Data/hora: 01/06/2024 07:22:02

Provedor de dados: 	56	
País: 	Brazil	
Título: 	Association among genetic predisposition, gut microbiota, and host immune response in the etiopathogenesis of inflammatory bowel disease	
Autores: 	Basso,P.J.; Fonseca,M.T.C.; Bonfá,G.; Alves,V.B.F.; Sales-Campos,H.; Nardini,V.; Cardoso,C.R.B.	
Data: 	2014-09-01	
Ano: 	2014	
Palavras-chave: 	Inflammatory bowel disease; Crohn's disease; Ulcerative colitis; Immune response; Etiology; Microbiota.	
Resumo: 	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.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2014000900727	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431X20143932	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.47 n.9 2014	
Fonte: 	info:eu-repo/semantics/openAccess