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Skin Inflammation (skin + inflammation)
Selected AbstractsTumor necrosis factor , blockade exacerbates murine psoriasis-like disease by enhancing Th17 function and decreasing expansion of Treg cellsARTHRITIS & RHEUMATISM, Issue 2 2010Hak-Ling Ma Objective Patients with psoriasis and psoriatic arthritis respond well to tumor necrosis factor , (TNF,) blockers in general; however, there is now mounting evidence that a small cohort of patients with rheumatoid arthritis who receive TNF, blockers develop psoriasis. This study was undertaken to explore the mechanisms underlying TNF, blockade,induced exacerbation of skin inflammation in murine psoriasis-like skin disease. Methods Skin inflammation was induced in BALB/c scid/scid mice after they received CD4+CD45RBhighCD25, (naive CD4) T cells from donor mice. These mice were treated with either anti,interleukin-12 (anti,IL-12)/23p40 antibody or murine TNFRII-Fc fusion protein and were examined for signs of disease, including histologic features, various cytokine levels in the serum, and cytokine or FoxP3 transcripts in the affected skin and draining lymph node (LN) cells. In a separate study, naive CD4+ T cells were differentiated into Th1 or Th17 lineages with anti-CD3/28 magnetic beads and appropriate cytokines in the presence or absence of TNF,. Cytokine gene expression from these differentiated cells was also determined. Results Neutralization of TNF, exacerbated skin inflammation and markedly enhanced the expression of the proinflammatory cytokines IL-1,, IL-6, IL-17, IL-21, and IL-22 but suppressed FoxP3 expression in the skin and reduced the number of FoxP3-positive Treg cells in the draining LNs. TNF, also demonstrated a divergent role during priming and reactivation of naive T cells. Conclusion These results reveal a novel immunoregulatory role of TNF, on Th17 and Treg cells in some individuals, which may account for the exacerbation of skin inflammation in some patients who receive anti-TNF treatments. [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] Polymorphisms in the interleukin-1 gene influence the stratum corneum interleukin-1, concentration in uninvolved skin of patients with chronic irritant contact dermatitisCONTACT DERMATITIS, Issue 5 2008Cindy M. DeJongh Background:, Interleukin (IL)-1, and its receptor antagonist IL-1ra play a role in skin inflammation. Several polymorphisms in the IL1 gene cluster, coding for IL-1,, IL-1ra, and IL-1,, influence their protein expression. Within this cluster, strong linkage disequilibrium has been shown. Objective:, We studied the association between the polymorphisms IL1A -889 (C,T) and IL1B -31 (T,C) and the concentration of IL-1, and IL-1ra in the stratum corneum (SC). Method:, In 124 patients with chronic irritant contact dermatitis, we genotyped the IL1A -889 and IL1B -31 polymorphisms and determined the amount of IL-1, and IL-1ra on tape strips obtained from uninvolved skin of the volar forearm. Results:, The SC IL-1, concentration was 23% and 47% lower in subjects with IL1A -889 C/T genotype and T/T genotype, respectively, compared with wild-type genotype. In subjects with IL1B -31 C/C genotype, the IL-1, concentration was 51% lower compared with C/T and T/T genotypes. The ratio IL-1ra/IL-1, increased twofold in IL1A -889 C/T genotype and threefold in T/T genotype compared with wild type. Conclusions:, We have shown a clear effect of IL1 genotype on protein expression in the SC. This altered expression may be responsible for the interindividual differences in the inflammatory response of the skin. [source] Suppression of inflammatory responses by celastrol, a quinone methide triterpenoid isolated from Celastrus regeliiEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2009D. H. Kim Abstract Background, Celastrol, a quinone methide triterpenoid isolated from the Celastraceae family, exhibits various biological properties, including chemopreventive, antioxidant and neuroprotective effects. In this study, we showed that celastrol inhibits inflammatory reactions in macrophages and protects mice from skin inflammation. Materials and methods, Anti-inflammatory effects of celastrol (0,1 ,M) were examined in lipopolysaccharide (LPS)-stimulated RAW 264·7 macrophages. To investigate the effects of celastrol (0,50 ,g per mice) in vivo, activation of myeloperoxidase (MPO) and histological assessment were examined in the 12- O -tetradecanoyl-phorbol-13-acetate (TPA)-induced mouse ear oedema model. Results, Our in vitro experiments showed that celastrol suppressed not only LPS-stimulated generation of nitric oxide and prostaglandin E2, but also expression of inducible nitric oxide synthase and cyclooxygenase-2 in RAW264·7 cells. Similarly, celastrol inhibited LPS-induced production of inflammatory cytokines, including tumour necrosis factor-, and interleukin-6. In an animal model, celastrol protected mice from TPA-induced ear oedema, possibly by inhibiting MPO activity and production of inflammatory cytokines. Conclusions, Our data suggest that celastrol inhibits the production of inflammatory mediators and is a potential target for the treatment of various inflammatory diseases. [source] Is there a ,gut,brain,skin axis'?EXPERIMENTAL DERMATOLOGY, Issue 5 2010Petra Arck Please cite this paper as: Is there a ,gut,brain,skin axis'? Experimental Dermatology 2010; 19: 401,405. Abstract:, Emerging evidence arising from interdisciplinary research supports the occurrence of communication axes between organs, such as the brain,gut or brain,skin axis. The latter is employed in response to stress challenge, along which neurogenic skin inflammation and hair growth inhibition is mediated. We now show that ingestion of a Lactobacillus strain in mice dampens stress-induced neurogenic skin inflammation and the hair growth inhibition. In conclusion, we are introducing a hypothesis, encouraged by our pilot observations and resting upon published prior evidence from the literature, which amalgamates previously proposed partial concepts into a new, unifying model, i.e. the gut,brain,skin axis. This concept suggests that modulation of the microbiome by deployment of probiotics can not only greatly reduce stress-induced neurogenic skin inflammation but even affect a very complex cutaneous phenomenon of (mini-) organ transformation, i.e. hair follicle cycling. These observations raise the intriguing prospect that feeding of just the right kind of bacteria can exert profound beneficial effects on skin homoeostasis, skin inflammation, hair growth and peripheral tissue responses to perceived stress. [source] Pimecrolimus , an anti-inflammatory drug targeting the skinEXPERIMENTAL DERMATOLOGY, Issue 12 2004M. Grassberger Abstract:, Pimecrolimus is the most recent member of calcineurin inhibitors available for the therapy for inflammatory skin diseases. It targets T-cells and mast cells and inhibits the production and release of cytokines and other inflammatory mediators, as well as the expression of signals essential for the activation of inflammatory T-lymphocytes. Pimecrolimus has a cell-selective mode of action. In contrast to corticosteroids, it does not affect, e.g., Langerhans'cells/dendritic cells (LC/DC), as demonstrated in vitro with human monocyte-derived DC and in vivo with epidermal LC in mice, nor human primary fibroblasts. As shown in vitro with human skin and by comparison of clinical pharmacokinetic data from patients with atopic dermatitis, pimecrolimus permeates less through skin than tacrolimus and much less than corticosteroids. It, thus, has a lower potential for transcutaneous resorption after topical administration, resulting in a lower risk of systemic effects. Pimecrolimus has high anti-inflammatory activity in animal models of skin inflammation, including a model reflecting neurogenic inflammation, but a more favourable balance of anti-inflammatory vs. immunosuppressive activity than tacrolimus. Pimecrolimus does not affect sensitization in a murine model of allergic contact dermatitis and has a lower potency in various models of immunosuppression after systemic administration, compared to tacrolimus. In conclusion, the results of preclinical studies show that pimecrolimus has a selective pharmacological profile, suited for effective and safe treatment for inflammatory skin diseases. [source] Cosmeceutical properties of polysaccharides from the root bark of Ulmus davidiana var. japonicaINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 2 2007Sang Yong Eom In Korea and China, Ulmus davidiana var. japonica has been used as a traditional oriental medicine for the treatment of difficulty in urination, skin inflammation, etc. In order to investigate the potential of a polysaccharide extract from Ulmus davidiana var. japonica as a cosmetic ingredient, we measured its moisturizing effect, photo-induced cytotoxicity, and anti-inflammatory effect. After hydrolysis, HPLC experiments showed that the composition of the polysaccharide extract was mainly rhamnose, galactose, and glucose. The molecular weight of the obtained Ulmus davidiana root extract was 20 000. The intrinsic viscosity was 90 dL/g. In a moisturizing test conducted through the measurement of water loss in a desiccator and of moisture content with a Corneometer CM820, Ulmus davidiana root extract showed almost the same moisturizing effect as hyaluronic acid. In an assay for inhibition of the H2O2-activated release of PGE2, IL-6, and IL-8 in normal human fibroblast cell lines, Ulmus davidiana root extract showed an inhibitory activity of PGE2 release in a dose-dependent manner (up to 85.9% at a concentration of 0.1%). The percent inhibition of the release of IL-6 was in the range of 45.6,64.5% (H2O2 was used as the positive control). Moreover, the release of IL-8 was completely inhibited in the entire concentration range (>0.0025%). In a test of recovery from photo-induced damage after UVA irradiation (3 J/cm2), the cell recovery of human fibroblasts increased to levels two times higher than that of the positive control, which was UVA-damaged cells in the absence of Ulmus davidiana root extract (up to 60.2% at 3.0% of Ulmus davidiana root extract). In a photo-induced cytotoxicity assay in the presence of promethazine as a photosensitizer, Ulmus davidiana root extract showed approximately 48% of the increased cell viability of the control. Therefore, Ulmus davidiana root extract may be useful for the development of a cosmetic ingredient. [source] Cosmeceutical properties of levan produced by Zymomonas mobilisINTERNATIONAL JOURNAL OF COSMETIC SCIENCE, Issue 3 2006K. H. Kim Levan, a polysaccharide that can be produced by both plants and micro-organisms, is a sugar polymer composed of fructose, with-2,6 linkages. Here, we have attempted to assess the possible use of levan produced by Zymomonas mobilis as a cosmeceutical ingredient. In service of this goal, we assessed a host of levan's properties, including its moisturizing effects, cell cytotoxicity, cell proliferation effects and anti-inflammation effects. Levan exhibited a moisturizing effect that was almost exactly the same as that evidenced by hyaluronic acid, as well as a similar cell proliferation effect in human fibroblast and keratinocyte cell lines. Moreover, in our cell proliferation test, which was conducted using bio-artificial skin constructed via 3-dimensional (3-D) culture after the induction of primary skin inflammation with 0.05% sodium lauryl sulphate (SLS), cell viability in the presence of levan (0.01 and 0.05 mg mL,1) was determined to be higher than cell viability in the absence of levan. In our anti-inflammation test, which was also conducted using 3-D artificial skin, and which involved the measurement of a quantity of secreted interleukin-1 (IL-1), a pre-inflammatory mediator induced by SLS, we determined that the quantity of IL-1 in the 3-D artificial skin treated with 0.01 and 0.05 mg mL,1 of levan was less than that registered in a skin sample that had been treated only with SLS. In this study, we determined that levan exerted an anti-inflammatory effect against inflammatory reactions to skin irritants, and also that levan exerted a cell-proliferative effect in bio-artificial skin, thereby indicating its potential applicability as a cosmeceutical agent. [source] What is a role of haeme oxygenase-1 in psoriasis?INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, Issue 2 2007Current concepts of pathogenesis Summary The skin is constantly exposed to endogenous and environmental pro-oxidant agents, which lead to harmful generation of reactive oxygen species (ROS). Healthy skin, being a potential target for oxidative stress, is equipped with a large number of defence mechanisms including antioxidant systems. This protection can be corrupted by an imbalance between ROS and antioxidants with pathological level of oxidants prevailing. There is a great body of evidence indicating that some inflammatory skin diseases, such as psoriasis, are mediated by oxidative stress. Keratinocytes of normal skin, the primary target for pro-oxidant agents, show strong expression of ROS-detoxifying enzymes. In addition, normal keratinocytes express haeme oxygenase (HO), an enzyme which might be involved in the protection of cells against oxidative stress. HO (inducible HO-1, constitutive HO-2 and HO-3) is the rate-limiting enzyme in haeme catabolism, which leads to the generation of biliverdin, iron, and carbon monoxide. HO-1 is a stress-responsive protein whose expression is induced by various oxidative agents. HO-1 is known for its cytoprotective, antioxidant and anti-inflammatory properties. Interestingly, a strong overexpression of HO-1 was observed in psoriatic skin. However, the role of HO-1 in psoriasis remains unclear. In this review, we will discuss some current concepts concerning pathogenesis of psoriasis and the contribution of HO-1 in skin inflammation to show the relationships between HO-1, ROS and cytokine network in psoriatic skin. We will try to answer a question whether enhanced HO-1 expression in keratinocytes results in beneficial or detrimental effect on the development and severity of psoriatic lesions. [source] Phycocyanin liposomes for topical anti-inflammatory activity: in-vitro in-vivo studiesJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 4 2009Maria Manconia Abstract Objectives The aim of this work was to investigate the anti-inflammatory activity of C-phycocyanin (C-PC) on skin inflammation after topical administration and the influence of liposomal delivery on its pharmacokinetic properties. Methods Liposomes of different size and structure were prepared with different techniques using soy phosphatidylcholine and cholesterol. Vesicular dispersions were characterised by transmission electron microscopy, optical and fluorescence microscopy for vesicle formation and morphology, dynamic laser light scattering for size distribution, and Zetasizer for zeta-potential. C-PC skin penetration and permeation experiments were performed in vitro using vertical diffusion Franz cells and human skin treated with either free or liposomal drug dispersed in a Carbopol gel. Key findings The protein was mainly localised in the stratum corneum, while no permeation of C-PC through the whole skin thickness was detected. Two percent C-PC-encapsulating liposomes showed the best drug accumulation in the stratum corneum and the whole skin, higher than that of the corresponding free 2% C-PC gel. Moreover, skin deposition of liposomal C-PC was dose dependent since skin accumulation values increased as the C-PC concentration in liposomes increased. The topical anti-inflammatory activity of samples was evaluated in vivo as inhibition of croton oil-induced or arachidonic acid-induced ear oedema in rats. Conclusions The results showed that C-PC can be successfully used as an anti-inflammatory drug and that liposomal encapsulation is effective in improving its anti-inflammatory activity. [source] In-vitro Antioxidant and In-vivo Photoprotective Effect of Three Lyophilized Extracts of Sedum telephium L. LeavesJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 10 2000FRANCESCO BONINA Sedum telephium L. is a medicinal plant used in antiquity to cure many types of inflammatory skin diseases. The leaves (without the external cuticle), are used to promote healing and reduce skin inflammation and pain, and contain various components. We found two major components: flavonol glycosides and polysaccharides, with molecular weight between 13 000 and 13 500 Da. We evaluated the in-vitro antioxidant and in-vivo skin photoprotective effects of three lyophilized extracts obtained from the juice of S. telephium L. leaves: a total lyophilized juice, a lyophilized flavonolic fraction, and a lyophilized polysaccharidic fraction. Two in-vitro models were used: the bleaching of the stable 2,2-diphenyl-1-picrylhydrazyl (DPPH*) radical, and the protective effect against UV-induced peroxidation on phosphatidylcholine multilamellar vesicles, as model membranes. The antioxidant/radical scavenging activity of each lyophilized extract was also assessed in-vivo by determining their ability to reduce UVB-induced skin erythema (monitored by reflectance spectrophotometry) in healthy human volunteers. The findings of the in-vitro experiments clearly demonstrated that, unlike the lyophilized polysaccharidic fraction, the lyophilized flavonolic fraction and total lyophilized juice possess strong antioxidant/free radical scavenging properties, which are likely due to phenolic compounds. Consistent with these findings, gel formulations of both the total lyophilized juice and, to a greater degree, the lyophilized flavonolic fraction appeared to possess a strong protective effect against UV-induced skin erythema in-vivo, whereas the lyophilized polysaccharidic fraction was completely ineffective. The in-vitro and in-vivo results suggest that, both the total lyophilized juice and, in particular, the lyophilized flavonolic fraction, but not the lyophilized polysaccharidic fraction of S. telephium L. leaves, have photoprotective effects against UVB-induced skin damage. [source] How the skin reacts to environmental factorsJOURNAL OF THE EUROPEAN ACADEMY OF DERMATOLOGY & VENEREOLOGY, Issue 2007L. Misery Abstract The skin is one of the main points of contact with the environment. Usually, interactions between skin and environmental factors are harmonious. But sometimes, the skin barrier is modified (dry or greasy skin) or skin inflammation can occur (irritated, reactive, allergic or atopic skin). [source] Stratum corneum TARC level is a new indicator of lesional skin inflammation in atopic dermatitisALLERGY, Issue 9 2010E. Morita To cite this article: Morita E, Takahashi H, Niihara H, Dekio I, Sumikawa Y, Murakami Y, Matsunaka H. Stratum corneum TARC level is a new indicator of lesional skin inflammation in atopic dermatitis. Allergy 2010; 65: 1166,1172. Abstract Background:, Management of atopic dermatitis (AD) requires judging the symptoms of local skin lesions and prescribing a suitable treatment. However, no method has been established in which objective measures can be used to evaluate the severity of local symptoms. We established a method for measuring thymus and activation-regulated chemokine (TARC) levels in the stratum corneum (scTARC), and examined whether the scTARC can be used as an indicator of the severity of local skin lesions in patients with AD. Methods:, Stratum corneum was obtained from patients with AD by tape-stripping, and scTARC was evaluated using a TARC-specific antibody followed by image analysis. The scTARC was examined to determine correlation with the severity of local skin lesions (the severity of erythema, edema/papule, oozing/crusts, excoriations, lichenification, and xerosis) as well as with the severity scoring of atopic dermatitis (SCORAD) index, serum TARC level, serum IgE level, serum lactate dehydrogenase (LDH) level, interleukin (IL)-4-producing T cell ratio (Th2 cell ratio), and blood eosinophil count. Results:, The scTARC was correlated with the severity of local skin lesions, especially with the erythema, edema/papule, and oozing/crusts score. The scTARC in the most severe lesions was also correlated with the SCORAD index, serum TARC level, serum IgE level, and blood eosinophil count. The scTARC was not, however, correlated with the serum LDH level and Th2 cell ratio. Conclusion:, An immunofluorescent technique combined with tape-stripping was used to measure scTARC. The scTARC can be used as an indicator of the severity of local acute inflammation in patients with AD. [source] Effector and regulatory mechanisms in allergic contact dermatitisALLERGY, Issue 12 2009M. Vocanson Allergic contact dermatitis (ACD), one of the commonest occupational diseases, is a T-cell-mediated skin inflammation caused by repeated skin exposure to contact allergens, i.e. nonprotein chemicals called haptens. Allergic contact dermatitis, also referred to as contact hypersensitivity, is mediated by CD8+ T cells, which are primed in lymphoid organs during the sensitization phase and are recruited in the skin upon re-exposure to the hapten. Subsets of CD4+ T cells endowed with suppressive activity are responsible for both the down-regulation of eczema in allergic patients and the prevention of priming to haptens in nonallergic individuals. Therefore, ACD should be considered as a breakdown of the skin immune tolerance to haptens. Recent advances in the pathophysiology of ACD have demonstrated the important role of skin innate immunity in the sensitization process and have revisited the dogma that Langerhans cells are mandatory for CD8+ T-cell priming. They have also introduced mast cells as a pivotal actor in the magnitude of the inflammatory reaction. Finally, the most recent studies address the nature, the mode and the site of action of the regulatory T cells that control the skin inflammation with the aim of developing new strategies of tolerance induction in allergic patients. [source] Differential effects of skin nerves on allergic skin inflammationALLERGY, Issue 3 2009R. Vieira dos Santos No abstract is available for this article. [source] Case of localized scleroderma associated with osteomyelitisTHE JOURNAL OF DERMATOLOGY, Issue 1 2010Eiji MUROI Abstract We report a 4-year-old girl presenting with progressive linear scleroderma affecting the right leg. Biopsy specimen disclosed typical histopathological findings of localized scleroderma. Right leg magnetic resonance imaging (MRI) showed high signal areas on T2 -weighted images on the subcutaneous fatty tissue, muscles and bone marrow, suggesting that skin inflammation extended to the bone marrow. Oral corticosteroid therapy was instituted with improvement of both skin sclerosis and MRI findings. Our observations suggest that MRI examination should be considered in patients with localized scleroderma to evaluate the extension of the inflammation. [source] Tumor necrosis factor , blockade exacerbates murine psoriasis-like disease by enhancing Th17 function and decreasing expansion of Treg cellsARTHRITIS & RHEUMATISM, Issue 2 2010Hak-Ling Ma Objective Patients with psoriasis and psoriatic arthritis respond well to tumor necrosis factor , (TNF,) blockers in general; however, there is now mounting evidence that a small cohort of patients with rheumatoid arthritis who receive TNF, blockers develop psoriasis. This study was undertaken to explore the mechanisms underlying TNF, blockade,induced exacerbation of skin inflammation in murine psoriasis-like skin disease. Methods Skin inflammation was induced in BALB/c scid/scid mice after they received CD4+CD45RBhighCD25, (naive CD4) T cells from donor mice. These mice were treated with either anti,interleukin-12 (anti,IL-12)/23p40 antibody or murine TNFRII-Fc fusion protein and were examined for signs of disease, including histologic features, various cytokine levels in the serum, and cytokine or FoxP3 transcripts in the affected skin and draining lymph node (LN) cells. In a separate study, naive CD4+ T cells were differentiated into Th1 or Th17 lineages with anti-CD3/28 magnetic beads and appropriate cytokines in the presence or absence of TNF,. Cytokine gene expression from these differentiated cells was also determined. Results Neutralization of TNF, exacerbated skin inflammation and markedly enhanced the expression of the proinflammatory cytokines IL-1,, IL-6, IL-17, IL-21, and IL-22 but suppressed FoxP3 expression in the skin and reduced the number of FoxP3-positive Treg cells in the draining LNs. TNF, also demonstrated a divergent role during priming and reactivation of naive T cells. Conclusion These results reveal a novel immunoregulatory role of TNF, on Th17 and Treg cells in some individuals, which may account for the exacerbation of skin inflammation in some patients who receive anti-TNF treatments. [source] Induction of scratching behaviour and dermatitis in various strains of mice cohabiting with NC/Nga mice with chronic dermatitisBRITISH JOURNAL OF DERMATOLOGY, Issue 1 2006Y. Hashimoto Summary Background, NC/Nga (NC) mice with similar pathological and behavioural features as seen in human atopic dermatitis are used as a model of the disease. Under normal circumstances, spontaneous and persistent scratching occurs in NC mice and this can lead to the onset of skin inflammation. Objectives, We examined the induction of scratching behaviour in NC, BALB/c, ICR and C3H/HeN mice, and of dermatitis in NC and BALB/c mice, by cohabitation with mice with dermatitis. Methods, NC, BALB/c, ICR and C3H/HeN mice were kept together with NC mice with chronic dermatitis (CNV-NC) for 2 weeks, and the numbers of scratching episodes were counted. NC and BALB/c mice were also kept together with CNV-NC mice for 24 weeks and the skin severity score was assessed. The score was assessed for a further 8 weeks after separation of these mice. Results, The number of scratching episodes in NC, BALB/c, ICR and C3H/HeN mice was increased by cohabitation with CNV-NC mice. Cohabitation with CNV-NC mice led to dermatitis in both NC and BALB/c mice. The number of scratching episodes and the skin severity score in BALB/c mice were about half of those in NC mice. When cohabitation with CNV-NC mice stopped, the number of scratching episodes and the skin severity score decreased in BALB/c mice, but not in NC mice. Changes in the histopathological data of BALB/c mice supported the severity of skin inflammation. Conclusions, Our study demonstrates that scratching behaviour and dermatitis can be induced in various strains of mice by cohabitation with CNV-NC mice, and that cessation of cohabitation leads to a recovery in BALB/c mice but not in NC mice. [source] Increased activity of plasma and tissue kallikreins, plasma kininase II and salivary kallikrein in pemphigus foliaceus (fogo selvagem)BRITISH JOURNAL OF DERMATOLOGY, Issue 4 2005T.B. Rosatelli Summary Background, Pemphigus foliaceus (PF) is an autoimmune blistering disease of unknown aetiology, which is endemic in Brazil. Although the pathogenesis of PF is still unknown, proteins of the contact system have been implicated. Objectives, As the components of the kinin system may interact with those of the contact system, in this study we evaluated the plasma levels of high-molecular-weight kininogen (HK) and low-molecular-weight kininogen (LK), and the activity of plasma kallikrein, tissue kallikrein and kininase II in plasma of patients with PF presenting with Nikolsky's sign. As kidneys and salivary glands are relevant sources of tissue kallikrein for plasma, we also evaluated urinary/salivary kallikrein and urinary kininase II activities. Methods, Fifteen patients and 15 age- and sex-matched controls were studied. Kininogen levels were determined by enzyme-linked immunosorbent assay, and the activities of kallikreins and kininase II were determined using selective chromogenic substrates. Results, Compared with controls, plasma HK levels were decreased (P = 0·031), whereas the activities of plasma kallikrein, tissue kallikrein and kininase II in plasma, and the activity of salivary kallikrein, were increased in patients (P < 0·001 for each comparison). Plasma levels of LK and the activities of urinary kallikrein and urinary kininase II were not significantly different from controls. Conclusions, Diminished levels of HK associated with increased activities of plasma kallikrein and kininase II indicate that the kinin system is activated at the systemic level in PF. As active plasma kallikreins may act on some proteins of the contact system, it is possible that the enzyme may contribute to blister formation. The further observation of an increased tissue kallikrein activity at the systemic and saliva levels may be interpreted as a systemic reflex of skin inflammation. Whether the activation of the kinin system is a cause or a consequence of blister formation needs further clarification. [source] Photoageing shows histological features of chronic skin inflammation without clinical and molecular abnormalitiesBRITISH JOURNAL OF DERMATOLOGY, Issue 4 2003S. Bosset Summary Background Photodamage is characterized by degradation of collagen and accumulation of abnormal elastin in the superficial dermis. Mast cells and macrophages, which are found in higher numbers in photoaged skin, have been implicated in this process. Objectives To analyse the phenotype of haematopoietic-derived infiltrating cells in photodamaged skin. Methods Chronically sun-exposed (preauricular) and control sun-protected (postauricular) skin was recovered from eight healthy subjects undergoing cosmetic surgery (facial lifting). Results Histological analysis showed that sun-exposed skin harboured more infiltrating mononuclear cells than sun-protected skin. Cellular infiltrates were found at the periphery of areas of elastolysis around hair follicles in sun-exposed sites, whereas they were found in the interfollicular dermis around blood vessels and around hair follicles in sun-protected samples. Immunohistochemical analysis revealed an increased number of mast cells, macrophages and CD4+ CD45RO+ T cells in sun-exposed dermis as well as a higher number of CD1a+ dendritic cells in sun-exposed epidermis, compared with the sun-protected samples. Thus photoageing displays histological features of chronic skin inflammation. However, no molecular sign of inflammation was observed and we even found a decreased expression of interleukin-1, mRNA in sun-exposed compared with sun-protected sites. Furthermore, the patients' skin looked normal and did not display any clinical inflammation. Conclusions Collectively, these data show that chronic ultraviolet irradiation induces alterations of innate immune cells which are recruited in sun-exposed skin without being activated. [source] Tea tree oil reduces histamine-induced skin inflammationBRITISH JOURNAL OF DERMATOLOGY, Issue 6 2002K.J. Koh Summary Background Tea tree oil is the essential oil steam-distilled from Melaleuca alternifolia , an Australian native plant. In recent years it has become increasingly popular as an antimicrobial for the treatment of conditions such as tinea pedis and acne. Objectives ,To investigate the anti-inflammatory properties of tea tree oil on histamine-induced weal and flare. Methods Twenty-seven volunteers were injected intradermally in each forearm (study and control assigned on an alternating basis) with histamine diphosphate (5 µg in 50 µL). Flare and weal diameters and double skin thickness were measured every 10 min for 1 h to calculate flare area and weal volume. At 20 min, 25 µL of 100% tea tree oil was applied topically to the study forearm of 21 volunteers. For six volunteers, 25 µL paraffin oil was applied instead of tea tree oil. Results Application of liquid paraffin had no significant effect on histamine-induced weal and flare. There was also no difference in mean flare area between control arms and those on which tea tree oil was applied. However, mean weal volume significantly decreased after tea tree oil application (10 min after tea tree oil application, P = 0·0004, Mann,Whitney U-test). Conclusions ,This is the first study to show experimentally that tea tree oil can reduce histamine-induced skin inflammation. [source] Localized erosive pustular dermatosis of the scalp at the site of a cochlear implant: successful treatment with topical tacrolimusCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 5 2009A. V. Marzano Summary Erosive pustular dermatosis of the scalp (EPDS) is a rare form of nonmicrobial pustulosis mainly occurring in elderly patients with long-term sun damage to the skin. Clinically, it is characterized by pustular lesions that progressively merge into erosive and crusted areas over the scalp. The histology of EPDS is nonspecific, and its pathophysiology remains undetermined, with various types of local trauma possibly acting as the triggering factor. We describe a 24-year-old woman who developed EPDS after cochlear implant surgery for profound sensorineural hearing loss. We speculate that either the cutaneous surgery during cochlear implantation or the skin inflammation that commonly occurs near the magnet might have triggered the disorder. It is of note that the patient's skin lesions healed completely after treatment with topical tacrolimus, a relatively novel immunosuppressive molecule. Thus, topical tacrolimus may be indicated as a therapeutic alternative to the widely used steroids for this disease, mainly to avoid steroid-related cutaneous atrophy. [source] MicroRNAs: novel regulators in skin inflammationCLINICAL & EXPERIMENTAL DERMATOLOGY, Issue 3 2008E. Sonkoly Summary Compelling evidence indicates that microRNAs (miRNAs), short, non-protein coding RNAs, are critical for the development and survival of multicellular organisms. Recently, miRNAs were implicated in the pathogenesis of psoriasis and atopic eczema (AE), the two most common chronic inflammatory disorders in skin. In particular, miR-203, the first skin-specific miRNA, showing an intriguing expression profile being confined to skin epithelium, is specifically overexpressed in psoriasis. MiR-146a, another miRNA showing specific upregulation in psoriasis, is involved in the regulation of innate immune responses and the tumour necrosis factor (TNF)-, pathway. Interestingly, miR-125b, another miRNA involved in the TNF-, pathway, is also deregulated in psoriasis and AE. As skin inflammation may serve as a model for chronic inflammatory disorders, it is likely that miRNAs involved in skin inflammation will eventually emerge in other inflammatory or autoimmune disorders, and some of these may become disease markers and therapeutic targets. In this review we present an overview of what is currently known about the roles of miRNAs in chronic inflammatory skin disorders. [source] A role for T cell-derived interleukin 22 in psoriatic skin inflammationCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 3 2007K. Boniface Summary Interleukin (IL)-22 is a T cell-derived cytokine that has been reported recently to induce cutaneous inflammation in an experimental murine model of psoriasis, and to induce in vitro an inflammatory-like phenotype. In the present study, we assessed the presence of IL-22 and the IL-22 receptor 1 (IL-22R1) in skin lesions, skin-derived T cells, as well as IL-22 levels in sera from patients with psoriasis. IL-22R1 and IL-10R2 transcripts are expressed at a similar level in psoriatic and healthy skin. In contrast, IL-22 mRNA expression was up-regulated in psoriatic skin lesions compared to normal skin, whereas IL-22 mRNA levels in peripheral blood mononuclear cells from psoriatic patients and normal subjects were similar. Circulating IL-22 levels were significantly higher in psoriatic patients than in normal subjects. T cells isolated from psoriatic skin produced higher levels of IL-22 in comparison to peripheral T cells isolated from the same patients. IL-10 was expressed at similar levels in skin biopsies and peripheral blood mononuclear cells of psoriatic patients and normal subjects. Finally, we show here that supernatants of lesional psoriatic skin-infiltrating T cells induce an inflammatory response by normal human epidermal keratinocytes, resembling that observed in psoriatic lesions. Taken together, the results reported in this study indicate that IL-22 is a cytokine produced by skin-infiltrating lymphocytes that is potentially involved in initiation and/or maintenance of the pathogenesis of psoriasis. [source] | |||||||||||||||||||||||||