LECT2 modulates dendritic cell function after Helicobacter pylori infection via the CD209a receptor.

BACKGROUND

Helicobacter pylori, a gram-negative bacterium persisting on the gastric mucosa, is involved in the pathogenesis of a variety of gastric diseases. Leukocyte cell-derived chemotaxin 2 (LECT2) treatment increased the phagocytic capacity of lymphocytes and improved immune function in bacterial infection. Whether the immune cells infected with H. pylori are affected by LECT2 is unclear.

METHODS

Bone marrow-derived dendritic cells (BMDCs) from wild-type C57BL/6 mice, CD209a knockout mice, or LECT2 knockout mice were exposed to H. pylori at a multiplicity of infection of 10 for 24 h. The maturity of DCs and the cytokines secreted by DCs were analyzed by flow cytometry, western blot, and real-time PCR. The signaling pathway underlying CD209a activation after LECT2 treatment were also detected.

RESULTS

LECT2 treatment promoted H. pylori-induced BMDC maturation and produced a high level of anti-inflammatory cytokine (IL-10) but a low level of pro-inflammatory cytokine (IL-23p40). Moreover, LECT2-pretreated DCs shifted the development of pro-inflammatory Th1/Th17 cells to Treg cells. CD209a mediated LECT2-induced maturation and secretion of DC in H. pylori-primed BMDCs. LECT2 was further confirmed to induce the secretion of certain cytokines via CD209a-JNK/P38 MAPK pathway.

CONCLUSION

This study reveals that LECT2 modulated the functions of H. pylori-primed DCs in a CD209a-dependent manner, which might hinder the clearance of H. pylori and contribute to its colonization.