Tolerance to contact hypersensitivity was induced by feeding of different DNCB doses in mice. A total of 40 mice were divided into 4 groups(control group, 6 mg feeding group, 10 mg feeding group, 14 mg feeding group) in experiment I, Degree of tolerance to contact hypersensitivity was rneasured by incremert rate of ear swelling after challenge with DNFB. Experiment 2 was performed in the same method of cxperiment: I with addition of 3 mg DNCB feeding group. The increment ratee were significantly decreased in DNCB feeding groups in experirnent 1 and 2(p<0.0l). But there were no differences statisticalIy between increment rates of DNCB feeding groups.
Animals ; Dermatitis, Contact ; Dinitrochlorobenzene* ; Dinitrofluorobenzene ; Ear ; Mice*

BACKGROUND: Vitamin C is an essential nutrient, taken as a daily supplement by many people. Recently, high-dose vitamin C is considered as a therapeutic regimen in some clinical situations. Until now, few studies have been done with the effects of high-dose vitamin C on the immune response. METHODS: In this experiment, the effects of high-dose vitamin C on cell-mediated immune response in immunologically competent mice were evaluated. After intraperitoneal injection of 2.5, 5, or 10 mg/day of vitamin C for 10 days, delayed type hypersensitivity (DTH) was provoked against DNFB in the pinnae as a model for cell-mediated immune response. Severity of DTH reaction was evaluated as the thickness of pinnae, and the vitamin C levels were measured in the serum, liver, kidney, lung, pinnae, and splenocytes. RESULTS: After challenge, the thickness increased at its peak on the 2(nd) day in all groups. On the first day, the pinnae were thicker in the injected groups than in the control. On the contrary, the increment of the pinnae thickness was attenuated and the number of cells infiltrated in the site of DTH decreased proportionately to the amount of vitamin C administered from the second day on. With vitamin C exogenously given, the serum level peaked at 30 min after injection, and returned abruptly to its basal level without accumulation. However, it accumulated in the liver, kidney, and especially in the pinnae inflamed and splenopcytes, proportionately to the amount administered. CONCLUSION: Based on these results, it is suggested that, in one hand, exogenously administered high-dose vitamin C accumulated in the splenocytes and presumably changed the function of them resulting in the augmented cell-mediated immune response, as was revealed in the first day of DTH reaction. On the other hand, it seems likely that the vitamin C also showed anti-inflammatory effects.
Animals ; Ascorbic Acid* ; Dinitrofluorobenzene ; Hand ; Hypersensitivity ; Injections, Intraperitoneal ; Kidney ; Liver ; Lung ; Mice* ; Vitamins*

Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.
Animals ; Dermatitis, Contact* ; Dinitrofluorobenzene ; Humans ; Lymph Nodes ; Mice ; Prostaglandins E ; Skin ; Tissue Donors

Contact hypersensitivity (CH) responsiveness to 24-dinitro-l-fluorobenzene(DNFB)is depressed in mice sensitized through unexposed skin sites after exposure to high dose of ultraviolet B radiation(UVB). Exposure of mice to ultraviolet A(UVA) radiation in combination with 8-methoxypsoralen(8-MOP) also results in a systemic suppression of CH. Our study was designed to determine whether a high dose of UVA radiation alone can induce a systemic suppression of CH, and if so, which phase of CH response is influenced by UVA radiation. Relatively large doses of UVA(400, 600, 800J/cm²) induced significant systemic suppression of CH when DNFB was applied to UVA-unirradiated abdominal skin. The duration of the rest period after UVA exposure did not cause any significant change in systemic suppresion of CH. Functional analyses showed that lymph node cells(LNCs) obtained from donors that were sensitized on the unirradiated skin site with DNFB 5 days after UVA treatment transferred normal ear-swelling responsiveness to non-primed recipients, thus implying that high doses of UVA can induce systemic suppression which is not affected in the induction phase of CH but affected in the elicitation phase of CH. UVA irradiation de-creased Langerhans cell(LC) numbers significantly with a dose of 100J/cm² or greater. LNCs obtained from donors that were sensitized on the irradiated skin site with DNFB 5 days after UVA treatment did not transfer normal ear-swelling responsiveness to non-primed recipients. This phenomenon may be related to the decreased number of LC after UV treatment. To look for possible mediators impairing the elicitation phase of the CH reaction, we checked prostaglandin E(PGE) levels in serum after 800J/cm² irradiation. A high dose of UVA did not increase the serum PGE level in mice as much as UVB irradiation, in which a significant increase of PGE may affect CH response.
Animals ; Dermatitis, Contact* ; Dinitrofluorobenzene ; Humans ; Lymph Nodes ; Mice ; Prostaglandins E ; Skin ; Tissue Donors

This experiment pursued the time course of contact hypersensitivity to 2,4-dinitro-1-fluorobenzene (DNFB) and histologic changes of the cutaneous reaction in mice. The contact hypersensitivity reached a maximum 4 days after sensitization (96.9 +/- 6.7% vs. 22.7 +/- 1.3% in control) and persisted for 3 weeks. The cutaneous hypersensitivity reaction showed peak reactivity at 24 hr after challenge (96.2 +/- 4.7% vs. 11.5 +/- 1.7% in control), and persisted up to 96 hr (13.2 +/- 2.1%). Prime histologic changes observed in this experiment were the exocytosis of lymphoid cells and epidermal thickening which appeared at 20 hr after challenge. Edema, vasodilatation and increased mast cells were observed within the dermis at 4-8 hr. However, edema and vasodilatation disappeared gradually, but numbers of mast cell increased up to 96 hr. The dermal infiltrates were maximum at the 28-72 hr after challenge.
Animals ; Dermatitis, Contact/immunology/*pathology ; Dinitrofluorobenzene/*pharmacology ; Ear ; Female ; Mice ; Mice, Inbred BALB C ; Nitrobenzenes/*pharmacology ; Time Factors

BACKGROUND: Evening primrose oil(EPO) is a rich source of cis-linoleic acid and gammalinolenic acid(GLA) and has been used as a therapeutic agent in various skin diseases such as atopic dermatitis. OBJECTIVE: The purpose of this study was to evaluate the suppressive effect of EPO on murine contact sensitivity. METHODS: BALB/c mice were divided into 3 groups, positive control, experimental and negative control groups: the positive control group represents a group of mice which were sensitized and challenged with DNFB, the experimental group represents EPO-pretreated positive control group and the negative control group represents a group of mice which were challenged only. The changes of ear thickness were measured, and H & E staining and immunohistochemical staining for ICAM-1 expression of ear skin were performed to evaluate the histological changes of each group. RESULTS: The Pretreatment of mice with EPO resulted in suppression of contact sensitivity by more than 82%. On H & E staining, only a mild inflammatory reaction was observed in the dermis. Also ICAM-1 expression of keratinocytes, the intensity of the staining was significantly decreased in the experimental group compared with positive group. CONCLUSIONS: Our study indicates that EPO was able to suppress the induction of contact sensitivity.
Animals ; Dermatitis, Atopic ; Dermatitis, Contact* ; Dermis ; Dinitrofluorobenzene ; Ear ; Intercellular Adhesion Molecule-1 ; Keratinocytes ; Mice ; Oenothera biennis* ; Skin ; Skin Diseases

BACKGROUND: Langerhans cells (LC), keratinocytes and Thy-1+ dendritic epidermal cells(DEC) are epidermal cells which are known to have important roles in inflammatory or immunologic skin disorders. Allergic contact dermatitis(ACD) is a prototype of a delayed hypersensitive reaction in which LC, keratinocytes and T lymphocytes play an important role. The role of LC in ACD is well known, but the role of Thy-1+ DEC is not yet fully revealed. Futhermore, the mechanism of irritant contact dermatitis(ICD) is not known and more study is required on the interaction between these epidermal cells in ICD. OBJECTIVE: The aim of this study is to observe the changes of these cells in ACD and ICD and to discuss their possible roles in the disease precess. MEHTODS: We evoked ACD with DNFB and ICD with croton oil in BALB/c mice and observed the morphologic changes of LC, Ia+ keratinocytes, and Thy-1+ DEC by immunoperoxidase staining when the inflammation was at its peak and at the resolution state. RESULTS: 1. In the control group, LC were evenly distributed and their average number was 1147+/-132/mm*. Thy-1+ DEC were slightly bigger than LC and showed uneven distribution. The average number of Thy-1+ DEC was 57+/-69/mm* Ia+ keratinocytes did not appeared. 2. On the 1st day of DNFB challenge, the number of LC was significantly decreased and their size and dendritic processes were increased when compared to those of the control group. Most of the keratinocytes showed Ia antigen expression on their surfaces. 3. On the 12th day of DNFB challenge, no significant changes in the number and morphologyof LC were noted when compared to the cotrol group, Ia+ keratinocytes were not observed. 4. there were no significant changes in the number and morphology of Thy-1+ DEC in ACD on the 1st and 12th day after DNFB challenge. 5. On the 2nd day after croton oil application, the number of LC was significantly decreased but the morphology not significantly changed. Ia+ keratinocytes were not observed. 6. On the 20th day after croton oil application, the number of LC was significantly increased but the morphology was not significantly changed. Ia+ keratinocytes were not observed. 7. There were no significant changes in th number and morphology of Thy-1+ DEC in ICD on the 2nd and 20th day after application of croton oil. Ia+ keratinocytes were not observed. CONCLUSION: In can be deduced that the LC have important roles in the mechanisms of both ACD and ICD reactions. Ia+ keratinocytes have an important role mainlyin the inflammatory precess of ACD. In addition, since the changes of the number of Langerhans cells in ACD and ICD showed different time courses and Ia+ keratinocytes appeared only in ACD, we hypothesized that different pathways of inflammation exist in ACD and ICD, and different cytokines may be responsible. It is probable that Thy-1+ DEC does not have any significant role in the inflammatory process of both ACD and ICD.
Animals ; Croton Oil ; Cytokines ; Dermatitis, Allergic Contact* ; Dermatitis, Contact* ; Dinitrofluorobenzene ; Histocompatibility Antigens Class II ; Inflammation ; Keratinocytes ; Langerhans Cells ; Mice ; Skin ; T-Lymphocytes

The injection of antigen into the anterior chamber of the eye results in a unusual pattern of systemic immune responses termed anterior chamber associated immune deviation(ACAID). This study was done to investigate the in vitro effect of bovine aqueous humor(BAR) on the proliferation response of murine spleen and thymus to mitogens, to determine in vivo effects of BAR on delayed-type hypersensitivity and hemagglutinin response to sheep red blood cells, and to examine contact hypersensitivity to dinitrofluorobenzene(DNFB). Also, the effect on in vivo exposure to BAH on the production of IL-2 and IL-6 of murine lymphocyte was investigated. As a result, various concentration of BAR inhibited or enhanced the proliferation response of mouse splenocytes to mitogens. BAR injection significantly enhanced 'Arthus reaction to SRBC, but failed to change DTR reaction to SRBC. Interestingly, however, BAR profoundly inhibited contact hypersensitivity to DNFB and HA response. BAR inhibited both IL-2 and IL-6 production of murine spleen and thymus cells. Taken together, these results suggest that BAR contains soluble factor(s) that can suppress or enhance immune response, depending on experimental conditions and that immunomodulatory activity of BAR is not species-specific.
Animals ; Anterior Chamber ; Aqueous Humor* ; Dermatitis, Contact ; Dinitrofluorobenzene ; Erythrocytes ; Hemagglutinins ; Hypersensitivity ; Interleukin-2* ; Interleukin-6* ; Lymphocytes ; Mice* ; Mitogens ; Sheep ; Spleen ; Thymus Gland

Animals ; Dinitrofluorobenzene ; Ear ; Electrons ; Erbium ; Gene Expression ; Humans ; Inflammation ; Interleukin-1beta ; Laser Therapy ; Lymphocytes ; Male ; Mice ; Skin ; Tumor Necrosis Factor-alpha

OBJECTIVETo investigate the therapeutic effect of mustard seed on allergic contact dermatitis (ACD) in mice and explore the mechanism.

METHODSEighteen BALB/c mice were randomly divided into normal control group, model group and mustard seed group. The mice in the normal control group and model group were fed with normal chow, and those in mustard seed group were given 5% mustard seed mixed in the chow. Three weeks later, ACD was induced on the ear using 2, 4-dinitrofluorobenzene. After 24 h, the swelling of the ear was examined, and the rats were sacrificed to collect the ear tissue ears and blood for histopathological and immunohistochemical examinations, RT-PCR and enzyme-linked immunosorbent assay.

RESULTSIn mice with ACD, feeding with mustard seeds significantly lessened the ear swelling, improved the tissue histopathology, lowered the number of infiltrating Langerhans cells, and reduced the expressions of IL-1β, TNF-α and IL-6 mRNA in the ear, but did not cause significant changes in serum levels of IL-4, IFN-γ and IL-17.

CONCLUSIONMustard seed inhibits ACD in mice possibly by suppressing the expressions of IL-1β, TNF-α and IL-6 mRNA and inhibiting Langerhans cell migration in the epidermis.

Animals ; Dermatitis, Allergic Contact ; drug therapy ; metabolism ; Dinitrofluorobenzene ; adverse effects ; Female ; Interleukin-1beta ; metabolism ; Interleukin-6 ; metabolism ; Mice ; Mice, Inbred BALB C ; Mustard Plant ; Seeds ; Tumor Necrosis Factor-alpha ; metabolism