Lactobacillus murinus alleviate intestinal ischemia/reperfusion injury through promoting the release of interleukin-10 from M2 macrophages via Toll-like receptor 2 signaling.
Lactobacillus murinus alleviate intestinal ischemia/reperfusion injury through promoting the release of interleukin-10 from M2 macrophages via Toll-like receptor 2 signaling.
复制标题
鼠乳杆菌通过 Toll 样受体 2 信号传导促进 M2 巨噬细胞释放白细胞介素 10，从而减轻肠道缺血/再灌注损伤
DOI：
10.1186/s40168-022-01227-w
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发表时间：
2022-03-03
期刊：
影响因子：
15.5
通讯作者：
Liu KX
中科院分区：
文献类型：
--
作者：
Hu J;Deng F;Zhao B;Lin Z;Sun Q;Yang X;Wu M;Qiu S;Chen Y;Yan Z;Luo S;Zhao J;Liu W;Li C;Liu KX
背景
Background
Intestinal ischemia/reperfusion (I/R) injury has high morbidity and mortality rates. Gut microbiota is a potential key factor affecting intestinal I/R injury. Populations exhibit different sensitivities to intestinal I/R injury; however, whether this interpopulation difference is related to variation in gut microbiota is unclear. Here, to elucidate the interaction between the gut microbiome and intestinal I/R injury, we performed 16S DNA sequencing on the preoperative feces of C57BL/6 mice and fecal microbiota transplantation (FMT) experiments in germ-free mice. The transwell co-culture system of small intestinal organoids extracted from control mice and macrophages extracted from control mice or Toll-like receptor 2 (TLR2)-deficient mice or interleukin-10 (IL-10)-deficient mice were established separately to explore the potential mechanism of reducing intestinal I/R injury.
Results
Intestinal I/R-sensitive (Sen) and intestinal I/R-resistant (Res) mice were first defined according to different survival outcomes of mice suffering from intestinal I/R. Fecal microbiota composition and diversity prior to intestinal ischemia differed between Sen and Res mice. The relative abundance of Lactobacillus murinus (L. murinus) at the species level was drastically higher in Res than that in Sen mice. Clinically, the abundance of L. murinus in preoperative feces of patients undergoing cardiopulmonary bypass surgery was closely related to the degree of intestinal I/R injury after surgery. Treatment with L. murinus significantly prevented intestinal I/R-induced intestinal injury and improved mouse survival, which depended on macrophages involvement. Further, in vitro experiments indicated that promoting the release of IL-10 from macrophages through TLR2 may be a potential mechanism for L. murinus to reduce intestinal I/R injury.
Conclusion
The gut microbiome is involved in the postoperative outcome of intestinal I/R. Lactobacillus murinus alleviates mice intestinal I/R injury through macrophages, and promoting the release of IL-10 from macrophages through TLR2 may be a potential mechanism for L. murinus to reduce intestinal I/R injury. This study revealed a novel mechanism of intestinal I/R injury and a new therapeutic strategy for clinical practice.
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影响因子：
29.4
作者：
Chen P;Torralba M;Tan J;Embree M;Zengler K;Stärkel P;van Pijkeren JP;DePew J;Loomba R;Ho SB;Bajaj JS;Mutlu EA;Keshavarzian A;Tsukamoto H;Nelson KE;Fouts DE;Schnabl B
通讯作者：
Schnabl B
影响因子：
24.5
作者：
Chen, Y;Lui, VCH;Tam, PKH
通讯作者：
Tam, PKH
DOI：
10.1097/shk.0000000000000477
发表时间：
2016-01
期刊：
Shock (Augusta, Ga.)
影响因子：
--
作者：
Goering J;Pope MR;Fleming SD
通讯作者：
Fleming SD
影响因子：
4.1
作者：
Aprahamian, Charles J.;Lorenz, Robin G.;Dimmit, Reed A.
通讯作者：
Dimmit, Reed A.
肠道微生物代谢物普伐他汀通过 IL-33/ST2 信号传导促进 II 型先天淋巴细胞释放 IL-13，从而减轻肠道缺血/再灌注损伤
影响因子：
7.3
作者：
Deng F;Hu JJ;Yang X;Sun QS;Lin ZB;Zhao BC;Yao ZW;Luo SD;Chen ZL;Liu Y;Yan ZZ;Li C;Liu WF;Liu KX
通讯作者：
Liu KX