Association among genetic predisposition, gut microbiota, and host immune response in the etiopathogenesis of inflammatory bowel disease

Author(s)

P.J. Basso ^[1] ; M.T.C. Fonseca ^[1] ; G. Bonfá ^[3] ; V.B.F. Alves ^[3] ; H. Sales-Campos ^[3] ; V. Nardini ^[3] ; C.R.B. Cardoso ^[3]

Affiliation

^[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Imunol & Bioquim, BR-14040903 Ribeirao Preto, SP - Brazil

^[2] Universidade de São Paulo. Faculdade de Medicina de Ribeirão Preto. Departamento de Imunologia e Bioquímica - Brasil

^[3] Univ Sao Paulo, Fac Ciencias Farmaceut Ribeirao Preto, Dept Anal Clin Toxicol & Bromatol, BR-14040903 Ribeirao Preto, SP - Brazil

• Document type: Journal article
• Source: Brazilian Journal of Medical and Biological Research; v. 47, n. 9, p. 727-737, 2014-07-25.

Abstract

Inflammatory bowel disease (IBD), which includes Crohn's disease (CD) and ulcerative colitis (UC), is a chronic disorder that affects thousands of people around the world. These diseases are characterized by exacerbated uncontrolled intestinal inflammation that leads to poor quality of life in affected patients. Although the exact cause of IBD still remains unknown, compelling evidence suggests that the interplay among immune deregulation, environmental factors, and genetic polymorphisms contributes to the multifactorial nature of the disease. Therefore, in this review we present classical and novel findings regarding IBD etiopathogenesis. Considering the genetic causes of the diseases, alterations in about 100 genes or allelic variants, most of them in components of the immune system, have been related to IBD susceptibility. Dysbiosis of the intestinal microbiota also plays a role in the initiation or perpetuation of gut inflammation, which develops under altered or impaired immune responses. In this context, unbalanced innate and especially adaptive immunity has been considered one of the major contributing factors to IBD development, with the involvement of the Th1, Th2, and Th17 effector population in addition to impaired regulatory responses in CD or UC. Finally, an understanding of the interplay among pathogenic triggers of IBD will improve knowledge about the immunological mechanisms of gut inflammation, thus providing novel tools for IBD control. (AU)

• FAPESP's process: 10/20162-7 - The role of hypothalamus-pituitary-adrenal (HPA) axis and exogenous glucocorticoids in the modulation of immune response in inflammatory bowel disease
• Grantee: Cristina Ribeiro de Barros Cardoso
• Support Opportunities: Research Grants - Young Investigators Grants