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The immunomodulatory properties of arsenic are nowadays supposed be associated with pathological injuries of this toxicant and the details have not been clarified. Our objective was to explore inflammation, differentiation of diverse T cell subsets, as well as the phenotypic molecules and functions of dendritic cells (DCs) by chronic arsenic exposure in vivo. We exposed different concentrations of arsenic (0, 0.1, 1 and 10 mg/L) in drinking water for 6 and 12 months in C57BL/6 mice. We first confirmed that low levels of arsenic induced excess inflammation evidenced by accumulation of macrophages and lymphocytes in bronchoalveolar lavage fluid (BALF), secretion of pro-inflammatory cytokine IL-1β in BALF and serum, as well as histological analysis. Flow cytometry analysis revealed that arsenic disturbed CD4/CD8 T-cell ratio in isolated pneumonocytes and splenocytes, as well as enhanced IFN-γ and reduced IL-4 in spleen. The mRNA expressions of transcription factors (T-bet, GATA3, ROR-γt) and cytokines (IFN-γ, IL-4, IL-10, IL-23, IL-22) showed the imbalanced Th1/Th2/Th17 differentiation in arsenic exposed lung and spleen. We further testified that arsenic enhanced the percentages of CD11c DCs, and promoted the expressions of antigen presentation molecule MHC II and cytokine IL-12, co-stimulatory molecules (CD86, CD80), and chemokine receptors (CCR7, CCR5) in vivo. Moreover, arsenic activated the expressions of immune-related MAPKs and NF-κB. Taken together, our study here demonstrated that chronic arsenic exposure could disrupt the immune homeostasis in vivo possibly by interfering with the differentiation of Th1/Th2/Th17 subsets as well as the function of DCs.
This article was published in the following journal.
Name: International immunopharmacology
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