The role of cytokine-induced neutrophil chemoattractant-1 in neutrophil-mediated remote lung injury after intestinal ischaemia/reperfusion in rats

Abstract

In the I/R group, the permeability index of the lung, the neutrophil count in pulmonary vascular lavage fluid and bronchoalveolar lavage fluid (BALF), lung myeloperoxidase activity and neutrophil oxidative production were all significantly greater than those in the sham group. Cytokine-induced neutrophil chemoattractant-1 levels in blood and BALF were significantly increased at 240 min after intestinal reperfusion. There was a significant relationship between neutrophils in BALF and CINC-1 level in BALE CONCLUSION: These findings suggest that intestinal reperfusion was associated with activation and accumulation of neutrophils in the lung and resulted in remote lung injury with increased microvascular permeability. Thus, CINC-1 in BALF may induce neutrophil migration from the pulmonary vessels to the interstitium and alveolar spaces in remote lung injury after intestinal I/R.

Sphingosine-1-Phosphate Attenuates Lung Injury Induced by Intestinal Ischemia/Reperfusion in Mice: Role of Inducible Nitric-Oxide Synthase

“…Ischemia and reperfusion involves the release of a large number of inflammatory mediators including TNF, IL-1, IL-6, IL-8, IL-10, platelet activating factor, arachidonic acid metabolites, NO, and so forth. The neutrophil and their enzymatic products are sequestrated in lung tissues, which causes increased microvascular permeability, perivascular and interstitial edema, and pulmonary edema [22,23]. The results that we obtained in our model were similar to previous studies in terms of the increasing plasma proinflammatory cytokines (TNF-α and IL-6) levels and pulmonary leukosequestration and edema in the lungs after SMA I/R.…”

Postconditioning of the Lower Limb—Protection Against the Reperfusion Syndrome

“…Neutrophils act as central mediators by local release of reactive oxygen species, leukotriene B 4 , tromboxane B 2 , and different proteolytic enzymes. These metabolites and other humoral agents (different cytokines, the cytokine-induced neutrophil chemoattractant-1 (CINC-1) and the complement system) act as potent activators of the neutrophil recruitment and the generalized inflammatory process [20,21]. TNF-a plays a major role in this process by activating neutrophils and up-regulating the expression of adhesion molecules in endothelial cells and granulocytes [22].…”

Protective effects of trapidil in lung after abdominal aorta induced ischemia–reperfusion injury: an experimental study

“…The lung injuries are PMN dependent and can be aggrevated by the prior depletion of circulating PMNs [20]. The mechanism of respiratory failure after IR injury is a complex process which is associated with the activation of systemic inflammatory mediators including bacteriotoxin, immunocytokines and inflammatory mediators such as TNF and interleukins [21,22]. TNF and NO are significant determinants of the lung injury process which is caused by lower extremity IR [4,15].…”