASFs via the activation of Rho. Such mechanisms could play a pivotal role in the marked proliferation of RASFs and hyperplasia of synovial tissue seen in RA synovium. [source] Association of mast cells with tumor angiogenesis in esophageal squamous cell carcinomaDISEASES OF THE ESOPHAGUS, Issue 2 2001M. Tomita The association of mast cells with tumor angiogenesis was investigated in patients with esophageal squamous cell carcinoma. Surgical specimens from 48 patients with esophageal squamous cell carcinoma were studied. Mast cells in tumor sections were stained with Alcian blue and safranin O. The number of mast cells was counted under light microscopy and the average count recorded. To highlight the microvessels, endothelial cells were stained with anti-human factor VIII antibody. Microvessel density was also counted. We found a significant correlation between mast cell count and microvessel density in patients with esophageal squamous cell carcinoma. Double staining of the microvessels revealed highly angiogenic areas densely populated with mast cells. There appears to be a direct correlation between the number of mast cells and tumor angiogenesis in patients with esophageal squamous cell carcinoma. [source] Osteopontin is produced by mast cells and affects IgE-mediated degranulation and migration of mast cellsEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 2 2008Akiko Nagasaka Abstract Osteopontin (OPN), originally discovered in bone as an extracellular matrix protein, was identified in many cell types in the immune system, presumably being involved in many aspects of pathogenesis of inflammatory and immune diseases. Mast cells are also involved in such pathological aspects by secreting multiple mediators. However, it has not been determined whether mast cells produce OPN and whether it affects their function. To test this, we used murine fetal skin-derived cultured mast cells (FSMC) and bone marrow-derived cultured mast cells. We found that OPN was spontaneously produced by FSMC and inducible by ionomycin and Fc,RI aggregation in bone marrow-derived cultured mast cells. In the presence of mast cell growth factors, FSMC were similarly generated from both OPN-deficient (OPN,/,) and -sufficient (OPN+/+) mice without significant differences in yield, purity, granularity, and viability. Using OPN,/, FSMC, we found that recombinant OPN augmented IgE-mediated degranulation and induced FSMC chemotaxis. Both effects were mediated by OPN receptors (i.e. CD44 and integrin,,v). IgE-mediated passive cutaneous anaphylaxis was significantly reduced in OPN,/, mice compared with OPN+/+ mice, indicating physiological relevance of OPN. These results indicate that OPN is a mast cell mediator, enhances mast cell responses to antigen, and thus may influence mast cell-related pathological conditions. See accompanying commentary at http://dx.doi.org/10.1002/eji200738131 [source] Mast cells play a key role in the developmentof late airway hyperresponsiveness through TNF-,in a murine model of asthmaEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 4 2007Young-Suk Kim Abstract We have investigated the role of TNF-, in mast cell-mediated late airway hyperresponsiveness (AHR) using mast cell-deficient WBB6F1- W/Wv (W/Wv) mice in a murine model of asthma, which exhibits a biphasic increase in AHR. TNF-, levels in the airway and magnitude of late AHR in response to airway allergen challenge were severely impaired in W/Wv mice compared to their littermates. In addition to TNF-,, cytosolic phospholipase A2 (cPLA2) phosphorylation and enzymatic activity in the lungs were also impaired in W/Wv mice. Either anti-TNF-, antibody or an inhibitor of cPLA2 abolished late AHR in congeneic +/+ mice. Intratracheal administration of TNF-, resulted in increases in late AHR, cPLA2 phosphorylation, cPLA2 activity, and phosphorylation of mitogen-activated protein kinases. Mast cell replacement restored airway TNF-, level, cPLA2 phosphorylation and enzymatic activity in the lungs as well as late AHR in W/Wv mice. These data indicate that mast cells play a key role in the development of late AHR through liberation of TNF-,. [source] Mast cells: novel clinical perspectives from recent insightsEXPERIMENTAL DERMATOLOGY, Issue 5 2009Manfred Kneilling Abstract:, Mast cells are still generally viewed as mediators of type I allergic or pseudoallergic reactions. Research over the past 10 years revealed that our view was too small and that mast cells are of key importance in innate immunity and also types II, III and IV adaptive immune reactions. Understanding their role in modulating and amplifying of inflammatory responses provides important insights into the pathogenesis of skin diseases such as psoriasis, atopic dermatitis, bullous pemphigoid or the control of infections. This helps us to understand the course of these diseases, their trigger mechanisms, and, the new role of agents, which can modulate the function of mast cells. These insights will help to develop new therapeutic approaches. [source] Exploring the mast cell enigma: a personal reflection of what remains to be doneEXPERIMENTAL DERMATOLOGY, Issue 2 2008Beate M. Henz Abstract: Mast cells are traditionally viewed as effector cells of allergic reactions and parasitic diseases, but their importance in host defense against bacteria, in tissue remodelling, their bone marrow and stem cell origin and a central role of the stem cell factor (SCF) as mast cell growth and chemotactic factor has been worked out only in recent years. Despite this, major aspects about the nature of the cells and their role in disease remain unclear. This holds in particular for the identification of mast cell precursors and the role of growth factors that stimulate specific mast cell commitment from stem cells, such as nerve growth factor, neutrotrophin-3 and certain interleukins, alone and during interaction with SCF. Early data suggesting also an involvement of specific transcription factors need to be expanded in this process. Furthermore, although mast cell proliferative disease (mastocytosis) has been shown to be often associated with SCF receptor c-kit mutations, reasons for the development of this disease remain unclear. This holds also for mast cell release mechanisms in many types of mast cell-dependent urticaria. Exciting new insights are emerging regarding the role of mast cells in bacterial infections, in defense against tumors, in wound healing and in the interplay with the nervous system, with hormones, and in the neurohormonal network. The aim of this reflection is to delineate the many known and unknown aspects of mast cells, with a special focus on their development, and to discuss in detail two mast cell-related diseases, namely mastocytosis and urticaria. [source] Mast cells and their role in the neuro-immune-endocrine axisEXPERIMENTAL DERMATOLOGY, Issue 9 2004J. Bienenstock It has become clear that the immune and nervous systems communicate constantly to maintain homeostasis and a coordinated and continuing adaptive response to an ever-changing environment. Evidence from mast cell nerve communication, as an example of this interaction, has been obtained in a variety of tissues and circumstances, most especially in the intestine and skin. Bidirectional communication has been shown in vivo, ex vivo, in vitro and in coculture experiments involving the two cell types. Examples will be given of these various situations and involve normal physiological situations and those involved in response to infection and inflammation as well as in response to ultraviolet light. More recent examples of the importance of mast cells in the regulation of central nervous activity including the secretion of hormones by the pituitary gland, and thereby the regulation of the HPA axis as well as involvement in behavioural change will be addressed. Through its potential communication with the nervous system, the mast cell can be regarded as a sentinel cell or receptor, especially located at surfaces exposed to the environment, which specifically and non-specifically react to molecules and substances, foreign to the organism, so as to help orchestrate the complex and integrated responses required to maintain homeostasis. [source] Synovial mast cells: role in acute and chronic arthritisIMMUNOLOGICAL REVIEWS, Issue 1 2007Peter A. Nigrovic Summary:, Mast cells reside in the normal synovium and increase strikingly in number in rheumatoid arthritis and other joint diseases. Given the broad spectrum of activity of this lineage, it has for decades been considered probable that mast cells are involved in the pathophysiology of synovitis. Recent work in murine arthritis has substantiated this suspicion, showing that mast cells can contribute importantly to the initiation of inflammatory arthritis. However, the role of the greatly expanded population of synovial mast cells in established arthritis remains unknown. Here we review the current understanding of mast cell function in acute arthritis and consider the potentially important influence of this cell on key processes within the chronically inflamed synovium, including leukocyte recruitment and activation, fibroblast proliferation, angiogenesis, matrix remodeling, and injury to collagen and bone. We also consider recent evidence supporting an immunomodulatory or anti-inflammatory role for mast cells as well as pharmacologic approaches to the mast cell as a therapeutic target in inflammatory arthritis. [source] Mast cells and eicosanoid mediators: a system of reciprocal paracrine and autocrine regulationIMMUNOLOGICAL REVIEWS, Issue 1 2007Joshua A. Boyce Summary:, When activated by specific antigen, complement, or other transmembrane stimuli, mast cells (MCs) generate three eicosanoids: prostaglandin (PG)D2, leukotriene (LT)B4, and LTC4, the parent molecule of the cysteinyl leukotrienes (cysLTs). These diverse lipid mediators, which are generated from a single cell membrane-associated precursor, arachidonic acid, can initiate, amplify, or dampen inflammatory responses and influence the magnitude, duration, and nature of subsequent immune responses. PGD2 and cysLTs, which were originally recognized for their bronchoconstricting and vasoactive properties, also serve diverse and pivotal functions in effector cell trafficking, antigen presentation, leukocyte activation, matrix deposition, and fibrosis. LTB4 is a powerful chemoattractant for neutrophils and certain lymphocyte subsets. Thus, MCs can contribute to each of these processes through eicosanoid generation. Additionally, MCs express G-protein-coupled receptors specific for cysLTs, LTB4, and another eicosanoid, PGE2. Each of these receptors can regulate MC functions in vivo by autocrine and paracrine mechanisms. This review focuses on the biologic functions for MC-associated eicosanoids, the regulation of their production, and the mechanisms by which eicosanoids may regulate MC function in host defense and disease. [source] Synaptotagmin regulates mast cell functionsIMMUNOLOGICAL REVIEWS, Issue 1 2001Dana Baram Summary: Synaptotagmin(s) (Syts), are products of a gene family implicated in the control of Ca2+ -dependent exocytosis. Mast cells, specialized secretory cells that release mediators of inflammatory and allergic reactions in a process of regulated exocytosis, express Syt homologues and SNAREs (Soluble NSF Attachment proteins Receptors), which together with Syt constitute the core complex which mediates exocytotic vesicle docking and fusion. Rat basophilic leukemia cells (RBL-2H3), a tumor analogue of mucosal mast cells, express the Syt homologues Syt II, Syt III and Syt V. Expression of Syt I, the neuronal Ca2+ sensor, in the RBL cells, resulted in its targeting to secretory granules and in prominent potentiation and acceleration of Ca2+ -dependent exocytosis. Syt II is localized to an amine-free lysosomal compartment, which is also subjected to regulated exocytosis. Lysosomal exocytosis is negatively regulated by Syt II: overexpression of Syt II inhibited Ca2+ -triggered exocytosis of lysosomes, while suppression of Syt II expression markedly potentiated this release. These findings implicate Syt homologues as key regulators of mast cell function. We thank Drs. T.C. Sudhof, R.H. Scheller and M. Takahashi for their generous gifts of antibodies and cDNAs. [source] Normal and abnormal secretion by haemopoietic cellsIMMUNOLOGY, Issue 1 2001Jane C. Stinchcombe Summary The secretory lysosomes found in haemopoietic cells provide a very efficient mechanism for delivering the effector proteins of many immune cells in response to antigen recognition. Although secretion shows some similarities to the secretion of specialized granules in other secretory cell types, some aspects of secretory lysosome release appear to be unique to melanocytes and cells of the haemopoietic lineage. Mast cells and platelets have provided excellent models for studying secretion, but recent advances in characterizing the immunological synapse allow a very fine dissection of the secretory process in T lymphocytes. These studies show that secretory lysosomes are secreted from the centre of the talin ring at the synapse. Proper secretion requires a series of Rab and cytoskeletal elements which play critical roles in the specialized secretion of lysosomes in haemopoietic cells. [source] Mast cells and transforming growth factor-, expression: a possible relationship in the development of porphyria cutanea tarda skin lesionsINTERNATIONAL JOURNAL OF DERMATOLOGY, Issue 6 2008Glalcyara Lançoni MD Background, Porphyria cutanea tarda (PCT) is a metabolic disease characterized by vesicles and blisters in sun-exposed areas and scleroderma-like lesions in sun-exposed and non-sun-exposed areas. Mast cells participate in the pathogenesis of bullous diseases and diseases that show sclerosis, including PCT. Moreover, transforming growth factor-, (TGF-,) is the main cytokine in the development of tissue sclerosis. The correlation of mast cells and TGF-, with the lesions of PCT has not been examined, however. The possible role of mast cells and TGF-, (and the relationship between them) in the development of PCT lesions is discussed. Methods, To quantify mast cells and cells expressing TGF-, in skin samples from patients with PCT and controls, immunohistochemical studies were performed in tissue sections allied to morphometric analyses. Results, The numbers of mast cells and cells expressing TGF-, per square millimiter were increased in the PCT group relative to controls, and there was a direct and significant correlation between the mast cell number and cells expressing TGF-, in PCT. Conclusions, The results suggest that the increased number of mast cells and of cells expressing TGF-,, as well as their direct correlation, may contribute to the pathogenesis of the skin lesions in PCT. [source] Mast cells in the amphibian brain during developmentJOURNAL OF ANATOMY, Issue 3 2010Claudia Pinelli Abstract This is the first descriptive study of ontogenesis and anatomical distribution of mast cells in the developing brain of three different amphibian species. In the toad and the green frog, mast cells are preferentially located in: (i) the meningeal lining (pia mater), (ii) the choroid plexuses, both anterior and posterior, and (iii) the neuropil, in close association with the epithelial cell lining of blood vessels. It is only in the perennially aquatic African clawed frog that mast cells never appear inside brain ventricles and within the neuropil. Mast cells first become identifiable in brain of different species in different stages of development. While there are differences in the number of mast cells in different species at different stages of development, the number nearly doubles in all three species during the transition from pro-metamorphic stage of larval development to the peak of metamorphic climax. Furthermore, the number of mast cells is comparatively higher in the toad and remarkably lower in the fully aquatic Xenopus laevis, in which species the first appearance of identifiable mast cells during larval development occurs much later than in equivalent stages of development of the toad and the green frog. The secretory nature of mast cells can be assumed by the presence of cytoplasmic granules, which may show species-specific texture. Further experimental analyses are required to unveil the usefulness of mast cells in the amphibian brain. [source] Consequences of eicosapentaenoic acid (n-3) and arachidonic acid (n-6) supplementation on mast cell mediatorsJOURNAL OF ANIMAL PHYSIOLOGY AND NUTRITION, Issue 7-8 2004T. Gueck Summary Mast cells are important players in the pathogenesis of atopic diseases. These cells release immediate-phase and late-phase mediators of inflammation. Fatty acids are incorporated in cellular membranes and therefore seem to influence mediator production and release. A study was conducted to assess the effects of eicosapentaenoic acid (EPA, 20:5n-3) and arachidonic acid (AA, 20:4n-6) on mast cell mediators in a canine mastocytoma cell line (C2). Cells were cultured in a basic medium (Dulbecco's modified Eagle's medium/HAM's F12 1 : 1, DEH), DEH supplemented with 14.0 ,m EPA (DEH-EPA) or 14 ,m AA (DEH-AA). The DEH-AA cultured cells had increased spontaneous and mastoparan-stimulated PGE2 production and histamine release. Furthermore, the tryptase activity was increased. The DEH-EPA cultured cells rendered elevated levels of PGE2 and histamine release compared with DEH only after stimulation. These levels were significantly lower in comparison to DEH-AA. The increased PGE2 production of C2 cultured in DEH-AA is the consequence of the AA enrichment, because AA is the precursor of PGE2. However, the different effects by AA and EPA on mast cell mediators possibly reflect the higher susceptibility of long chain polyunsaturated fatty acids (PUFA) to undergo lipid peroxidation, because it is known that altered cellular redox state influences mediator production and release. [source] Neovascularization and mast cells with tryptase activity increase simultaneously in human pterygiumJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 3 2007Domenico Ribatti Abstract Mast cells (MC) have been implicated in both normal and pathological angiogenesis, such as that in chronic inflammatory diseases and tumors. This assumption is partially supported by the close structural association between MC and blood vessels and the recruitment of these cells during tumor growth. MC release a number of angiogenic factors among which tryptase, a serine protease stored in MC granules, is one of the most active. In this study, we correlate the extent of angiogenesis with the number of tryptase-reactive MC in tissue fragments from pterygium and normal bulbar conjunctiva investigated by immunohistochemistry, using two murine monoclonal antibodies against the endothelial cell marker CD31 and the MC marker tryptase. Angiogenesis, measured as microvessel density, was highly correlated with MC tryptase-positive cell count in pterygium tissues. These results suggest that the characteristic neovascularization observed in pterygium may be sustained, at least in part, by MC angiogenic mediators, in particular tryptase. [source] Nitric oxide synthesis inhibition alters rat cutaneous wound healingJOURNAL OF CUTANEOUS PATHOLOGY, Issue 7 2006Thaís P. Amadeu Background:, Nitric oxide (NO) is an important molecule that participates in wound repair, but its effects on cutaneous wound healing are not well understood. The aim of this study was to investigate the effects of NO synthesis blockade on rat cutaneous wound healing by the administration of NG -nitro- l -arginine methyl ester (l -NAME), a non-selective inhibitor of NO synthases. Methods:, NO synthesis was inhibited by administration of l -NAME (20 mg/kg/day) in drinking water. An excisional wound was done, and the animals were killed 7, 14, and 21 days later. Wound contraction and blood pressure were evaluated. The lesion and adjacent skin were formalin fixed and paraffin embedded. Mast cells were quantified, and vessels were evaluated using stereological methods. Results:,l -NAME-treated animals presented delayed wound contraction, alterations in collagen organization, and neoepidermis thickness. The inhibition of NO synthesis increased mast cell migration 7 days after wounding, but decreased 21 days after wounding. Volume density of vessels was decreased in l -NAME-treated animals, 21 days after lesion. Surface density of vessels was frequently smaller in l -NAME-treated animals than in controls. Conclusion:, The blockade of NO synthesis impaired cutaneous wound healing, acting in early and late phases of wound repair. [source] Host response to the chondracanthid copepod Chondracanthus goldsmidi, a gill parasite of the striped trumpeter, Latris lineata (Forster), in TasmaniaJOURNAL OF FISH DISEASES, Issue 3 2010M Andrews Abstract The chondracanthid copepod, Chondracanthus goldsmidi is an ectoparasite of gills, inner opercula and nasal cavities of cultured striped trumpeter, Latris lineata (Forster). Whilst often present in high numbers (up to 60 parasites per host), little is known about its effect on striped trumpeter. In this study C. goldsmidi was associated with extensive epithelial hyperplasia and necrosis. Pathological changes were most pronounced near the parasite's attachment site, with papilloma-like growths surrounding the entire parasite resulting in deformation of the filament. The number of mucous cells increased near the parasite attachment sites on both the opercula and gills. Mast cells were absent in healthy gills; in contrast numerous mast cells were identified in the papilloma-like growths. Immunostaining identified piscidin-positive mast cells in the papilloma-like growths, presenting the first evidence of piscidin in the family Latridae. [source] Deficiency of KIT-positive cells in the colon of patients with diabetes mellitusJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2002MASANORI NAKAHARA Abstract Background Diabetes mellitus is a well-known cause of gastrointestinal dysmotility. The pathogenesis of diabetic gastroenteropathy is mainly considered to be a neuropathy, but the cause of dysmotility remains unknown. Interstitial cells of Cajal (ICC), which express c-kit receptor tyrosine kinase (KIT), are considered to be pacemaker cells for the gastrointestinal movement. Therefore, we investigated a possible involvement of ICC in the pathogenesis of diabetic gastroenteropathy in humans. Methods The KIT-positive cells in the proper muscle layer of the colon were detected by immunohistochemistry in patients with diabetes mellitus and normal control subjects. Mast cells, which are also known to express KIT, were detected by staining with Alcian blue. The numbers of KIT-positive cells and Alcian blue-positive cells in the proper muscle layer were counted under the microscope and the number of KIT-positive cells apart from Alcian blue-positive cells was calculated. Results In the normal control subjects, KIT-positive cells were located at the myenteric plexus region and in the circular muscle layer of the colon. Their distribution pattern was similar to that of ICC. The average number of KIT-positive cells, apart from mast cells (which reflects the number of ICC), in patients with diabetes mellitus was approximately 40% of that found in normal subjects. Conclusions Deficiency of ICC might be related to the pathogenesis of diabetic gastroenteropathy in humans. [source] Mast cells and IgE-containing cells in gastric mucosa of Helicobacter pylori infected and non-infected patients with chronic urticariaJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 1 2004M Liutu ABSTRACT Background, Several studies have indicated that antibiotic therapy aimed at eradication of Helicobacter pylori has effects on symptoms of chronic urticaria (CU) patients. However, the possible connections and pathomechanism by which H. pylori might be linked to CU have remained largely unknown. The IgE-mediated pathway might be a possible link between H. pylori infection and CU. We therefore clarified the role of H. pylori as an inducer of IgE response. Materials and methods, Gastroscopy was performed and mucosal biopsy specimens were taken to evaluate the histology, as well as the presence of H. pylori bacteria, mast cells and IgE-containing cells in the antral mucosa, in 21 CU patients. Controls (n = 48) included 19 patients with lichen planus, nine patients with atopic dermatitis and 20 patients with no skin or allergic disease. Results, The mean densities of IgE-containing cells were significantly higher in H. pylori- infected patients and in patients with skin disease compared to non- H. pylori -infected patients with no skin or allergic disease. No significant difference was found in the number of IgE-containing cells between H. pylori -infected and non-infected patients with CU. There was no significant difference in the mean densities of mast cells in the different patient groups. Conclusions, Our findings suggest that H. pylori gastritis leads to increased IgE production. However, we could not show a significant difference in IgE staining between H. pylori -infected and non-infected patients with CU. [source] Duodenal mastocytosis, eosinophilia and intraepithelial lymphocytosis as possible disease markers in the irritable bowel syndrome and functional dyspepsiaALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 7 2009M. M. WALKER Summary Background, Irritable bowel syndrome (IBS) and functional dyspepsia (FD) are common functional disorders without defined pathology. Mast cells and eosinophils interact with T lymphocytes and may alter enteric nerve and smooth muscle function. Aim, To examine mast cell, eosinophil and intraepithelial lymphocyte populations in duodenal biopsies of subjects with IBS and FD. Methods, A random sample of an adult Swedish population (n = 1001; mean age 54 years; 51% female) underwent upper endoscopy and biopsy; 51 cases with FD and 41 cases with IBS were compared with 48 randomly selected controls. Eosinophils were identified by light microscopy; mast cells by immunocytochemistry (CD117). Intraepithelial lymphocytes were counted per 100 enterocytes. Cell counts were quantified by counting the number per high power field (HPF) in 5HPFs in the bulb (D1) and second part of duodenum (D2), summed over 5HPFs at each site. Results, Cases and controls showed similar demographics. Compared to controls, IELs in IBS-constipation were significantly increased (P = 0.005). Mast cells were significantly increased in IBS in D2 (P < 0.001), while eosinophils were significantly increased in FD in D1 and D2 (P < 0.001). Conclusion, Duodenal mast cell hyperplasia is linked to IBS and eosinophilia to FD, and duodenal biopsy may identify subsets of these disorders. [source] Comparison of Four Staining Methods for Detection of Mast Cells in Equine Bronchoalveolar Lavage FluidJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2006Mathilde Leclere Mast cells normally are present in equine bronchoalveolar lavage fluid (BALF), but usually represent <2% of all cells in healthy horses. An increased percentage of mast cells has been associated with airway hyperactivity and inflammatory airway diseases, but marked differences are reported between studies in normal and diseased horses. Because an abnormal mast cell count may be of clinical relevance, we compared the ability of a fast Romanowsky method to stain mast cell granules with that of 3 metachromatic stains: automated Romanowsky, May-Grünwald Giemsa, and toluidine blue stains. The BALF cells from 24 horses were studied. A differential cell count was performed blindly on 400 cells. The percentages of mast cells obtained were analyzed by means of repeated-measures analysis of variance and Fischer's PLSD test. The Bland and Altman method was used to assess agreement among stains. The mean percentage of mast cells in BALF was significantly lower with the fast Romanowsky than with the automated Romanowsky, May-Grünwald Giemsa, and toluidine blue stains. With the fast Romanowsky stain, the metachromatic granules of mast cells were not stained, and their identification was based on morphologic criteria. Toluidine blue staining allowed detection of the highest mean percentage of mast cells, but was inadequate for performing a differential cell count on other cell types. In conclusion, fast Romanosky stain may be inadequate for detection of mast cells in equine BALF, whereas automated Romanowsky, May-Grünwald Giemsa, and toluidine blue stains provide metachromatic staining of mast cell granules. [source] Expression and release of IL-29 by mast cells and modulation of mast cell behavior by IL-29ALLERGY, Issue 10 2010S. He To cite this article: He S, Zhang H, Chen H, Yang H, Huang T, Chen Y, Lin J, Wang F, Chen X, Li T-L, Yang P. Expression and release of IL-29 by mast cells and modulation of mast cell behavior by IL-29. Allergy 2010; 65: 1234,1241. Abstract Background:, The role of interleukin (IL)-29 in innate immunity has been recognized recently, and it is regarded as a potent bioactive molecule. However, little is known about its role in the pathogenesis of allergy. Because mast cells are recognized as primary effector cells of allergy, we investigated the potential relationship between IL-29 and mast cells in this study. Objective:, To examine the expression of IL-29 in mast cells and the influence of IL-29 on mast cell mediator release and accumulation. Methods:, Expression of IL-29 in mast cells was determined by double-labeling immunohistochemistry and flow cytometry analysis. Mast cell cell-line was cultured to examine the mediator release, and mouse peritoneal model was employed to observe the mast cell accumulation. Results:, Large proportions of mast cells expressing IL-29 were localized in human tissue including the colon, tonsil and lung. Mast cells can release substantial quantity of IL-29 upon challenge with proteolytic allergens. Extrinsic IL-29 provoked IL-4 and IL-13 release from mast cell line P815 cells through PI3K/Akt and (JAK)/STAT3 signaling pathways, but failed to induce mast cell histamine release from human mast cells. Extrinsic IL-29 also induced mast cell infiltration in mouse peritoneum by a CD18- and ICAM1-dependent mechanism. Conclusion:, Mast cell-derived IL-29 has the potential to be involved in the pathogenesis of allergic inflammation. [source] A granular variant of CD63 is a regulator of repeated human mast cell degranulationALLERGY, Issue 10 2010T. Schäfer To cite this article: Schäfer T, Starkl P, Allard C, Wolf RM, Schweighoffer T. A granular variant of CD63 is a regulator of repeated human mast cell degranulation. Allergy 2010; 65: 1242,1255. Abstract Background:, Mast cells are secretory immune cells whose degranulation can provoke acute allergic reactions. It is presently unclear, however, whether an individual mast cell can repeatedly degranulate or turns dysfunctional after a single antigen stimulus. This work thus aims to better define the mast cell life cycle, with particular focus on new target structures for therapeutic or diagnostic approaches in allergy. Methods:, Monoclonal antibodies were raised against degranulated cord blood-derived human mast cells. A subset of these antibodies that exclusively recognized degranulated mast cells, but did not cross-react with quiescent mast cells or other hematopoietic cell types, became key reagents in subsequent experiments. Results:, We identified a granular variant of tetraspanin CD63 as an exclusive molecular marker of degranulated human mast cells. Mutant analyses indicate that a cysteine cluster around residue C170 and protein glycosylation at residue N172 account for the antibody specificity. Here, we show that mast cells, which underwent an initial Fc,RI-mediated degranulation, can be degranulated for at least another cycle in vitro. Repeated degranulation, however, requires an IgE/antigen stimulus that differs from the preceding one. Furthermore, the new variant-specific anti-CD63 antibodies effectively impair repeated cycles of mast cell degranulation. Conclusion:, Our findings indicate that mast cells are stable, multiple-use cells, which are capable of surviving and delivering several consecutive hits. Surface expression of the novel CD63 variant is a distinguishing feature of such primed cells. Reagents directed against this molecular hallmark may thus become valuable diagnostic and therapeutic agents. [source] Mast cell adhesion to bronchial smooth muscle in asthma specifically depends on CD51 and CD44 variant 6ALLERGY, Issue 8 2010P.-O. Girodet To cite this article: Girodet P-O, Ozier A, Trian T, Begueret H, Ousova O, Vernejoux J-M, Chanez P, Marthan R, Berger P, Tunon de Lara JM. Mast cell adhesion to bronchial smooth muscle in asthma specifically depends on CD51 and CD44 variant 6. Allergy 2010; 65: 1004,1012. Abstract Background:, Mast cells infiltrate the bronchial smooth muscle (BSM) in asthmatic patients, but the mechanism of mast cell adhesion is still unknown. The adhesion molecules CD44 (i.e. hyaluronate receptor) and CD51 (i.e. vitronectin receptor) are widely expressed and bind to many extracellular matrix (ECM) proteins. The aims of the study are (i) to identify the role of ECM in mast cell adhesion to BSM and (ii) to examine the role of CD51 and CD44 in this adhesion. Methods:, Human lung mast cells, human mast cell line (HMC-1), and BSM cells from control donors or asthmatic patients were cultured in the presence/absence of various cytokines. Mast cell,BSM interaction was assessed using 3H-thymidine-pulsed mast cells, confocal immunofluorescence, or electron microscopy. Adhesion molecules expression and collagen production on both cell types were evaluated by quantitative RT-PCR, western blot, and flow cytometry. Results:, Mast cell adhesion to BSM cells mostly involved type I collagen of the ECM. Such an adhesion was increased in normal BSM cells under inflammatory condition, whereas it was maximal in asthmatic BSM cells. Blockade of either CD51 or CD44 significantly decreased mast cell adhesion to BSM. At the molecular level, protein and the transcriptional expression of type I collagen, CD51 or CD44 remained unchanged in asthmatic BSM cells or in mast cells/BSM cells under inflammatory conditions, whereas that of CD44 variant isoform 6 (v6) was increased. Conclusions:, Mast cell,BSM cell adhesion involved collagen, CD44, and CD51, particularly under inflammatory conditions. CD44v6 expression is increased in asthmatic BSM cells. [source] | |||||||||||||||||||||||||||||||||||||||||||