Am. J. Respir. Crit. Care Med., Volume 156, Number 4, October 1997, 1230-1234

Interleukin-1 in Ischemia-Reperfusion Acute Lung Injury

DEH-MING CHANG, KANG HSU, YU-AN DING, and CHI-HUEI CHIANG

Rheumatology/Immunology/Allergy Division, Pulmonary Division, and Cardiovascular Division, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China

Interleukin-1 (IL-1) is a proinflammatory cytokine produced by blood-borne and resident inflammatory lung tissue involved in the thrombotic occlusion of the pulmonary microcirculation and the increase of the vascular permeability following a wide variety of injuries and sepsis. The locally accentuated, organ-related activation of this cytokine seems to be responsible for the development of acute lung injury. The present study was conducted to determine if IL-1 was produced in an ischemia-reperfusion (I/R) rat model subjected to lung injury. We measured sequential perfusate levels of IL-1 by ELISA and we measured IL-1 gene expression in the rat lung tissue by a reverse-transcriptase polymerase chain reaction method. Little IL-1 gene expression was observed in normal rat lung tissue. Perfusate IL-1 slightly increased 2 h after induced ischemia and 3 h after reperfusion. IL-1 gene expression rapidly increased as early as 30 min after ischemia and continued to increase for up to 120 min. IL-1 gene expression was dramatically upregulated during reperfusion after cessation of ischemia, reached a peak at 1 h, and then gradually decreased (2 to 3 h) to near baseline levels. During ischemia, the increased IL-1 gene expression was not significantly different between the ventral and dorsal sites of the lung. However, IL-1 gene expression markedly increased on the dorsal part (the dependent site for a rat in a supine position) after reperfusion. From these results, it appears that IL-1 may have an important role in I/R lung injury.

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