Postdoctoral Fellow, Georgia State University, Institute for Biomedical Sciences, 2012-2015
PhD, Cellular and Molecular Microbiology, Auvergne University, 2011
B.S. Genetic and Physiology, Auvergne University, 2008
Intestinal and neuro-Inflammation
Benoit Chassaing was born and raised in Clermont-Ferrand, France. He obtained his PhD in microbiology at the Auvergne University, identifying factors involved in the virulence of adherent and invasive Escherichia coli strains (pathovar involved in the etiology of Crohn’s disease).
Following his PhD completion in 2011, he joined Georgia State University (Atlanta) where he worked with Dr. Andrew T. Gewirtz on various aspects of the intestinal microbiota and mucosal immunology, trying to decipher how genetic and environmental factors can perturb the intestinal microbiota composition in a detrimental way, leading to intestinal inflammation.
Benoit was appointed Assistant Professor in 2015, and he recently joined the Neuroscience Institute in order to pursue his research on the Role of the microbiota in health and disease, with a particular focus on intestinal inflammation, carcinogenesis and neuro-inflammation.
Environmental factors-mediated modulation of the intestinal microbiota
We are highly interested in studying some environmental factors that can alter the intestinal microbiota. We have previously reported that emulsifiers, highly used by the food industry, are able to detrimentally alter the intestinal microbiota, characterized by an increased ability to penetrate the normally protective mucus layer and an increase pro-inflammatory potential. We reported that the consumption of emulsifying agent is sufficient to induce intestinal inflammation that will manifest as chronic colitis in genetically susceptible host. Moreover, in unimpaired host, such food additives are inducing the development of metabolic syndrome characterized by diabetes and an increase in body weight, as well as by an increased susceptibility to colonic carcinogenesis.
Our ongoing research on this area is focusing on the mechanisms beyond such observations:
– how dietary emulsifiers are able to directly impact the intestinal microbiota?
– how the altered microbiota will subsequently drive deleterious phenotypes?
The gut brain axis: a dietary point of view
We are developing our research toward the gut and brain axis in order to understand how alterations of the intestinal microbiota by dietary components can be detrimental for the brain and behavior. Our preliminary data support a central role played by the microbiota on anxiety-related behavior.
We are now trying to:
– better characterize the consequences of an altered microbiota on behavior
– how diet-induced alterations of the intestinal microbiota can lead to neuro-inflammation
– what are the molecular mechanisms connecting the altered microbial community and the associated altered behaviors ?
Innate immunity / microbiota relationship in health and disease
We have studied for many years how the host is controlling the intestinal microbiota in order to keep it under control and at a proper/safe distance from the intestinal mucosa. We have for example demonstrated that the flagellin receptor TLR5 is playing a central role in keeping the intestinal microbiota under control. Animals lacking the TLR5 receptor develop intestinal inflammation that can manifest with the development of chronic colitis or metabolic syndrome. In the liver, we have recently demonstrated that TLR5 is playing an important protective role during western-style diet consumption.
Our current research is focusing on:
– characterizing the microbiota members driving intestinal inflammation
– identifying some therapeutic approaches to beneficially alter the intestinal microbiota
Modulation of the intestinal microbiota using pre- and pro-biotics approach
While our research is mainly focusing on detrimental impacts of the microbiota, our expertise in this field of research, our data-set of identified detrimental bacteria and metabolites, as well as the numerous animal models available in the laboratory lead us to work on the development of tools aiming to beneficially alter the intestinal microbiota.
Among other approaches, we are:
– using dietary factor to modulate the microbiota and prevent its deleterious effects
– using probiotics to beneficially modulates the host/microbiota relationship
– using approaches to in vivo modulate bacterial gene expression in order protect against intestinal inflammation and neuro-inflammation.
Dietary emulsifiers directly alter human microbiota composition and gene expression ex vivo potentiating intestinal inflammation. Chassaing B, Van de Wiele T, De Bodt J, Marzorati M, Gewirtz AT. Gut. 2017 Aug;66(8):1414-1427.
Colonic Microbiota Encroachment Correlates With Dysglycemia in Humans. Chassaing B, Raja SM, Lewis JD, Srinivasan S, Gewirtz AT. Cell Mol Gastroenterol Hepatol. 2017 Apr 13;4(2):205-221.
Supplementation of Low- and High-fat Diets with Fermentable Fiber Exacerbates Severity of DSS-induced Acute Colitis. Miles JP, Zou J, Kumar MV, Pellizzon M, Ulman E, Ricci M, Gewirtz AT, Chassaing B. Inflamm Bowel Dis. 2017 Jul;23(7):1133-1143.
Vasopressin deletion is associated with sex-specific shifts in the gut microbiome. Fields CT, Chassaing B, Paul MJ, Gewirtz AT, de Vries GJ. Gut Microbes. 2017 Jul 31:0.
Hepatocyte Toll-Like Receptor 5 Promotes Bacterial Clearance and Protects Mice Against High-Fat Diet-Induced Liver Disease. Etienne-Mesmin L, Vijay-Kumar M, Gewirtz AT, Chassaing B. Cell Mol Gastroenterol Hepatol. 2016 May 5;2(5):584-604.
Dietary Emulsifier-Induced Low-Grade Inflammation Promotes Colon Carcinogenesis. Viennois E, Merlin D, Gewirtz AT, Chassaing B. Cancer Res. 2017 Jan 1;77(1):27-40.
Microbiota-Dependent Hepatic Lipogenesis Mediated by Stearoyl CoA Desaturase 1 (SCD1) Promotes Metabolic Syndrome in TLR5-Deficient Mice. Singh V, Chassaing B, Zhang L, San Yeoh B, Xiao X, Kumar M, Baker MT, Cai J, Walker R, Borkowski K, Harvatine KJ, Singh N, Shearer GC, Ntambi JM, Joe B, Patterson AD, Gewirtz AT, Vijay-Kumar M. Cell Metab. 2015 Dec 1;22(6):983-96.
Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome. Chassaing B, Koren O, Goodrich JK, Poole AC, Srinivasan S, Ley RE, Gewirtz AT. Nature. 2015 Mar 5;519(7541):92-6.
Viral infection. Prevention and cure of rotavirus infection via TLR5/NLRC4-mediated production of IL-22 and IL-18. Zhang B, Chassaing B, Shi Z, Uchiyama R, Zhang Z, Denning TL, Crawford SE, Pruijssers AJ, Iskarpatyoti JA, Estes MK, Dermody TS, Ouyang W, Williams IR, Vijay-Kumar M, Gewirtz AT. Science. 2014 Nov 14;346(6211):861-5.
Intestinal epithelial cell toll-like receptor 5 regulates the intestinal microbiota to prevent low-grade inflammation and metabolic syndrome in mice.
Chassaing B, Ley RE, Gewirtz AT. Gastroenterology. 2014 Dec;147(6):1363-77.e17.
AIEC pathobiont instigates chronic colitis in susceptible hosts by altering microbiota composition. Chassaing B, Koren O, Carvalho FA, Ley RE, Gewirtz AT. Gut. 2014 Jul;63(7):1069-80.
Crohn disease–associated adherent-invasive E. coli bacteria target mouse and human Peyer’s patches via long polar fimbriae. Chassaing B, Rolhion N, de Vallée A, Salim SY, Prorok-Hamon M, Neut C, Campbell BJ, Söderholm JD, Hugot JP, Colombel JF, Darfeuille-Michaud A. J Clin Invest. 2011 Mar;121(3):966-75.