title: Type 1 and Type 2 cytokines imbalance in adult male C57BL/6 mice following a 7-day oral exposure to perfluorooctanesulfonate (PFOS).
abstract: Previous studies indicate that exposure to perfluorooctanesulfonate (PFOS), a ubiquitous and highly persistent environmental contaminant induces immunotoxicity in mice. However, clear mechanisms to explain any PFOS-induced immunotoxicity are still unknown. The study here sought to examine the ability of PFOS to potentially perturb T-helper (T(H))-1 and -2 cell cytokine secreting activities, as well as to cause shifts in antibody isotype levels, as possible mechanisms involved in PFOS-induced immunotoxicity. Adult male C57BL/6 mice were given by gavage 0, 5, or 20 mg PFOS/kg/d for 7 days. One day after the final exposure, spleens from these hosts were isolated and used for analyses of the ex vivo production of T(H)1-type (interleukin-2 (IL-2), interferon-γ (IFNγ), T(H)2-type (IL-4), and IL-10 cytokines by isolated splenocytes. In addition, serum was isolated from these mice in order to assess their levels of immunoglobulin M (IgM) and IgG antibodies. In all studies, levels of the cytokines of the antibodies were quantified via enzyme-linked immunosorbent assay or enzyme-linked immunosorbent spot. The results here showed that IL-2 and IFNγ formation was reduced, but that IL-4 production increased by the 5 and 20 mg PFOS/kg/d treatments. Serum IgM levels decreased significantly (in dose-related manner) as a result of the PFOS exposures; serum IgG levels increased markedly with 5 mg PFOS/kg/d, but decreased slightly with the 20 mg PFOS/kg/d regimens PFOS exposure increased serum corticosterone levels in a dose-dependent manner. These results indicated that, after a high-dose short-term exposure to PFOS, a host's immune state is likely to be characterized by a shift toward a more T(H)2-like state that, in turn, may lead to suppression of their cellular response and enhancement of their humoral response.
authors.affiliation: Department of Immunology, College of Basic Medical Science, China Medical University, Shenyang, PR China.
authors.forename: Li
authors.initials: L
authors.lastname: Zheng
authors.forename: Guang-Hui
authors.initials: GH
authors.lastname: Dong
authors.forename: Ying-Hua
authors.initials: YH
authors.lastname: Zhang
authors.forename: Zai-Fu
authors.initials: ZF
authors.lastname: Liang
authors.forename: Yi-He
authors.initials: YH
authors.lastname: Jin
authors.forename: Qin-Cheng
authors.initials: QC
authors.lastname: He
mesh_terms: D000284:Administration, Oral; D017738:Alkanesulfonic Acids / Q000633:toxicity*; D000818:Animals; D016207:Cytokines / Q000276:immunology*; D004305:Dose-Response Relationship, Drug; D004785:Environmental Pollutants / Q000633:toxicity*; D005466:Fluorocarbons / Q000633:toxicity*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D013154:Spleen / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D018417:Th1 Cells / Q000187:drug effects* / Q000276:immunology; D018418:Th2 Cells / Q000187:drug effects* / Q000276:immunology
chemical_list: D017738:Alkanesulfonic Acids; D016207:Cytokines; D004785:Environmental Pollutants; D005466:Fluorocarbons; C076994:perfluorooctane sulfonic acid