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Abstract: Perfluorooctanoic acid (PFOA) has unique physical and chemical characteristics, water and oil repellency, thermal stability, and surfactant properties. PFOA has been regularly found in the blood of animals and humans worldwide, and has become an increasing concern because of its adverse effects in immune system. However, the role of PFOA in the allergic inflammation is not well-known. To further extend the immunotoxicity of PFOA, we examined the role of PFOA on the mast cell-mediated allergic inflammation and studied the possible mechanism of action. PFOA dose- and time-dependently increased histamine release from mast cells and serum histamine by the induction of intracellular calcium. PFOA exacerbated the IgE-dependent local allergic reaction in the mouse allergy model. PFOA induced gene expression of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 in mast cells. The inducing effect of PFOA on the pro-inflammatory cytokines was nuclear factor-κB, p38 mitogen-activated protein kinase, and caspase-1 dependent. Furthermore, the activation of cyclooxygenase-2 by PFOA suggests the induction of allergic inflammatory mediators by the PFOA. Our findings provide evidence that PFOA, the known immunotoxic agent, induces mast cell-derived allergic inflammatory reactions by histamine release and expression of pro-inflammatory cytokines. [Copyright &y& Elsevier]

Abstract: Ethnopharmacological relevance: The Lindera obtusiloba has been used in traditional medicine for the treatment of inflammation and dermatitis. In this study, we investigated the effect of topical application of Lindera obtusiloba water extract (LOWE) on the house dust mite extract (Dermatophagoides farinae extract, DFE) and 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD). Materials and methods: We established AD model in BALB/c mice by repeated local exposure of DFE/DNCB to the ears. After a topical application of LOWE on the skin lesions, the epidermal thickness, mast cell infiltration, and serum immunoglobulin E (IgE) and histamine were measured. In addition, the gene expression of interleukin (IL)-4, IL-13, IL-31, and tumor necrosis factor (TNF)-α in the ears was assayed. Results: LOWE reduced AD symptoms based on ear thickness, histopathological analysis, and serum IgE levels. LOWE inhibited mast cell infiltration into the ear and elevation of serum histamine in AD model. Moreover, LOWE suppressed DFE/DNCB-induced expression of IL-4, IL-13, IL-31, and TNF-α in the ears. Conclusions: Our results showed that topical application of LOWE exerts beneficial effects in AD symptoms, suggesting that LOWE might be a candidate for the treatment of AD. [Copyright &y& Elsevier]

Mercuric sulfide (HgS) is a major component of cinnabar, which has been used as a sedative drug in China for more than 2000 years. Because its toxicological effects are still unclear, we attempted to verify the toxic effects of HgS, focused on liver and immune organs such as the spleen and thymus. Male ICR mice were administered HgS (0.02, 0.2, 2.0 g/kg/day) by gavage for 4 weeks. During the administration period, HgS-treated mice did not reveal overt signs of clinical toxicity. HgS had no significant effect on body weight, food consumption, water consumption, and organ weights. In spite of its known insolubility, HgS was absorbed by the gastrointestinal tract and accumulated in the liver, spleen and thymus in a dose-dependent manner. In the biochemical and histological examination, HgS did not cause hepatotoxicity. However, HgS significantly increased both CD8+ T lymphocytes and CD4+CD8+ lymphocyte populations in the spleen without changing in the thymus. In the histological evaluation, HgS induced enlargement with marked hyperplasia and increase of lymphoid follicles in the spleen. In addition, HgS induced the gene expression of pro-inflammatory cytokines in the spleen and thymus. Our results suggest that insoluble HgS was absorbed by the gastrointestinal tract, accumulated in the spleen and thymus, and thus could affect immune systems. [ABSTRACT FROM AUTHOR]