M2 macrophages participate in ILC2 activation induced by Helicobacter pylori infection

ABSTRACT

Helicobacter pylori (H. pylori) causes a diversity of gastric diseases. The host immune response evoked by H. pylori infection is complicated and can influence the development and progression of diseases. We have reported that the Group 2 innate lymphocytes (ILC2) were promoted and took part in building type-2 immunity in H. pylori infection-related gastric diseases. Therefore, in the present study, we aim to clarify how H. pylori infection induces the activation of ILC2. It was found that macrophages were necessary for activating ILC2 in H. pylori infection. Mechanistically, H. pylori infection up-regulated the expression of indoleamine 2,3-dioxygenase (IDO) in macrophages to induce M2 polarization, and the latter secreted the alarmin cytokine Thymic Stromal Lymphopoietin (TSLP) to arouse ILC2.

KEYWORDS:

• Group 2 innate lymphoid cells
• M2 macrophages
• Helicobacter pylori

Acknowledgments

We thank Professor Xie Yong (Department of Gastroenterology, First Affiliated Hospital of Nanchang University, Jiangxi, China) for donating the H. pylori strains SS1 (Western type) and ATCC43504 to us.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author contribution

Ruyi Peng performed the experiments and drafted the manuscript. Canxia Xu designed the study. Linfang Zhang and Xiaoming Liu assisted with data analysis. Dongzi Peng and Xingcen Chen assisted with the animal experiments and data analysis. Deliang Liu revised the manuscript. Rong Li designed the study and checked the manuscript. All authors read and approved the final version of the manuscript.

Data availability statement

The authors confirm that the data supporting the findings of this study are available within the article and its supplementary materials.

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/19490976.2024.2347025

Additional information

Funding

This work was supported by the National Natural Science Foundation of China under Grant No. 81900501, No. 81570509, and No. 82070547; the Natural Science Foundation of Hunan Province under Grant No. 2023JJ30765.