Division of Gastroenterology

Stephen M. Collins


Professor, Department of Medicine

Distinguished Professor, Michael G. Degroote School of Medicine

Director, Farncombe Family Digestive Health Research Institute

GlaxoSmithKline Chair in Gastroenterology

Gastroenterologist, Hamilton Health Sciences

Member, Farncombe Family Digestive Health Research

Academic Biography

Dr. Collins obtained his medical training at London University in England where he later specialized in internal medicine. He trained in gastroenterology at McMaster University in Canada before completing 3 years of research training in cell biology at the Digestive Diseases Branch, National Institutes of Health (NIH) in Bethesda, Maryland USA. He has been on staff at McMaster University since 1981 where he was the Director of the Intestinal Diseases Research Unit from 1983-1993, and Head of the Division of Gastroenterology since 1993-2006. He is past president of the Canadian Association of Gastroenterology. His areas of interest include:  the impact of inflammation on gut function, neuron-immune interactions, and the role of commensal bacteria in health and disease.  He has over 200 publications including papers in Nature Medicine, Lancet, JCI, Gastroenterology and Gut. He has received continuous CIHR funding for over 20 years, has been a member of the MRC Science & Research Committee, and chaired the CIHR Experimental Medicine grants review committee for 5 years. He has also been an advisor to the Crohn’s and Colitis Foundation of America and Chaired the Strategic Initiatives Committee for The Crohn’s and Colitis Foundation of Canada. He was the Associate Dean for Research at the Faculty of Health Sciences, McMaster University and holds the title of Distinguished University Professor - the highest rank awarded by the University.

Research Interests

Main research area: The immune modulation of enteric nerve and muscle function.

Specific topics: Inflammation of the intestine results in a widespread disturbance of function, including involvement of nerves (pain) and muscle (stricture formation and diarrhea). Research addresses mechanisms underlying the changes in these tissues during experimental inflammation. Studies include the roles of specific cells, such as lymphocytes, and cytokines on nerve and muscle function in vitro, with measurements of changes in physiology and biochemistry of these cell types. Participation of muscle and nerves in the inflammatory process via activation of lymphocytes through antigen presentation, adhesion molecule expression and cytokine production. The role of stress in the inflammatory process. These studies are pertinent to the understanding of inflammatory bowel diseases such as Crohn's disease and ulcerative colitis.

Methods used include: RT- PCR, immunohistochemistry, cell culture and co-culture, physiological studies on muscle (contraction) and nerves (neurotransmitter release) and second messenger systems.

Selected Publications 2006-2008

  1. Akiho H, Blennerhassett P, Deng Y, Collins SM. Role of IL-4, IL-13, and STAT6 in inflammation-induced hypercontractility of murine smooth muscle cells. Am J Physiol Gastrointest Liver Physiol. 2002;282:G226-32.
  2. Khan WI, Blennerhassett PA, Deng Y, Gauldie J, Vallance BA, Collins SM. IL-12 gene transfer alters gut physiology and host immunity in nematode-infected mice. Am J Physiol Gastrointest Liver Physiol 2001;281:G102-10.
  3. Barbara G, De Giorgio R, Deng Y, Vallance B, Blennerhassett P, Collins SM. Role of immunologic factors and cyclooxygenase 2 in persistent postinfective enteric muscle dysfunction in mice. Gastroenterology. 2001;120:1729-36.
  4. Collins SM. Stress and the Gastrointestinal Tract IV. Modulation of intestinal inflammation by stress: basic mechanisms and clinical relevance. Am J Physiol Gastrointest Liver Physiol. 2001;280:G315-8. Review.
  5. Barbara G, Xing Z, Hogaboam CM, Gauldie J, Collins SM. Interleukin 10 gene transfer prevents experimental colitis in rats. Gut 2000;46:344-9.
  6. Qiu BS, Vallance BA, Blennerhassett PA, Collins SM. The role of CD4+ lymphocytes in the susceptibility of mice to stress-induced reactivation of experimental colitis. Nature Med 1999;5:1178-82.