Helminth-induced CD9+ B-cell subset alleviates obesity-associated inflammation via IL-10 production

• Published in: International journal for parasitology Vol. 52; no. 2-3; pp. 111 - 123
• Main Authors: Li, Maining, Wang, Huiquan, Ni, Yangyue, Li, Chen, Xu, Xuejun, Chang, Hao, Xu, Zhipeng, Hou, Min, Ji, Minjun
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.02.2022
• Subjects: Animals; Antigens, CD19 - metabolism; B-lymphocytes; B-Lymphocytes, Regulatory; CD9; helminthiasis; Helminths; Helminths - metabolism; high fat diet; homeostasis; Immunometabolism; Inflammation; insulin resistance; interleukin-10; Interleukin-10 - genetics; Interleukin-10 - metabolism; Mice; Mice, Inbred C57BL; obesity; Obesity - complications; Obesity - metabolism; parasitology; Regulatory B cell; Schistosoma japonicum; sequence analysis; spleen; Immunometabolism; CD9; Regulatory B cell; Helminths
• ISSN: 0020-7519; 1879-0135; 1879-0135
• DOI: 10.1016/j.ijpara.2021.08.009

[Display omitted] •Schistosome infection could expand regulatory B cells (Bregs) in mice.•CD19±CD9± B cells produced more IL-10 than conventional B10 cells.•Adoptive transfer of CD9± B cells from infected mice had the capacity to markedly alleviate obesity-related inflammation.•CD9± B cells induced by helminth infection play a role in regulation of host metabolic disorders through IL-10 production. It has been shown that helminth infection can protect against obesity and improve insulin sensitivity to a certain extent, based on epidemiological investigations and animal experiments. Meanwhile, helminths induce a network of regulatory immune cells, including regulatory B cells (Bregs). However, the molecule characteristics and function of these Bregs in improving whole-body metabolic homeostasis remains largely unclear. We established a mouse model with chronic Schistosoma japonicum infection, and compared the differences in B10 cells (CD19+CD5+CD1dhi) and B10− cells (CD19+CD5−CD1d−) from splenic B cells of infected mice using RNA-seq. A unique Breg population was identified. Furthermore, these Bregs were evaluated for their ability to produce inhibitory cytokines in vitro and suppress obesity when adoptively transferred into mice on a high-fat diet. We found that schistosome infection could expand Breg cell populations in mice. CD9 was demonstrated to be a key surface marker for most murine IL-10+ B cells in spleen. CD19+CD9+ B cells produced more IL-10 than conventional B10 cells. Adoptive transfer of CD9+ B cells had the capacity to alleviate obesity-associated inflammation via promoting Tregs, Th2 cells and decreasing Th1, Th17 cells in high-fat diet mice. In conclusion, schistosome infection can induce regulatory CD9+ B cell production, which plays a critical role in the regulation of metabolic disorders through IL-10 production.