作者@article {Yanagawa1211 = {Yanagawa, HYano, S and Haku, T and Ohmoto, Y and Sone, S}, title = {Interleukin-1 receptor antagonist in pleural effusion due to inflammatory and malignant lung disease}, volume = {9}, number = {6}, pages = {1211--1216}, year = {1996}, publisher = {European Respiratory Society}, abstract = {Interleukin (IL)-1 is a key cytokine in inflammatory reactions. To clarify the mechanism of inflammation in the pleural cavity, we investigated the contribution of IL-1 and its antagonism to inflammatory processes in the pleural cavity. Interleukin-1 receptor antagonist (IL-1Ra) levels as well as IL-1 beta and interferon-gamma (IFN-gamma) levels were measured by enzyme immunoassay in pleural effusions from 70 patients. Pleural macrophages were also examined as possible sources of these cytokines in 10 patients. IL-1Ra was detectable in 28 patients (40\%) out of 70 patients with pleural effusions. Patients with tuberculosis had significantly higher IL-1Ra as well as IFN-gamma levels in pleural effusion than patients with lung cancer. Transudative pleural effusions had low or undetectable IL-IRa levels. On the other hand, IL-1 beta levels were low, except in cases of parapneumonic pleural effusion. Spontaneous production of IL-1Ra pleural macrophages was observed in six patients, and IL-4 significantly augmented its production. Although spontaneous production of IL-1 beta was observed in only two patients, pleural macrophages produced significant amounts of IL-1 beta in response to lipopolysaccharide in all 10 patients examined. These results suggest that interleukin-1 receptor antagonist regulates various reactions by interleukin-1 in pleural effusion, and that pleural macrophages may act in situ as a source of interleukin-1 receptor antagonist.}, issn = {0903-1936}, URL = {//www.qdcxjkg.com/content/9/6/1211}, eprint = {//www.qdcxjkg.com/content/9/6/1211.full.pdf}, journal = {European Respiratory Journal} }