Chen Jiezhong, Vitetta Luis
Medlab Clinical Ltd, Sydney 2015, Australia.
The University of Sydney, Faculty of Medicine and Health, Sydney 2006, Australia.
Immune Netw. 2020 Feb 4;20(2):e15. doi: 10.4110/in.2020.20.e15. eCollection 2020 Apr.
An excessive hyperinflammatory response-caused septic shock is a major medical problem that is associated with pathogenic bacterial infections leading to high mortality rates. The intestinal microbiota and the associated elaborated metabolites such as short chain fatty acid butyrate have been shown to relieve pathogenic bacterial-caused acute inflammation. Butyrate can down-regulate inflammation by inhibiting the growth of pathobionts, increasing mucosal barrier integrity, encouraging obligate anaerobic bacterial dominance and decreasing oxygen availability in the gut. Butyrate can also decrease excessive inflammation through modulation of immune cells such as increasing functionalities of M2 macrophages and regulatory T cells and inhibiting infiltration by neutrophils. Therefore, various approaches can be used to increase butyrate to relieve pathogenic bacterial-caused hyperinflammation. In this review we summarize the roles of butyrate in attenuating pathogenic bacterial-caused hyperinflammatory responses and discuss the associated plausible mechanisms.
由过度的高炎症反应引起的脓毒症休克是一个主要的医学问题,与致病性细菌感染相关,导致高死亡率。肠道微生物群以及相关的精细代谢产物,如短链脂肪酸丁酸,已被证明可缓解致病性细菌引起的急性炎症。丁酸可通过抑制致病共生菌的生长、增强黏膜屏障完整性、促进专性厌氧菌占优势以及降低肠道内的氧可用性来下调炎症。丁酸还可通过调节免疫细胞来减少过度炎症,如增加M2巨噬细胞和调节性T细胞的功能,并抑制中性粒细胞的浸润。因此,可采用各种方法来增加丁酸以缓解致病性细菌引起的高炎症。在本综述中,我们总结了丁酸在减轻致病性细菌引起的高炎症反应中的作用,并讨论了相关的合理机制。