The digestive tract as the origin of systemic inflammation.


Por: de Jong PR, Gonzalez J and Jansen NJ

Publicada: 18 oct 2016
Categoría: Critical care and intensive care medicine

Resumen:
Failure of gut homeostasis is an important factor in the pathogenesis and progression of systemic inflammation, which can culminate in multiple organ failure and fatality. Pathogenic events in critically ill patients include mesenteric hypoperfusion, dysregulation of gut motility, and failure of the gut barrier with resultant translocation of luminal substrates. This is followed by the exacerbation of local and systemic immune responses. All these events can contribute to pathogenic crosstalk between the gut, circulating cells, and other organs like the liver, pancreas, and lungs. Here we review recent insights into the identity of the cellular and biochemical players from the gut that have key roles in the pathogenic turn of events in these organ systems that derange the systemic inflammatory homeostasis. In particular, we discuss the dangers from within the gastrointestinal tract, including metabolic products from the liver (bile acids), digestive enzymes produced by the pancreas, and inflammatory components of the mesenteric lymph.

Filiaciones:
de Jong PR:
 Department of Pediatric Intensive Care, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, The Netherlands.

 Sanford Burnham Prebys Medical Discovery Institute, 10901 N Torrey Pines Rd, La Jolla, CA, 92037, USA.

Gonzalez J:
 Networked Biomedical Research Center for Hepatic and Digestive Diseases (CIBERehd), Hospital General Universitario de Alicante, Alicante, Spain

 Alicante Institute of Health and Biomedical Research (ISABIAL - FISABIO Foundation), Alicante, Spain

Jansen NJ:
 Department of Pediatric Intensive Care, Wilhelmina Children's Hospital, University Medical Center Utrecht, Utrecht, The Netherlands
ISSN: 13648535





CRITICAL CARE
Editorial
BIOMED CENTRAL LTD, 236 GRAYS INN RD, FLOOR 6, LONDON WC1X 8HL, ENGLAND, Reino Unido
Tipo de documento: Article
Volumen: 20 Número: 1
Páginas: 279-279
WOS Id: 000385723700001
ID de PubMed: 27751165
imagen Open Access

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