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PubMed1997

Immunophenotyping of skin-infiltrating T-cell subsets in dogs with atopic dermatitis.

Atopic dermatitis in dogs has many clinical features that are identical to those of the same disorder in man. To investigate the pathogenesis of this disease in dogs and the possibility of similarities to the pathogenesis in humans we compared the presence and ratio of CD4+ and CD8+ T-cells in the cutaneous infiltrate of lesional and non-lesional skin of atopic dogs with that in the skin of healthy dogs. In ten dogs with atopic dermatitis and ten healthy dogs the skin was biopsied at the predilection sites for atopic dermatitis and histological sections were immunohistochemically stained for CD4 and CD8. The staining showed an increase in CD4+ and CD8+ T-cells in canine lesional atopic skin, with a predominance of CD4+ T-cells in the epidermis. In non-lesional atopic skin there was also an infiltration with CD4+ and CD8+ T-cells, but without predominance of CD4+ T-cells. The results in the separate predilection sites did not differ substantially from the mean results. These observations indicate further similarities in the immunopathogenesis of atopic dermatitis in dogs and humans, which may have consequences for the control of atopic dermatitis in dogs and contributes to a possible role of the dog as a model for human atopic dermatitis.

Animals↗
PubMedDate not supplied

[New horizons in the treatment of atopic dermatitis].

Nearly fifty years after their introduction, corticoids continue to be one of the main pillars of dermatological therapy in general and in atopic dermatitis in particular. However, their use is limited by local and systemic adverse effects.There is enormous demand for anti-inflammatory agents not belonging to the corticoid group that would be useful in the different inflammatory dermatoses.In the last few years the therapeutic arsenal for atopic dermatitis has increased with two distinct groups of drugs: topical immunomodulators and leukotriene inhibitors. Both groups of drugs are new and new compounds belonging to these types of drugs will probably appear in the next few years.Among the alternatives to corticoids are the immunomodulators and the most promising of these are macrolide antibiotics. Tacrolimus (FK 506) and pimecrolimus (ASM 981) belong to this group of substances with a high capacity to inhibit T lymphocyte activation. Although they also act on other cells playing a role in atopic dermatitis (mastocytes, Langerhans' cells, B lymphocytes) their action on T lymphocytes seems to be the most important. In T lymphocytes, these drugs act by inhibiting the action of calmodulin, a vital enzyme in the activation chain of these cells that ends in the production of interleukin 2 and other proinflammatory cytokines.The accumulated evidence of the various publications seems to indicate that tacrolimus is a safe and effective treatment of atopic dermatitis in patients aged 2 years or more. The drug was approved for clinical use 3 years ago in Japan and more than 1 year ago in the United States. The number of randomized clinical trials comparing this drug with placebo or various corticoids demonstrate that its action is overwhelming. Its anti-inflammatory action is similar to that of high-potency topical corticoids. Two doses daily are required and the drug has been tested in patients with moderate-to-severe atopic dermatitis. Published data from more than 10,000 patients guarantee its safety. The most frequent short-term adverse effect is a burning sensation in the site of application lasting a few minutes.Pimecrolimus has not yet been commercialized in any country and is currently undergoing phase III clinical investigations. It has been tested in three clinical trials in patients aged more than 3 months old with mild-moderate atopic dermatitis. Its safety profile is good and similar to that of tacrolimus.The number and quality of the data provided by studies of treatment with leukotriene inhibitors (zafirlukast, montelukast and zileuton) is much lower but these substances seem to warrant further investigation. Only five small series undergoing treatment with these products have been published.

Allergy and Immunology↗
PubMed2003

Seborrheic dermatitis.

Seborrheic dermatitis is present in 1% to 3% of immunocompetent adults, and is more prevalent in men than in women. Seborrheic dermatitis may be seen in conjunction with other skin diseases, such as rosacea, blepharitis or ocular rosacea, and acne vulgaris. Malassezia yeasts have been associated with seborrheic dermatitis. Abnormal or inflammatory immune system reactions to these yeasts may be related to development of seborrheic dermatitis. Treatment modalities for seborrheic dermatitis include keratolytic agents, corticosteroids, and more recently, antifungal agents. Antifungal agents do not carry a risk of skin atrophy or telangiectasia with prolonged use, and it is more prudent to consider antifungals than corticosteroid preparations. The wide range of antifungal formulations available (creams, shampoos, or oral) provides safe, effective, and flexible treatment options for seborrheic dermatitis.

Administration, Cutaneous↗
PubMed2001

Inflammation in stasis dermatitis upregulates MMP-1, MMP-2 and MMP-13 expression.

Stasis dermatitis is a common disorder, which is a consequence of impaired venous drainage of the legs. It is characterized histologically by proliferation of small blood vessels in the papillary dermis. This neovascularization may lead occasionally to the formation of discrete papules due to inflammatory processes. In order to evaluate the role of matrix metalloproteinases (MMPs) in the acute phase of chronic venous insufficiency, we examined the production of MMP-1, -2, -13 and tissue inhibitors of metalloproteinase (TIMP)-1 and -2 in lesional skin of stasis dermatitis. A total of 19 patients affected by stasis dermatitis were included in this experimental study. Polymerase chain reaction, western blot and immunohistochemical studies on tissue specimen were performed. In lesional skin of stasis dermatitis, there was elevated gene expression and immunoreactivity for MMP-1, -2 and -13 in comparison to healthy controls. In contrast, genexpression and immunoreactivity for TIMP-1 and -2 were diminished in stasis dermatitis in comparison with healthy controls. Overexpression and production of MMP-1, -2 and -13 without inhibitory effects could be the result of cytokine mediated induction. Matrix metalloproteinases (MMPs) may play an important role in the remodeling of lesional skin in stasis dermatitis.

Aged↗
PubMed2002

The effect of antibiotics on the production of superantigen from Staphylococcus aureus isolated from atopic dermatitis.

Staphylococcus aureus (S. aureus) often colonizes on the skin of patients with atopic dermatitis. It is known that superantigens which are staphylococcal enterotoxins can activate T cells without processing by antigen presenting cells. It has been suggested that activated T cells release various cytokines which may exacerbate or prolong the cutaneous inflammation associated with atopic dermatitis. Reduction of bacterial colonization from skin lesions has been reported to be effective in the treatment of atopic dermatitis. Therefore, antimicrobial therapy using antibiotics may be a treatment option for atopic dermatitis in selected patients. We examined the effect of antibiotics on the production of superantigen from S. aureus in vitro to determine the action mechanism of antibiotics in the treatment of atopic dermatitis. It was found that antibiotics with inhibitory effect on protein synthesis can suppress the production of superantigen. On the other hand, the superantigen production was not suppressed by antibiotics having either the inhibitory effect on cell wall synthesis or on nucleic acid synthesis. Levels of the suppressive effect on superantigen production by S. aureus varied with strains tested in this study. Moreover, we demonstrated that replication of DNA coding of superantigen produced by S. aureus was suppressed only by roxithromycin (ROX), which is a new macrolide. This finding suggests that ROX may have an effect at the gene level. These results suggested that the suppressive effects of antimicrobial agents that act as inhibitors of protein synthesis on superantigen production from S. aureus may be useful in the treatment of atopic dermatitis.

Anti-Bacterial Agents↗
PubMed2003

Heterogeneity of interleukin 5 genetic background in atopic dermatitis patients: significant difference between those with blood eosinophilia and normal eosinophil levels.

BACKGROUND: Blood eosinophil levels in patients with atopic dermatitis vary widely during exacerbation of the disease. We considered that in addition to environmental factors, the genetic background involved with elevating blood eosinophil levels might be heterogeneous among atopic dermatitis patients. OBJECTIVE: We attempted to determine whether a polymorphism of the interleukin (IL)5 gene plays a role in atopic dermatitis, particularly in those patients with blood eosinophilia. Due to the close relation of blood eosinophilia to high IgE productivity, we also assessed these polymorphisms in patients with high IgE concentrations. METHODS: We determined the genotype of the IL5 polymorphism -703C/T in 451 atopic dermatitis patients and 116 normal subjects. The patients were classified into three groups by blood eosinophil levels; less than 7%, from 7 to 15%, and more than 15%, as well as by serum IgE concentrations; less than 500 IU/ml, from 500 to 2000 IU/ml, and more than 2000 IU/ml. RESULTS: IL5 -703C/T was not significantly associated with either total atopic dermatitis patients or individual patients who had both blood eosinophilia and high IgE productivity. However, the distribution of the IL5 -703C/T genotype was significantly different between patients with either blood eosinophilia or high IgE productivity and those without either condition (P=0.0476, P=0.0088, respectively). CONCLUSION: These results suggest that the IL5 gene may play a role in blood eosinophilia associated with atopic dermatitis. We also considered that the IL5 -703C/T gene polymorphism does not have a direct relationship to disease specificity.

Adolescent↗
PubMed1999

Fur mites induce dermatitis associated with IgE hyperproduction in an inbred strain of mice, NC/Kuj.

An inbred strain of mice, NC, has been introduced as an animal model for atopic dermatitis because the mice develop dermatitis associated with severe scratch preceded by elevated serum IgE level when kept in conventional conditions. Although hypersensitivity to some environmental factors is suggested to cause dermatitis, the precise factor remains unclear. As the mice maintained under conventional conditions were often infected with fur mites, we investigated whether an infection of fur mites induces skin lesions in NC. Infection with the fur mites induced NC to develop skin lesions associated with highly elevated serum IgE, whereas no obvious skin lesions were observed in BALB/c and C57BL/6, and the elevation of serum IgE level was minimal in these two strains of mice. The role of the fur mites in the manifestation of skin lesions and IgE hyperproduction was confirmed by eliminating the fur mites by treatment with ivermectin. In addition, the existence of specific IgE antibody to Myocoptes musculinus antigen in the sera of mite-infested NC was detected by the antigen-induced histamine release from bone marrow-derived cultured mast cells after sensitization with the serum. These results suggest that continuous exposure to fur mite antigen is a potential factor in the development of dermatitis in NC. We provide a new model system of antigen-induced dermatitis for investigating the role of IgE in eliciting dermatitis.

Animals↗
PubMed1997

IgE-binding components of staphylococcal enterotoxins in patients with atopic dermatitis.

BACKGROUND: The exacerbation of atopic dermatitis may be associated with infection of the skin with Staphylococcus aureus (S.aureus). S. aureus isolated from the skin of patients with atopic dermatitis secretes enterotoxin A, B, and toxic shock syndrome toxin 1. This is of interest because these patients may develop specific IgE antibodies against components from staphylococci. OBJECTIVE: The objective was to demonstrate IgE-sensitization to components of Staphylococcus aureus enterotoxins A and B (purified and partially purified), toxic shock syndrome toxin 1, and the bacterial cell component lipoteichoic acid, in patients with atopic dermatitis. METHODS: Blood samples from 34 patients with atopic dermatitis and 10 controls were tested by leukocyte histamine release to the enterotoxins and lipoteichoic acid. The toxins were separated by sodium dodecylsulfate polyacrylamide gel electrophoresis and analyzed by IgE-immunoblotting with sera from the same patients. RESULTS: The majority of patients (96%) with clinical signs of skin infection produced specific IgE-antibodies to all three toxins. Nearly half of the patients produced IgE to enterotoxin A and B. Only 63% of the patients with atopic dermatitis showed cellular response judged by the release of histamine from patient basophils when challenged in vitro with the toxins. This may indicate clinically unimportant sensitization in a number of patients. The immunoblotting revealed that the major allergens of the toxins were 24 and 28 kD proteins. Partially purified toxins showed a higher frequency of leukocyte histamine release responses than purified toxin. The only obvious difference was a difference in the content of pure toxin of the two preparations. Lipoteichoic acid showed nonspecific activity. CONCLUSION: These findings suggest that staphylococcal enterotoxins may act as specific allergens and induce IgE-antibodies to enterotoxins that may exacerbate the skin inflammation in some patients with atopic dermatitis.

Allergens↗
PubMed2003

In patients with dermatitis herpetiformis distribution of transglutaminase in cutaneous tissue does not differ from controls.

BACKGROUND: Dermatitis herpetiformis may be regarded as the cutaneous counterpart of coeliac disease. These conditions are related to the ingestion of gluten and both are characterised by circulating antibodies against tissue transglutaminase. AIMS: To study the distribution of tissue transglutaminase in the skin of dermatitis herpetiformis patients and controls, and to investigate whether the dermal IgA deposits, diagnostic for dermatitis herpetiformis, are related to tissue transglutaminase expression in the skin. METHODS: A series of 11 patients with dermatitis herpetiformis had a 4 mm punch biopsy taken from the uninvolved perilesional skin. A group of 16 controls, undergoing surgical removal of benign nevi, gave perilesional skin. Biopsies were covered with OCT and frozen at -80 degrees C. After washing, skin biopsy sections were incubated with an IgG anti-tissue transglutaminase mouse monoclonal antibody. After washing, sections were incubated with anti-mouse IgG. RESULTS: The anti-tissue transglutaminase monoclonal antibody specifically recognised the basal epidermal cells. This staining was no different between patients and controls. CONCLUSION: Our results suggest that tissue transglutaminase can be recognised in the basal epidermal layer both of patients with dermatitis herpetiformis and controls. Since this distribution does not correspond to the distribution of dermal IgA deposits, it is concluded that dermatitis herpetiformis dermal IgA deposits are not due to antibodies directed against cutaneous tissue transglutaminase.

Adult↗
PubMed2000

The relevance of skin prick tests for Pityrosporum ovale in patients with head and neck dermatitis.

BACKGROUND: Patients with atopic dermatitis often develop immunoglobulin E antibodies against the yeast Pityrosporum ovale. This organism may produce positive skin prick reactions in a higher rate in patients with atopic dermatitis of the head, scalp, and neck region. METHODS: We investigated whether positive prick tests to P. ovale were associated with a specific localization in the head and neck region. A total of 589 consecutive patients were prick tested with a P. ovale extract from ALK Abelló. RESULTS: Thirty-seven patients (6.3%) showed a positive reaction to the P. ovale extract. We could not find significant differences in the localizations of the dermatitis and the pattern of reaction to the tested intracutaneous allergens between the 37 patients positive to P. ovale and the control group of 55 subjects with negative reactions. In a subgroup, we found an elevated level of P. ovale-specific IgE in 100.0% of the patients with head and neck dermatitis, compared with 13.6% in the atopic dermatitis patients with lesions in any other localization. CONCLUSIONS: Our results clearly show that P. ovale-specific IgE is strongly related to the head and neck localization of atopic dermatitis, but RAST seems more sensitive than a prick test with the extract we used.

Adolescent↗
PubMed2002

Parthenium dermatitis presenting as photosensitive lichenoid eruption. A new clinical variant.

Parthenium hysterophorus is the commonest cause of airborne contact dermatitis (ABCD) in India. The disease usually manifests as itchy erythematous, papular, papulovesicular and plaque lesions on exposed areas of the body. Rarely, however, the disease may present as actinic reticuloid or photocontact dermatitis. We have observed a different clinical variant of this disease where certain patients with Parthenium dermatitis have presented with discrete, flat, violaceous papules and plaques on exposed areas of the body closely simulating photosensitive lichenoid eruption. We had 8 patients, 6 males and 2 females between 30 and 62 years of age, with itchy, violaceous, papules and plaques on the face, neck, ears, upper chest and dorsa of the hands for 6 months to 6.5 years. Four of these patients had a history of improvement of the lesions up to 30% in winter and aggravation of lesions on exposure to sunlight. There was no personal or family history of atopy. Cutaneous examination in all patients revealed multiple flat, violaceous, mildly erythematous papules and plaques on the forehead, sides and nape of neck, ears, 'V' area of the chest, and extensor aspects of the forearms and hands. Skin biopsies from these lesions showed features of chronic non-specific dermatitis. Patch testing with standardized plant antigens showed a positive patch test reaction to Parthenium hysterophorus in all patients, with a titre of contact hypersensitivity (TCH) varying from undiluted to 1 : 100. We conclude that Parthenium dermatitis may occasionally present with lesions very similar to the lesions of photosensitive lichenoid eruption in morphology and distribution. This clinical presentation of Parthenium dermatitis needs to be recognized to avoid misdiagnosis.

Adult↗
PubMed2003

Nickel-elicited systemic contact dermatitis.

20 patients with systemic contact dermatitis due to nickel are described. Of these patients, 15 were female and 5 were male. Their mean age was 24.8 years (16-51 years). All had experienced contact dermatitis in the umbilical area due to continual contact with metal belt-buckles or buttons. Then, with long- or short-term aggravation of such periumbilical dermatitis, commonly in summer, lesions spread to other sites such as the side of the neck, the flexures of the extremities, etc. All patients showed a positive patch test to nickel sulphate (2.5% in petrolatum) and the dimethylglyoxime test demonstrated the presence of free nickel on metal buttons or belt-buckles. Punch biopsies performed in 7 patients showed subacute dermatitis. After avoidance of continual exposure to objects containing nickel and foods rich in nickel, as well as treatment with oral antihistamines and topical corticosteroids, all patients improved or cleared. It has been reported that nickel can cause systemic contact dermatitis by some internal systemic route, such as oral intake, transfusion, inhalation, implantation of metal medical devices, etc. In our patients, we found that continual local skin contact could also elicit systemic contact dermatitis.

Adolescent↗
PubMed2001

Expression of interleukin-4 in the epidermis of transgenic mice results in a pruritic inflammatory skin disease: an experimental animal model to study atopic dermatitis.

Atopic dermatitis, a common, chronic, inflammatory skin disease that occurs with increasing prevalence, is characterized by hyperactivated cytokines of helper T cell subset 2 and is frequently associated with staphylococcal infection. An experimental animal model of atopic dermatitis induced by transgenically introduced cytokine is not available. We generated a transgenic mouse line expressing epidermal interleukin-4, a critical cytokine of helper T cell subset 2. Here we show that transgenic mice spontaneously developed a pruritic inflammatory skin disease reproducing all key features of human atopic dermatitis, including xerosis, conjunctivitis, inflammatory skin lesions, Staphylococcus aureus infection, histopathology of chronic dermatitis with T cell, mast cell, macrophage-like mononuclear cell, and eosinophil infiltration, and elevation of total serum IgE and IgG1. The onset and early progression of skin disease coincided with increased total serum IgE and IgG1. The mouse disease occurred at a 43% annual incidence rate and primarily affected the poorly haired skin: ear (100%), neck (65%), eye (53%), face (29%), tail (12%), leg (12%), and torso (6%). As a group the affected transgenic mice manifested with a skin disorder that fulfilled the clinical diagnostic criteria established for atopic dermatitis in human patients. Pending further characterization to authenticate it as a model of atopic dermatitis, this experimental animal model of pruritic inflammatory skin disease may facilitate investigations for the roles of interleukin-4 in cutaneous inflammation and skin infection in human patients.

Animals↗
PubMed2001

Anti-mycotics suppress interleukin-4 and interleukin-5 production in anti-CD3 plus anti-CD28-stimulated T cells from patients with atopic dermatitis.

It is reported that anti-mycotic agents are effective for the treatment of patients with atopic dermatitis. We studied the in vitro effects of anti-mycotics on T helper-1 and T helper-2 cytokine production in anti-CD3 plus anti-CD28-stimulated T cells from atopic dermatitis patients and normal donors. The amounts of interleukin-4 and interleukin-5 secreted by anti-CD3/CD28-stimulated T cells were higher in atopic dermatitis patients than in normal donors. Azole derivatives, ketoconazole, itraconazole, miconazole, and nonazole terbinafine hydrochloride, and tolnaftate reduced interleukin-4 and interleukin-5 secretion without altering that of interferon-gamma and interleukin-2 in anti-CD3/CD28-stimulated T cells from both atopic dermatitis patients and normal donors. The azole derivatives were more inhibitory than nonazole anti-mycotics. These anti-mycotics reduced the anti-CD3/CD28-induced mRNA expression and promoter activities for interleukin-4 and interleukin-5. The 3',5'-cyclic adenosine monophosphate analog dibutyryl 3',5'-cyclic adenosine monophosphate reversed the inhibitory effects of the anti-mycotics on interleukin-4 and interleukin-5 secretion, mRNA expression, and promoter activities. Anti-CD3/CD28 transiently (< or = 5 min) increased intracellular 3',5'-cyclic adenosine monophosphate in T cells, and the increase was greater in atopic dermatitis patients than in normal donors. The increase of 3',5'-cyclic adenosine monophosphate by anti-CD3/CD28 correlated with interleukin-4 and interleukin-5 secretion by anti-CD3/CD28. The transient 3',5'-cyclic adenosine monophosphate increase was suppressed by anti-mycotics, and azole derivatives were more suppressive than nonazoles. Azole derivatives inhibited the activity of cyclic adenosine monophosphate-synthesizing adenylate cyclase whereas terbinafine hydrochloride and tolnaftate enhanced the activity of 3',5'-cyclic adenosine monophosphate-hydrolyzing cyclic nucleotide phosphodiesterase in atopic dermatitis and normal T cells. These results suggest that the anti-mycotics may suppress interleukin-4 and interleukin-5 production by reducing 3',5'-cyclic adenosine monophosphate signal, and stress their potential use for the suppression of T helper-2-mediated allergic reactions.

Adenylyl Cyclases↗
PubMed2002

Oral administration of persimmon leaf extract ameliorates skin symptoms and transepidermal water loss in atopic dermatitis model mice, NC/Nga.

BACKGROUND: We have previously shown that persimmon leaf extract and its major flavonoid constituent, astragalin, inhibited histamine release by basophils and that oral administration of these substances prior to the onset into an atopic dermatitis (AD) model mouse, NC/Nga, prevented development of dermatitis. OBJECTIVES: This study was designed to assess the clinical therapeutic effect of persimmon leaf extract and astragalin in NC/Nga mice suffering from dermatitis and the dose-response preventive effects of persimmon leaf extract on dermatitis and transepidermal water loss (TEWL). METHODS: The efficacy of persimmon leaf extract or astragalin in NC/Nga mice was judged by measurement of skin severity, scratching behaviour, serum IgE levels or TEWL. RESULTS: Oral administration of persimmon leaf extract (250 mg kg(-1)) or astragalin (1.5 mg kg-1) for 4 weeks into NC/Nga mice with overt dermatitis resulted in a decrease in the severity of the condition. The preventive effect of persimmon leaf extract on the dermatitis was dose-dependent and continuous intake of persimmon leaf extract significantly decreased its onset and development. In addition, TEWL was also suppressed at a persimmon leaf extract dose of 250 mg kg(-1). No significant adverse reaction by these substances could be observed. CONCLUSIONS: These observations suggest that persimmon leaf extract or the flavonoid astragalin may be alternative substances for the management of AD.

Administration, Oral↗
PubMed2001

Distribution of HLA-A, B alleles and polymorphisms of TAP and LMP genes in Korean patients with atopic dermatitis.

BACKGROUND: Atopic dermatitis has been seen to result from multifactorial inheritance, with interaction between genetic and environmental factors. The genetic association may differ according to the ethnic backgrounds. OBJECTIVE: The purpose of this study was to investigate the genetic factors in Korean atopic dermatitis patients by studying the human leucocyte antigen (HLA) class I association and polymorphisms of transporters associated with antigen presentation (TAP) and low-molecular-weight polypeptide (LMP) genes. METHODS: HLA-A and B genotyping was performed in 53 atopic dermatitis patients and 184 healthy controls using the standard microlymphocytotoxicity technique. TAP1, TAP2, LMP2, and LMP7 gene polymorphisms were anaylzed using the polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP), PCR-amplification refractory mutation system (ARMS), and PCR-restriction fragment length polymorphism (RFLP). RESULTS: Allele frequency of HLA-A24 was significantly increased in patients with atopic dermatitis compared to controls (P < 0.05). HLA-B alleles showed no differences in distribution between patients and controls. Genotype, phenotype, and allele frequencies of TAP1 gene also revealed no differences in distribution between patients and controls. Analysis of TAP2 gene polymorphisms showed increased frequencies of the TAP2*C allele and TAP2*A/TAP2*C genotype in atopic dermatitis patients compared to controls (P < 0.05). Distribution of LMP2 and LMP7 gene polymorphisms was similar for patients and controls. CONCLUSION: This study demonstrates an association of atopic dermatitis with HLA-A24 and TAP2*C alleles in Korean patients. Discrepancy with the previous reports might be related to different patient characteristics and ethnic variations.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2002

Transforming growth factor-beta1 suppresses atopic dermatitis-like skin lesions in NC/Nga mice.

BACKGROUND: Atopic dermatitis is a chronic, relapsing inflammatory disorder characterized by pruritic and eczematous skin lesions. Transforming growth factor (TGF)-beta1 has been implicated in the suppression of inflammatory responses. OBJECTIVE: The purpose of this study is to determine whether TGF-beta1 suppresses skin lesions in a mouse model of atopic dermatitis. METHODS: We used the NC/Nga strain of mice as an in vivo model of atopic dermatitis. The effects of exogenous TGF-beta1 on atopic dermatitis-like skin lesions in NC/Nga mice were evaluated clinically, histologically and immunologically. RESULTS: Subcutaneous injection of recombinant TGF-beta1 macroscopically suppressed eczematous skin lesions in NC/Nga mice associated with reduced serum immunoglobulin E (IgE) levels. Histological analysis showed that TGF-beta1 significantly inhibited the infiltration of inflammatory cells such as mast cells and eosinophils into the skin of NC/Nga mice. Spontaneous interferon (IFN)-gamma production from splenocytes of NC/Nga mice was down-regulated by the treatment with TGF-beta1 and neutralizing antibody against IFN-gamma inhibited skin lesions in NC/Nga mice. The inhibitory effect of TGF-beta1 on the skin lesions lasted at least 1 week after cessation of the treatment. CONCLUSION: These findings indicate that TGF-beta1 suppressed atopic dermatitis-like skin lesions in NC/Nga mice at least in part through down-regulation of IFN-gamma. These results suggest that TGF-beta1 may have a therapeutic potential for atopic dermatitis.

Animals↗
PubMed1998

Outbreak of rat mite dermatitis in medical students.

BACKGROUND: The tropical rat mite, Ornithonyssus bacoti (0. bacoti), is an ectoparasite on many rodents, but when the rodent is not available, humans may become the victim of the mite's bite. The bite induces a nonspecific dermatitis; therefore, it is not easy to diagnose rat mite dermatitis unless the parasites are found. MATERIALS AND METHODS: Ten cases of rat mite dermatitis were found in medical students who had studied in the same room of the library. Their nonspecific dermatitis consisted of small papules, and parasites were found in the skin or in the environment. The mites were collected and identified as O. bacoti, female. Histopathologic studies showed moderate perivascular lymphohistiocytic infiltrations intermingled with some eosinophils. The presence of rodents in or around the room was confirmed by the students, but there had been no preceding rodent eradication. Although the rats were not captured in the library, insecticides were sprayed, and no further problem with either mites or dermatitis developed during the follow-up period. CONCLUSIONS: Rat mite dermatitis can occur in clusters that involve a common source of exposure to the rat mite epidemiologically. Prompt identification of rat mites and the eradication of mites and rodents from the environment can prevent further spreading of the disease.

Adult↗