The association between type 2 DM (T2DM) and susceptibility to tuberculosis (TB) is well recognized.Patients with DM have 2-3 fold increased susceptibility to TB, treatment is longer and the outcome is worse than in non-diabetic TB patients. Here, we report that aerosol infection withM. tuberculosisis followed by leukocyte infiltration and proliferation, and expression of inflammatory markers in adipose tissue of lean mice leading to disrupted lipid metabolism and the induction of adipocyte hypertrophy.RNA-sequencing (RNAseq) in whole pgWAT adipose tissue at 8 wk after aerosol challenge revealed an upregulation of genes that were associated with antigen presentation, Th1 and type-1 interferon response, indicated the induction of T cell activation. This was found to be due to activated mTORC2/Akt signaling. By depleting Rictor (mTORC2 subunit) in adipocytes we noticed the restoration of inflammation and cell hypertrophy. Our study suggests that TB-induced inflammation in the adipose tissue is associated with improved glucose tolerance and is mediated by mTORC2/Akt pathway. SOURCE: Michael Poidinger (michael_poidinger@immunol.a-star.edu.sg) -  Singapore Immunology Network

Pluto Bioinformatics

GSE106611: mTORC2/Akt Activation in Adipocytes is Required forMycobacterium tuberculosisDerived Inflammation in Adipose Tissue