Investigation of regulation and mechanism of miR-223 on autophagy of CD4 + T lymphocytes in septic mice.

payth.elady61 shared this article with you from Inoreader Investigation of regulation and mechanism of miR-223 on autophagy of CD4 + T lymphocytes in septic mice. Via pubmed: autophagy Investigation of regulation and mechanism of miR-223 on autophagy of CD4 + T lymphocytes in septic mice. Cell Mol Biol (Noisy-le-grand). 2020 Oct 31;66(7):207-215 Authors: Li Q, Xiang G, Peng C, Xie L, Ji W Abstract T-lymphocyte dysfunction is most important part of immune dysfunction in sepsis, where dynamic change, especially autophagy of CD4+T lymphocytes is found to be related to disease fate. Our study is to i nvestigate the changes of CD4 + T lymphocytes and their autophagy levels in septic miR-223 -/- mouse model injected intraperitoneally with E. coli.120 male C57BL/6J wild-type. Twenty male miR-223 knockout(miR-223-/-) mice were randomly divided into, according to intraperitoneal injection of normal saline (NS) and E. coli solution, normal saline (WT NS) group, sepsis (WT Sep) group, miR-223 -/- NS group and miR-223 -/- Sep group, respectively. The autophagy related protein was monitored with flow cytometry to observe the autophagy of CD4+T lymphocytes. Flow cytometry showed the proportion of CD4 + T lymphocytes in peripheral blood circulation, alveoli, and spleen of mice in the WT Sep group gradually decreased after surgery, the proportion of cells with autophagic activity in t his population of cells was significantly higher than that in the WT NS group, and the proportion of CD4 + T lymphocytes with active autophagic activity in miR-223 -/- mice were significantly decreased, but higher than that in the miR-223 -/- NS group and lower than the level of autophagy in CD4 + T cells of wild-type mice. Thus, miR-223 can up-regulate the level of autophagy in CD4 + T lymphocytes of septic mice, suggesting that miR-223 may be used as a potential target for the prevention and treatment of sepsis. PMID: 33287944 [PubMed - in process] View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.