2. Academic Validation
  3. Extracellular vesicles of Bacteroides fragilis regulated macrophage polarization through promoted Sema7a expression

Extracellular vesicles of Bacteroides fragilis regulated macrophage polarization through promoted Sema7a expression

  • Microb Pathog. 2023 Dec 30:106527. doi: 10.1016/j.micpath.2023.106527.
Cong Chen 1,  Yu-Qi He 1,  Yan Gao 2,  Qun-Wen Pan 3,  Jing-Song Cao 4
Affiliations

Affiliations

  • 1 The First Affiliated Hospital, Department of Laboratory Medicine, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
  • 2 The First Affiliated Hospital, Institute of Endocrinology and Metabolism, Center for Clinical Research in Diabetes, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China.
  • 3 Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, Institute of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
  • 4 The First Affiliated Hospital, Institute of Endocrinology and Metabolism, Center for Clinical Research in Diabetes, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China. Electronic address: [email protected].
PMID: 38163490 DOI: 10.1016/j.micpath.2023.106527
Abstract

Abnormal activation of macrophage and gut Bacteroides fragilis (BF) are the important induction factors in the occurrence of type 2 diabetes (T2D) and vascular complications. However, it remains unknown whether BF involves in macrophage polarization. In this study, we found that BF extracellular vesicles (EV) can be uptaken by macrophage. BF-EV promote macrophage M1/M2 polarization significantly, and increase STING expression significantly. Bioinformatics analysis found that Sema7a is an important gene involving in macrophage polarization. The expression of Sema7a can be induced by BF-EV and can be inhibited after C-176 treated. The inhibition expression of Sema7a prevent BF-EV to induce macrophage polarization. Further analysis reveals that there is no direct interaction between STING and Sema7a, but Sgpl1 can interact with STING or Sema7a. BF-EV promote the expression of Sgpl1, which the phenomenon can be inhibited after C-176 treated. Importantly, overexpression of Sgpl1 reversed the effect of C-176 for Sema7a expression, while inhibit Sema7a expression has limitation influence for STING and Sgpl1 expression. In conclusion, this study confirms that Sting-Sgpl1-Sema7a is a key mechanism by which BF-EV regulates macrophage polarization.

Keywords

Bacteroides fragilis; Extracellular vesicles; Macrophage; Type 2 diabetes.

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