• G M Swank and E A Deitch.
• Department of Surgery, UMDNJ-New Jersey Medical School, MSB G-506, 185 South Orange Avenue, Newark, New Jersey, 07103-2714, U.S.A.
• World J Surg. 1996 May 1; 20 (4): 411-7.

AbstractIt is clear that increased gut permeability and bacterial translocation play a role in multiple organ failure (MOF). Failure of the gut barrier remains central to the hypothesis that toxins escaping from the gut lumen contribute to activation of the host's immune inflammatory defense mechanisms, subsequently leading to the autointoxication and tissue destruction seen in the septic response characteristic of MOF. However, the role of the gut is more than that of a sieve, which simply allows passage of bacteria and endotoxin from the gut lumen to the portal or systemic circulation. It appears, in addition, that the translocation of bacteria and endotoxin may lead to local activation of the immune inflammatory system and the local production of cytokines and other immune inflammatory mediators. These intestinally derived mediators may then exacerbate the systemic inflammatory response and potentially lead to a further increase in gut permeability. A vicious cycle of increased intestinal permeability, leading to toxic mediator release, resulting in a further increase in gut permeability is generated. Additionally, the systemic and local inflammatory cells that become activated in the gut contribute to the systemic response characteristic of the sepsis syndrome and MOF. Thus even if the immune inflammatory system, rather than the gut, is the "motor of" MOF, the gut remains one of the major pistons that turns the motor.

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