Abstract

Although many studies have focused on the protective function of H pylori in some allergic diseases, it remains unknown as whether H pylori infection exerts a similar protective effect on atopic dermatitis(AD). Thus, the aim of this study was to evaluate the association between H pylori infection and AD. An animal model of H pylori infection-AD was established by epicutaneous sensitization with calcipotriol after infection with H pylori by gavage. The Treg cells were analyzed by flow cytometry and immunohistochemistry. The expression of key inflammatory cytokines in dermal tissues was investigated at the mRNA level by real-time PCR. Compared with that in the H pylori-negative AD group, the severity of skin lesions, such as hyperemia, erythema, and swelling, was lower in the H pylori-positive AD group, while the serum IgE level decreased significantly in the H pylori-positive AD group. The percentage of CD4+ CD25+ Foxp3+ Treg cells in the peripheral blood and the number of Foxp3+ cells in dermal tissues increased significantly in the H pylori-positive AD group. The expression of IL-10 and TGF-β was upregulated, while the expression of IL-4 mRNA was downregulated in dermal tissues in the H pylori-positive AD group. The adoptive transfer assay showed that the number of CFSE+ Treg cells in the cervical lymph nodes of AD mice was significantly higher than that in normal mice, indicating the Tregs in H pylori-positive mice had a tendency to migrate to the skin tissue. It was also found that H pylori infection induced CCR4+ Treg cells expansion synchronously in gastric lymph nodes, spleen, blood, mesenteric lymph node (MLN), and cervical lymph nodes by the time of H pylori infection. H pylori infection alleviated calcipotriol-inducing AD manifestations by inducing the amplification of CD4+ CD25+ Foxp3+ Treg cells in the peripheral blood. H pylori showed possible protection against atopic dermatitis, suggesting an immune dialogue between gastrointestinal tract and skin.

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