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Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
Published on: May 21, 2012
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LECT2 modulates dendritic cell function after Helicobacter pylori infection via the CD209a receptor
Xiaofen Zhang1, Kefang Sun1, Chenxi Tang1
1Department of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, Zhejiang Province, China.
Journal of Gastroenterology and Hepatology
|February 6, 2023
Summary
Leukocyte cell-derived chemotaxin 2 (LECT2) influences Helicobacter pylori infection by modulating dendritic cell function. This interaction, dependent on CD209a, may impede bacterial clearance and promote colonization.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Helicobacter pylori (H. pylori) is a gastric pathogen linked to various diseases.
- Leukocyte cell-derived chemotaxin 2 (LECT2) enhances immune responses in bacterial infections.
- The effect of LECT2 on H. pylori-infected immune cells remains unclear.
Purpose of the Study:
- To investigate the role of LECT2 in H. pylori-infected dendritic cells (DCs).
- To elucidate the mechanism of LECT2 action in H. pylori infection.
Main Methods:
- Bone marrow-derived dendritic cells (BMDCs) from wild-type, CD209a knockout, and LECT2 knockout mice were infected with H. pylori.
- DC maturation and cytokine secretion were analyzed using flow cytometry, western blot, and real-time PCR.
- The CD209a signaling pathway (JNK/P38 MAPK) involved in LECT2 treatment was investigated.
Main Results:
- LECT2 promoted H. pylori-induced BMDC maturation.
- LECT2 treatment led to increased IL-10 and decreased IL-23p40 secretion.
- LECT2-treated DCs shifted T cell differentiation from pro-inflammatory Th1/Th17 to Treg cells.
- CD209a mediated LECT2-induced DC maturation and cytokine secretion via the JNK/P38 MAPK pathway.
Conclusions:
- LECT2 modulates H. pylori-primed DC function in a CD209a-dependent manner.
- This modulation may hinder H. pylori clearance and contribute to its gastric colonization.
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