Intestinal Cytokine Response After Gut Ischemia

Abstract

These results directly document that the levels of tumor necrosis factor-alpha and interleukin-6 released from the gut increase after an ischemic or I/R injury, such as SMAO, and that there is a relation between the magnitude of the gut ischemic or I/R insult and the cytokine response.

Organ-Specific Cytokine Gene Expression in Sepsis – an Experimental Study in a Two-Hit Septic Model

“…In summary, the mRNA results of this experimental study confirm previous findings of our research group concerning the gut as a site of TNF-α and IL-6 liberation after ischemic injury [14,17]. However, an intestinal mRNA expression of cytokines IL-1 and IL-10 was not found in either of the experimental groups.…”

“…Together with previous studies published by our research group, these findings suggest that the intestinal tract produces and liberates pro-and anti-inflammatory cytokines in a biologically active form after ischemic injury [14,17]. However, the importance of the gut as a cytokine-generating organ needs to be confined: the lung has been identified as the primary site of cytokine gene expression in this two-hit animal model of sepsis.…”

“…These findings have changed the idea of a "passive" role of the gut into an "active" role (cytokine production) in the cascades leading to systemic inflammation and organ dysfunction. In line with these concepts, we have recently documented the existence of cytokine liberation by the intestinal mucosa itself induced by gut ischemia or the presence of bacteria [17]. Likewise, Shenkar et al [18,19] have shown a significant increase in mRNA for pro-inflammatory and immunoregulatory cytokines in Peyer's patches and mesenteric lymph nodes (MLN) after hemorrhage and resuscitation.…”

Local and remote tissue injury upon intestinal ischemia and reperfusion depends on the TLR/MyD88 signaling pathway

“…Second, intestinal injury may expose the basolateral membrane of the intestinal epithelium expressing TLRs allowing the activation of TLR locally by commensal products leading to a systemic inXammation [3]. Third, a massive disruption of the intestinal barrier including damage to the microvasculature may allow the escape of several TLR agonists produced by intestinal commensals or a direct translocation of intestinal microbes into circulation, which lead to systemic inXammation and sepsis [28].…”

The Value of Plasma Cytokine Measurement for the Detection of Strangulation in Patients With Bowel Obstruction: A Prospective, Pilot Study

“…[15][16][17] The majority of them were experimental studies using animal models. Fevang et al 15 found that bowel strangulation was followed by greatly increased venous concentration and release of IL-6 in the strangulated loop in a pig model.…”