The Role of Butyrate in Attenuating Pathobiont-Induced Hyperinflammation.
Jiezhong ChenLuis VitettaPublished in: Immune network (2020)
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.
Keyphrases
- regulatory t cells
- oxidative stress
- septic shock
- fatty acid
- healthcare
- weight gain
- microbial community
- type diabetes
- dendritic cells
- intensive care unit
- liver failure
- cardiovascular disease
- cardiovascular events
- wastewater treatment
- immune response
- respiratory failure
- endothelial cells
- heavy metals
- body mass index
- coronary artery disease
- physical activity
- sewage sludge
- aortic dissection
- anaerobic digestion