Andy
Retired committee member
Abstract
Gut microbiota is essential for the function of peripherally-induced regulatory T (pTreg) cells. However, how commensal bacteria affect thymically derived fat-resident Treg cells that harbor a unique expression of peroxisome proliferator-activated receptor (PPAR)-γ and suppress inflammation in visceral adipose tissue (VAT), is not well defined.
Here it is revealed that microbiota depletion causes a drastic decline in Treg cell population in VAT, particularly those expressing ST2 (ST2+ Treg), which are largely restored after gut microbiome reconstruction. Mechanistically, gut microbiota-derived butyrate increases VAT ST2+ Treg cells through binding PPARγ. Butyrate supplementation and high fiber diet increase VAT ST2+ Treg population in obese mice, and ameliorated glucose tolerance and visceral inflammation. Furthermore, human omental adipose Treg cells show positive correlation with fecal butyrate and certain butyrate-producing microbes.
This study identifies the critical role of gut microbiota-butyrate-PPARγ axis in maintaining VAT Treg population, pinpointing a potential approach to augment VAT Treg population and ameliorate inflammation.
Open access
Gut microbiota is essential for the function of peripherally-induced regulatory T (pTreg) cells. However, how commensal bacteria affect thymically derived fat-resident Treg cells that harbor a unique expression of peroxisome proliferator-activated receptor (PPAR)-γ and suppress inflammation in visceral adipose tissue (VAT), is not well defined.
Here it is revealed that microbiota depletion causes a drastic decline in Treg cell population in VAT, particularly those expressing ST2 (ST2+ Treg), which are largely restored after gut microbiome reconstruction. Mechanistically, gut microbiota-derived butyrate increases VAT ST2+ Treg cells through binding PPARγ. Butyrate supplementation and high fiber diet increase VAT ST2+ Treg population in obese mice, and ameliorated glucose tolerance and visceral inflammation. Furthermore, human omental adipose Treg cells show positive correlation with fecal butyrate and certain butyrate-producing microbes.
This study identifies the critical role of gut microbiota-butyrate-PPARγ axis in maintaining VAT Treg population, pinpointing a potential approach to augment VAT Treg population and ameliorate inflammation.
Open access