Alveolar macrophage activation is a key initiation signal for acute lung ischemia-reperfusion injury

Abstract

activation is a key initiation signal for acute lung ischemia-reperfusion injury.

Inhaled Hydrogen Gas Therapy for Prevention of Lung Transplant-Induced Ischemia/Reperfusion Injury in Rats

“…2A). Recruitment and sequestration of activated alveolar macrophages play critical roles in lung I/R injury (14,15). Immunohistochemical staining using ED1 (anti-CD68) was performed to evaluate differences in macrophage infiltration in the lung graft tissue.…”

Neutrophil Depletion Causes a Fatal Defect in Murine Pulmonary Staphylococcus aureus clearance

“…A "wet" weight was immediately obtained. Lungs were then dried in a 60 degree oven for 7 days and reweighed (23). The ratio of dry/wet weight was then calculated.…”

Pulmonary Transplantation and Ischemia-Reperfusion Injury

“…Several studies suggest that lung IR injury is biphasic, with distinct acute macrophage-mediated injury followed later by neutrophil-dependent injury (Eppinger, et al, 1995(Eppinger, et al, , 1997Fiser, et al, 2001aFiser, et al, , 2001b. Abundant evidence suggests that alveolar macrophages in the donor lung are quickly activated by IR to subsequently release pro-inflammatory chemokines and cytokines, and it has been demonstrated that depletion of alveolar macrophages attenuates lung IR injury Zhao, et al, 2006). This acute pulmonary damage is followed by a cascade of events leading to activation of the recipient inflammatory system against the already damaged vascular endothelium and airway epithelium.…”

“…This acute pulmonary damage is followed by a cascade of events leading to activation of the recipient inflammatory system against the already damaged vascular endothelium and airway epithelium. A number of studies have strengthened a position for alveolar macrophages and TNF-α in acute IR injury (Eppinger, et al, 1997;Maxey, et al, 2004;Zhao, et al, 2006). One possible mechanism for decreased injury after suppression of macrophage function involves the attenuation of TNF-α or IFN-γ in respiratory burst activity and other inflammatory functions of macrophages (Arenzana-Seisdedos, et al, 1985;Eden & Turino, 1986;Issekutz & Issekutz, 1993;Mayer, et al, 1993;Phillips, et al, 1990).…”