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Tuberc Respir Dis > Volume 43(1); 1996 > Article
Tuberculosis and Respiratory Diseases 1996;43(1):46-53.
DOI: https://doi.org/10.4046/trd.1996.43.1.46    Published online February 1, 1996.
Priming Effect of Endotoxin in Human Alveolar Macrophage.
Man Pyo Chung, Chul Gyu Yoo, Young Whan Kim, Sung Koo Han, Young Soo Shim, Yong Chol Han
Department of Internal Medicine and Tuberculosis Research Institute, Seoul National University College of Medicine, Seoul, Korea.
Abstract
BACKGROUND
Endotoxin or lipopolysaccharide(LPS) can prime phagocytic cells such as polymorphonuclear leukocytes, monocytes or animal peritoneal macrophages to generate increased amounts of secretory products such as oxygen free radicals and tumor necrosis factor, which play an important role in developing adult respiratory distress syndrome in gram negative sepsis. Human alveolar macrophages(HAM) are continuously exposed to various stimuli inhaled into the alveoli, and the response to LPS might be different in HAM. Therefore, we investigated the effect of LPS pre-exposure on HAM adhered to plastic surface and A549 cell(type II human alveolar epithelial cell line) monolayer. METHODS: HAM were isolated from bronchoalveolar lavage fluid from normal lung of the patients with localized lung cancer and esophageal cancer. LPS was exposed to HAM for 2hrs before or after adherence to plastic surface of 24-well Linbro plate and A549 cell monolayer. And then HAM was stimulated with PMA(phorbol myristate acetate) or fMLP(N-formyl-methionyl- leucyl-phenylalanine). The amount of hydrogen peroxide(H2O2) production in the supernatant was measured on the principle of peroxidase-dependent oxidation of phenol red by hydrogen peroxide. RESULTS: LPS pre-exposure could not enhance H2O2 production in neither HAM adhered to plastic surface nor one to A549 cell monolayer. But LPS even in the absence of PMA or fMLP stimulation directly increased H2O2 release in HAM if added after the adherence to A549 cell monolayer. CONCLUSION: Endotoxin does not prime HAM, but may directly activate HAM adhered to alveolar epithelial cells. Further investagation will be necessary.
Key Words: Human alveolar macrophage, Priming, Lipopolysaccharide


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