Chemokine Involvement in Lung Injury Secondary to Ischaemia/Reperfusion

Abstract

The present study demonstrates that activated neutrophils, as well as MCP-1, MIP-2, and ICAM-1, are involved in inflammatory response induced by ischaemia-reperfusion-induced lung injury.

The relationship between low survival and acute increase of tumor necrosis factor α expression in the lung in a rat model of asphyxial cardiac arrest

“…This inflammation involves activation of leukocytes, secretions of cytokines, leukocytes adhesions to microvascular endothelium, and leukocytes extravasation, which develop tissue damage in final [ 2 6 21 22 ]. In addition, immune cells are rapidly activated upon reperfusion and induce direct tissue injury or augment inflammation via production of pro-inflammatory cytokines.…”

“…Elevated plasma levels of TNF-α, interleukin (IL)-6, IL-8 are strongly correlated with pulmonary dysfunction [ 10 21 22 ]. Those cytokines cause generation of polymorphonuclear cells and their entrapment in pulmonary capillaries, and eventually result in cell swelling, plasma and protein extravasation into the interstitial tissue, release of proteolytic enzymes, congestion of alveoli with plasma, erythrocytes and inflammatory debris which alter capillary permeability [ 6 23 ]. Finally, these abnormal pathophysiological processes lead to massive interstitial pulmonary edema, pulmonary fibrosis, and acute respiratory distress syndrome (ARDS), which is acute, non-cardiogenic and high-permeability lung injury, and associated with high mortality [ 21 24 ].…”

“…Systemic IR injury after RoSC triggers the release of inflammatory cytokines and eventually leads to systemic inflammatory response syndrome even in the absence of infection [ 5 ]. Ischemia and subsequent reperfusion in multiple organs are unavoidable during CA and RoSC, which commonly results in acute and sterile systemic inflammation, and IR activates and infiltrates innate immune cells [ 2 6 ]. Increased pro-inflammatory cytokines have been reported following resuscitation [ 7 ].…”

“…TNF-α increases shortly in myocardium after RoSC and is predictive of early death, especially, plasma levels of TNF-α have been shown to be inversely correlated with myocardial function after CA [ 9 ]. In addition, cytokines including TNF-α are secreted by alveolar macrophages and amplify the response of endothelial and epithelial cells in the lung [ 2 6 10 ]. However, the role of TNF-α in other organs is still unclear after CA.…”

The placenta in intrauterine demise

“…This pattern likely represents ‘postmortem chorioamnionitis,’ in which there is maternal neutrophil activation by non‐infectious tissue ischemia. Though scientific evidence for this in the context of retained placentas post‐fetal demise is lacking, by analogy there is a body of literature regarding neutrophil activation in ischemia/reperfusion models of other human and animal organ systems (e.g., ).…”