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Mast Cell Number (mast + cell_number)
Selected AbstractsEpithelioid cell histiocytoma , histogenetic and kinetics analysis of dermal microvascular unit dendritic cell subpopulationsJOURNAL OF CUTANEOUS PATHOLOGY, Issue 7 2003Jeffrey S. Silverman Background:, Epithelioid cell histiocytoma (ECH), also known as epithelioid fibrous histiocytoma, is a peculiar dermal tumor, which can mimic melanocytic, vascular, epithelial, or other histiocytic lesions. Thought to arise from dermal dendrocytes, most ECH contain approximately 50% FXIIIa+ histiocytic dendrocytes, but not all lesional cells express FXIIIa. A putative fibroblastic component has not been characterized. Methods:, We analyzed the differentiation and cell kinetics of dermal microvascular unit cells in 12 previously reported ECH using antibodies to FXIIIa, CD68 (KP1), CD34, CD117, CD31, smooth muscle actin, collagen type 1 aminopropeptide, and MIB-1, using single and double immunostains. Results:, In ECH, many variably sized CD34/CD31+ tumor vessels with actin+ myopericytes were surrounded by epithelioid-to-dendritic cells of three types. About 5,80% were dendritic histiocytes that expressed FXIIIa but not CD31 or KP1. Fibroblasts, in some cases showing mild nuclear pleomorphism, were usually collagen type 1+, but CD34 and actin, in 11/12 cases. One ,early' ECH had 40% CD34+ epithelioid cells, admixed with 50% FXIIIa+ histiocytes. Most ECH had about 2,20% KP1+, CD117+ mast cells. Mast cell numbers increased with FXIIIa+ histiocyte numbers and the intensity of FXIIIa expression. MIB-1/FXIIIa double-labeling showed only rare cycling histiocytes, with numerous cycling fibroblasts and endothelial cells. Conclusions:, Our findings support the impression that ECH is a vascular fibrous histiocytoma. The constituent cells appear to arise from the activation of resident microvascular CD34+ dermal fibroblasts and the accumulation of FXIIIa+ dendritic stromal assembly histiocytes. The CD34+ cells appear to differentiate toward collagenous fibrocytes in association with histiocytes and mast cells in forming collagenous stroma and vessels. ECH is a tumor composed of all requisite cell types consistent with the origin from the dermal microvascular unit. [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] Mucosal mast cells mediate motor response induced by chronic oral exposure to ovalbumin in the rat gastrointestinal tractNEUROGASTROENTEROLOGY & MOTILITY, Issue 1 2010E. Traver Abstract, We previously demonstrated that oral chronic exposure to ovalbumin (OVA) causes intestinal hypermotility in Sprague-Dawley rats. In this study, the objective was to determine the mechanism of action of OVA and the role of mucosal mast cells in the regulation of motor activity in this model. Rats were orally exposed to OVA during 6 weeks. Intestinal mucosal mast cells (IMMCs) were counted and rat mast cell protease II (RMCPII) measured in duodenum, jejunum, ileum and colon. Anti-OVA IgE, IgG, and IL-4 were measured in serum. Eosinophils and IgE+ cells were counted in jejunum. In an additional study rats were treated with the mast cell stabilizer ketotifen and mast cell number, RMCPII concentration and motor activity in vitro were evaluated. OVA exposed rats showed an increase in mucosal mast cell number and in RMCPII content in small intestine and colon. However, variables of a Th2 type response were not affected by exposure to OVA: (i) neither OVA specific IgE nor IgG were found; (ii) IL-4 did not increase and, (iii) the number of eosinophils and IgE+ cells was identical in the exposed and unexposed groups. These results brought us to hypothesize a possible non-Ig-mediated action of OVA on mast cells. Ketotifen significantly diminished the response to OVA: Ketotifen reduced the number of mast cells and the RMCPII content and blocked increased intestinal contractility. In addition ketotifen modified motor response in both OVA exposed and unexposed animals giving evidence of the importance of mast cells in intestine motor activity driving. [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] Lesional and nonlesional skin from patients with untreated juvenile dermatomyositis displays increased numbers of mast cells and mature plasmacytoid dendritic cellsARTHRITIS & RHEUMATISM, Issue 9 2010Sheela Shrestha Objective To investigate the distribution of mast cells and dendritic cell (DC) subsets in paired muscle and skin (lesional/nonlesional) from untreated children with juvenile dermatomyositis (DM). Methods Muscle and skin biopsy samples (4 skin biopsy samples with active rash) from 7 patients with probable/definite juvenile DM were compared with muscle and skin samples from 10 healthy pediatric controls. Mast cell distribution and number were assessed by toluidine blue staining and analyzed by Student's t -test. Immunohistochemical analysis was performed to identify mature DCs, myeloid DCs (MDCs), and plasmacytoid DCs (PDCs) by using antibodies against DC-LAMP, blood dendritic cell antigen 1 (BDCA-1), and BDCA-2, respectively. Myxovirus resistance protein A (MxA) staining indicated active type I interferon (IFN) signaling; positive staining was scored semiquantitatively and analyzed using the Mann-Whitney U test. Results Both inflamed and nonlesional skin from patients with juvenile DM contained more mast cells than did skin from pediatric controls (P = 0.029), and comparable numbers of mast cells were present in lesional and nonlesional skin. Interestingly, mast cell numbers were greater in skin than in paired muscle tissue from patients with juvenile DM (P = 0.014) and were not increased in muscle from patients with juvenile DM compared with control muscle. Both muscle and skin from patients with juvenile DM showed more mature PDCs and MxA staining than did their corresponding control tissues (P < 0.05). In both muscle and skin from patients with juvenile DM and in pediatric control muscle, there were fewer MDCs than PDCs, and the distributions of MDCs and PDCs were similar in pediatric control skin samples. Conclusion The identification of mast cells in skin (irrespective of rash) from patients with juvenile DM, but not in paired muscle tissue, suggests that they have a specific role in juvenile DM skin pathophysiology. In skin from patients with juvenile DM, increased numbers of PDCs and increased expression of type I IFN,induced protein suggest a selective influence on T cell differentiation and subsequent effector function. [source] Percutaneous application of peptidoglycan from Staphylococcus aureus induces an increase in mast cell numbers in the dermis of miceCLINICAL & EXPERIMENTAL ALLERGY, Issue 3 2005K. Matsui Summary Background Atopic dermatitis (AD) is a chronic inflammatory skin disease with immunopathologic features that vary depending on the duration of the lesion. The dermis of lesional skin of AD patients shows an increased number of inflammatory cells such as mast cells, eosinophils and mononuclear cells and superficial Staphylococcus aureus colonization. Objective The purpose of this study was to determine the effects of peptidoglycan (PEG) from S. aureus on mast cell induction in murine skin. Methods PEG was applied to barrier-disrupted abdominal skin of mice every 5 days and the number of mast cells in the abdominal skin was counted 20 days after the first application. The cytokine response was investigated by RT-PCR and immunohistologic analysis. Results The number of mast cells in the skin of mice treated with PEG was increased significantly compared with that of mice given phosphate-buffered saline. In addition, application of PEG to the abdominal skin increased the expression of mRNA for transforming growth factor-,1 (TGF-,1), which supports mast cell migration, but not that for IL-3 or stem cell factor, which support both mast cell proliferation and mast cell migration. Immunohistologic analysis demonstrated that levels of TGF-,1 transcripts corresponded with those of protein synthesis in the epidermis. TGF-,1 was found to be highly expressed in keratinocytes of the basal epidermis of PEG-treated skin. Furthermore, intraperitoneal injection of anti-TGF-,1 antibodies neutralized the induction of mast cells into the skin. Conclusion These results suggest that PEG may have the ability to induce an increase in mast cell numbers in the skin through TGF-,1 production by epidermal keratinocytes. Skin inflammation might therefore be linked to colonization with S. aureus in AD patients. [source] | ||||||||||