Oral Cadmium Intake Enhances Contact Allergen-induced Skin Reaction in Rats

Objective The effect of oral cadmium(Cd)intake to influence contact skin allergies was examined,since it is known that Cd is a heavy metal that affects many tissues,including the skin,in which it disturbs homeostasis,thus resulting in inflammation and injury.Methods Male rats were evoked with experimental contact hypersensitivity reaction(CHS)to hapten dinitrochlorobenzene(DNCB),after prolonged(30 day)oral exposure to an environmentally relevant Cd dose(5 ppm).The ear cell population was analyzed with flow cytometry.Cytokine production by ear skin cells and the activity of skin-draining lymph node(DLN)cells were measured using enzyme-linked immunosorbent assay(ELISA).Results Orally acquired Cd(5 ppm)increased CHS intensity only in Dark Agouti(DA)rats by affecting inflammatory responses in both the sensitization(an increase of IFN-γ and IL-17 cytokine production)and challenge(an increase of CD8^(+)and CD4^(+)cell number and TNF,IFN-γ and IL-17 cytokine production)phases.An increased CHS reaction was seen in Albino Oxford(AO)rats only at a high Cd dose(50 ppm),during the challenge phase(an increase of CD8^(+)and CD4^(+)cell number and TNF,IFN-γ and IL-17 cytokine production).Conclusion These novel data indicate that oral Cd intensifies the skin response to sensitizing chemicals such as DNCB.

Inhibitory activity of Cinnamomum Cassia extract on hypersensitivity in mice

OBJECTIVE Cinnamomum cassia has been used in traditional medicine in East Asian countries to treatallergic disease.Previous studies have demonstrated that C.cassiainhibits the development of mite antigen-induced skin lesions in NC/Nga mice by suppressing the Thelper 2cell response.The objective of this study is to investigate whether C.cassia has an efficient inhibition on systemic anaphylaxis and contact hypersensitivity in mice.METHODS To induce systemic anaphylaxis,mice were injected intraperitoneally with compound 48/80.Mortality was monitored for 1h after the injection.Contact hypersensitivity reaction was induced by topical application of 2,4-dinitrofluorobenzene(DNFB)to the ears of mice.After DNFBchallenge,ear thickness was measured 0,24 and 48h.RESULTS We discovered that C.cassia significantly inhibited compound 48/80-induced anaphylaxis and DNFB-induced ear swelling.Compound 48/80-induced anaphylaxiswas completely inhibited at the dose of 60mg·kg-1 body weight.Ear swelling at 24 h after DNFB-challenge was significantly less than that in the control group(0.16±0.03 vs.0.32±0.03 mm,P<0.01),while C.cassia was administered at the dose of 200mg·kg-1.CONCLUSION These findings indicate that C.cassiasuppresses allergic reactions,thus has potential value for mitigation of atopic dermatitis.

Long-term dermal exposure to diisononyl phthalate exacerbates atopic dermatitis through oxidative stress in an FITC-induced mouse model

Diisononyl phthalate （DINP）, considered to be an environmentally friendly plasticizer, is now widely used. However, the toxic effects of DINP need to be examined, particularly the effects of long-term dermal DINP exposure. Research into the mechanisms underlying these effects is urgently needed. In this study we examined the exacerbation effect of long-term dermal exposure to DINP in flnorescein isothiocyanate （FITC）-induced contact hypersensitivity （CHS） in mice, and sought the potential molecular mechanisms. Forty-nine male Balb/c mice were subjected to a 40-day dermal exposure to saline or one of three concentrations of DINP and then three rounds of sensitization with vehicle or 0.5% FITC. The results of a histopathological examination and measurement of ear swelling as well as immunological and inflammatory biomarkers （total-immunoglobulin （Ig）E and Th cytokines） supported the notion that high doses of DINP may aggravate atopic dermatitis. We also showed that melatonin, an antioxidant, could decrease the levels of oxidative stress and alleviate FITC-induced CHS suggesting that oxidative stress may be one of the molecular mechanisms to explain the exacerbation effect induced by DINP.