TY  - JOUR
  - Shanahan, F.
  - 2012
  - August
  - The microbiota in inflammatory bowel disease: friend, bystander, and sometime-villain
  - Validated
  - ()
  - 70
  - Ulcerative colitis and Crohn's disease, collectively known as inflammatory bowel disease, represent the heterogeneous outcome of three colliding influences: genetic risk factors, environmental modifiers, and immune effector mechanisms of tissue injury. The nature of these inputs is complex, with each having distinct and overlapping contributions to ulcerative colitis and Crohn's disease. Identification of specific genetic risk factors has improved the understanding of specific pathways to disease, but the primacy of environmental or lifestyle factors linked to changes in the gut microbiota, particularly in early life, is increasingly evident. Clarification of the molecular basis of host-microbe interactions in health and in susceptible individuals promises novel therapeutic strategies.Ulcerative colitis and Crohn's disease, collectively known as inflammatory bowel disease, represent the heterogeneous outcome of three colliding influences: genetic risk factors, environmental modifiers, and immune effector mechanisms of tissue injury. The nature of these inputs is complex, with each having distinct and overlapping contributions to ulcerative colitis and Crohn's disease. Identification of specific genetic risk factors has improved the understanding of specific pathways to disease, but the primacy of environmental or lifestyle factors linked to changes in the gut microbiota, particularly in early life, is increasingly evident. Clarification of the molecular basis of host-microbe interactions in health and in susceptible individuals promises novel therapeutic strategies.
  - 0029-66430029-6643
  - ://WOS:000307107200006://WOS:000307107200006
DA  - 2012/08
ER  - 

@article{V235378917,
   = {Shanahan,  F. },
   = {2012},
   = {August},
   = {The microbiota in inflammatory bowel disease: friend, bystander, and sometime-villain},
   = {Validated},
   = {()},
   = {70},
   = {{Ulcerative colitis and Crohn's disease, collectively known as inflammatory bowel disease, represent the heterogeneous outcome of three colliding influences: genetic risk factors, environmental modifiers, and immune effector mechanisms of tissue injury. The nature of these inputs is complex, with each having distinct and overlapping contributions to ulcerative colitis and Crohn's disease. Identification of specific genetic risk factors has improved the understanding of specific pathways to disease, but the primacy of environmental or lifestyle factors linked to changes in the gut microbiota, particularly in early life, is increasingly evident. Clarification of the molecular basis of host-microbe interactions in health and in susceptible individuals promises novel therapeutic strategies.Ulcerative colitis and Crohn's disease, collectively known as inflammatory bowel disease, represent the heterogeneous outcome of three colliding influences: genetic risk factors, environmental modifiers, and immune effector mechanisms of tissue injury. The nature of these inputs is complex, with each having distinct and overlapping contributions to ulcerative colitis and Crohn's disease. Identification of specific genetic risk factors has improved the understanding of specific pathways to disease, but the primacy of environmental or lifestyle factors linked to changes in the gut microbiota, particularly in early life, is increasingly evident. Clarification of the molecular basis of host-microbe interactions in health and in susceptible individuals promises novel therapeutic strategies.}},
  issn = {0029-66430029-6643},
   = {://WOS:000307107200006://WOS:000307107200006},
  source = {IRIS}
}