Professional Education


  • Doctor of Philosophy, Unlisted School (2014)
  • Master of Science, University Of Lucknow (2007)
  • Bachelor of Science, Kanpur University (2005)

Stanford Advisors


All Publications


  • Dysbiosis-Induced Secondary Bile Acid Deficiency Promotes Intestinal Inflammation. Cell host & microbe Sinha, S. R., Haileselassie, Y., Nguyen, L. P., Tropini, C., Wang, M., Becker, L. S., Sim, D., Jarr, K., Spear, E. T., Singh, G., Namkoong, H., Bittinger, K., Fischbach, M. A., Sonnenburg, J. L., Habtezion, A. 2020

    Abstract

    Secondary bile acids (SBAs) are derived from primary bile acids (PBAs) in a process reliant on biosynthetic capabilities possessed by few microbes. To evaluate the role of BAs in intestinal inflammation, we performed metabolomic, microbiome, metagenomic, and transcriptomic profiling of stool from ileal pouches (surgically created resevoirs) in colectomy-treated patients with ulcerative colitis (UC) versus controls (familial adenomatous polyposis [FAP]). We show that relative to FAP, UC pouches have reduced levels of lithocholic acid and deoxycholic acid (normally the most abundant gut SBAs), genes required to convert PBAs to SBAs, and Ruminococcaceae (one of few taxa known to include SBA-producing bacteria). In three murine colitis models, SBA supplementation reduces intestinal inflammation. This anti-inflammatory effect is in part dependent on the TGR5 bile acid receptor. These data suggest that dysbiosis induces SBA deficiency in inflammatory-prone UC patients, which promotes a pro-inflammatory state within the intestine that may be treated by SBA restoration.

    View details for DOI 10.1016/j.chom.2020.01.021

    View details for PubMedID 32101703

  • Saffron: The Golden Spice with Therapeutic Properties on Digestive Diseases NUTRIENTS Ashktorab, H., Soleimani, A., Singh, G., Amin, A., Tabtabaei, S., Latella, G., Stein, U., Akhondzadeh, S., Solanki, N., Gondre-Lewis, M. C., Habtezion, A., Brim, H. 2019; 11 (5)

    View details for DOI 10.3390/nu11050943

    View details for Web of Science ID 000471021600003