Dialogue between gastrointestinal tract and skin: New insights into the Helicobacter pylori and atopic dermatitis.

BACKGROUND

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.

MATERIALS AND METHODS

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.

RESULTS

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.

CONCLUSIONS

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.