Influence of the critically ill state on host-pathogen interactions within the intestine: Gut-derived sepsis redefined

Abstract

Severe and prolonged states of catabolic stress have been shown to have profound effects on the intestinal tract microflora and intestinal function. Gut-derived sepsis is a term used to describe a state of systemic inflammation with organ dysfunction after severe catabolic stress hypothesized to be initiated and perpetuated by the intestinal tract microflora. Popular notions of the mechanism of this process have suggested that stress promotes the translocation of intestinal bacteria or their toxins into the systemic compartment resulting in the release of proinflammatory cytokines which participate in the systemic inflammatory response syndrome. This review is an attempt to redefine the mechanism of gut-derived sepsis by focusing on molecular events that result from host-pathogen interactions within the intestinal tract itself. This evidence-based review posits that gut-derived bacteremia, even with potent nosocomial pathogens, is an event of low proinflammatory potential and, itself, is an insufficient stimulus for the systemic inflammatory response and organ failure state typically seen after severe and prolonged catabolic stress. Mechanisms of this apparent paradox are discussed.

Perioperative synbiotic treatment to prevent infectious complications in patients after elective living donor liver transplantation: a prospective randomized study

“…These functions might all be important for reduction of infections in surgical patients. However, definite mechanism regarding the reduction of urinary tract infection should await further investigation 3,25,29,30). …”

“…1 Bacterial translocation can occur if the intact environment is compromised, thus leading to the provocation of several cytokine networks and multiple organ failure in the end. [2][3][4][5] Especially, liver transplant recipients usually have a long history of liver disease and suffer portal hypertension, which leads to malnutrition. 6 Therefore, the mucosa of their bowel could be atrophic and more susceptible to bacterial translocation, which leads to endotoxenemia and multi-organ failure.…”

Efek Probiotik terhadap Mortalitas, Derajat Inflamasi Intestinal, dan Kadar IgA pada Mencit Model Sepsis

“…Penyebab utama kematian penderita rawat inap di Intensive Care Unit (ICU) adalah systemic inflammatory response syndrome (SIRS), sepsis, dan MODS. 1 Peran mikrobiota intestinal dalam inisiasi dan perjalanan penyakit kritis sudah semakin diakui dalam dekade terakhir. Beberapa penelitian yang telah dilakukan membuktikan pentingnya strain endogen bakteri probiotik seperti Bifidobacterium dan Lactobacillus dalam mempertahankan fungsi sawar intestinal serta memodulasi mukosa dan respons imun sistemik.…”

Critical Care Nutrition: Getting Involved as a Gastrointestinal Endoscopist

“…1). In an animal model, Alverdy 14 has shown that the number and type of bacteria colonizing the gut at the time the host goes into shock determines the degree of the inflammatory response generated by the gut. Progressing from a normal number of commensal bacteria, to bacterial overgrowth of commensal bacteria, to bacterial overgrowth of pathogenic organisms (a sequence which would occur naturally in response to failure to use the gut in critical illness), there is a steady increase in the volume of cytokines (tumor necrosis factor and interleukin-6) that are released from the gut.…”

“…Direct protection is provided by organisms such as Escherichia coli, that produce a disaccharidase enzyme that breaks down the toxin produced by Pseudomonas. 14 Alverdy 14 has shown that bacteria in the gut can sense decreases in pH or oxygen levels as the host goes into shock, and in response switch on virulence genes. When these genes are expressed, the bacteria go into an adherent phase, attach to the intestinal wall, and cause a contact-dependent activation of the intestinal epithelial cells (IECs).…”