丁酸梭菌通过调节CD4 + CD25 + FOXP3 + Treg减轻脓毒症小鼠lps诱导的心肌损伤。

IF 2.5 4区 医学 Q3 IMMUNOLOGY
Jinglin Zhao , Liuli Wu , Rupan Zhang , Mei Yuan , Junchao Huang , Xiongfei Jia , Xiaoqin Mao
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引用次数: 0

摘要

脓毒症引起的心肌损伤已成为威胁患者健康和安全的主要疾病。肠道菌群失衡在脓毒症的调节中起着至关重要的作用。利用16srRNA技术,我们研究了28天内丁酸梭菌的肠道定植对lps诱导的脓毒症小鼠的影响。小鼠肠道菌群发生显著变化,提示丁酸梭菌对脓毒性心肌损伤模型的免疫状态有积极影响。细菌通过调节CD4 + CD25 + FOXP3 + Treg细胞来预防脓毒症后期肠黏膜损伤和缓解免疫抑制状态的能力尤其值得注意。这表明丁酸梭菌在脓毒症管理中的治疗作用是通过保护心肌损伤和改善免疫调节。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Clostridium butyricum attenuates LPS-induced myocardial injury in septic mice by modulating CD4 + CD25 + FOXP3 + Treg
Sepsis-induced myocardial injury has become a major threat to patient health and safety. Intestinal microbiota imbalance plays a crucial role in sepsis regulation. Using 16srRNA technology, we explored how intestinal colonization of Clostridium butyricum over 28 days impacted mice with LPS-induced sepsis. Significant changes were noted in the gut microbiota of the mice, highlighting that C. butyricum can positively influence the immune state in septic myocardial injury models. The bacterium's ability to prevent intestinal mucosal damage and alleviate the immunosuppressive state during the later stages of sepsis by regulating CD4 + CD25 + FOXP3 + Treg cells is particularly noteworthy. This suggests a therapeutic role for C. butyricum in sepsis management by protecting against myocardial injury and improving immune regulation.
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来源期刊
Immunobiology
Immunobiology 医学-免疫学
CiteScore
5.00
自引率
3.60%
发文量
108
审稿时长
55 days
期刊介绍: Immunobiology is a peer-reviewed journal that publishes highly innovative research approaches for a wide range of immunological subjects, including • Innate Immunity, • Adaptive Immunity, • Complement Biology, • Macrophage and Dendritic Cell Biology, • Parasite Immunology, • Tumour Immunology, • Clinical Immunology, • Immunogenetics, • Immunotherapy and • Immunopathology of infectious, allergic and autoimmune disease.
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