In vivo hydroquinone exposure impairs allergic lung inflammation in rats.

Hydroquinone (HQ) is naturally found in the diet, drugs, as an environmental contaminant and endogenously generated after benzene exposure. Considering that HQ alters the immune system and its several source of exposures in the environment, we hypothesized that prolonged exposure of HQ could affect the course of an immune-mediated inflammatory response. For this purpose, male Wistar rats were intraperitoneally exposed to vehicle or HQ once a day, for 22 days with a 2-day interval every 5 days. On day 10 after exposure with vehicle or HQ, animals were ovalbumin (OA)-sensitized and OA-aerosolized challenged on day 23. HQ exposure did not alter the number of circulating leukocytes but impaired allergic inflammation, evidenced by lower number of leukocytes in the bronchoalveolar lavage fluid 24h after OA-challenge. Reduced force contraction of ex vivo tracheal segments upon OA-challenge and impaired mesentery mast cell degranulation after in situ OA-challenge were also detected in tissues from HQ exposed animals. The OA-specificity on the decreased responses was corroborated by normal trachea contraction and mast cell degranulation in response to compound 48/80. In fact, lower levels of circulating OA-anaphylactic antibodies were found in HQ exposed rats, as assessed by passive cutaneous anaphylaxis assay. The reduced level of OA-anaphylactic antibody was not dependent on lower number or proliferation of lymphocytes. Nevertheless, lower expression of the co-stimulatory molecules CD6 and CD45R on OA-activated lymphocytes from HQ exposed rats indicate the interference of HQ exposure with signaling of the humoral response during allergic inflammation. Together, these data indicate specific effects of HQ exposure manifested during an immune host defense.

Absence of CD4+ T cells impairs host defence of mice infected with Fonsecaea pedrosoi.

Chromoblastomycosis is a human chronic, often debilitating, suppurative, granulomatus mycosis of the skin and subcutaneous tissues beginning after inoculation trauma. It occurs worldwide, but is more frequently observed in tropical countries such as Brazil. Some studies have focused on fungus-host interaction, showing a predominantly cell-mediated immune response, with the activation of macrophages involved in fungus phagocytosis. Immunization with live conidia produced a high influx of CD4 T cells into the draining lymph node. The sensitized T cells proliferate in vitro when restimulated with specific antigen and preferentially produce IFN- gamma. To better characterize the role played by T cells on the chromoblastomycosis infection we used mice deficient for CD4 and CD8. Data determined by CFU counts associated with decreased DTH and IFN-gamma production of infected mice clearly demonstrated that, during experimental F. pedrosoi infection, absence of CD4(+) cells induces a more severe disease.