Pneumocystis carinii induces ICAM-1 expression in lung epithelial cells through a TNF-alpha-mediated mechanism

The American Journal of Physiology
M L Yu, A H Limper

Abstract

Inflammatory cell recruitment contributes to respiratory impairment during Pneumocystis carinii pneumonia. We evaluated expression of intercellular adhesion molecule-1 (ICAM-1), a key participant in leukocyte accumulation, in rats with P. carinii pneumonia. Immunostaining for ICAM-1 was most marked on bronchiolar epithelium but was also evident on type II pneumocytes, endothelium, and macrophages. Lung from normal and dexamethasone-treated uninfected animals exhibited markedly less ICAM-1. We hypothesized that P. carinii promoted ICAM-1 expression in epithelium through tumor necrosis factor-alpha (TNF-alpha) release from macrophages or that P. carinii directly stimulated ICAM-1 expression. Alveolar macrophages were incubated with P. carinii, and the medium was added to A549 epithelial cells. Treatment of macrophages with P. carinii enhanced A549 ICAM-1, which was inhibited with antibody to TNF-alpha. To determine whether P. carinii alone also stimulated ICAM-1, A549 cells were cultured with P. carinii, also augmenting ICAM-1. Of note, A549 ICAM-1 expression from P. carinii alone was less than with P. carinii-exposed macrophages. Thus ICAM-1 is enhanced in lung epithelium during P. carinii infection, in part, through TNF-alpha-m...Continue Reading

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Citations

Apr 6, 2001·American Journal of Physiology. Lung Cellular and Molecular Physiology·N E VlahakisR D Hubmayr
Mar 11, 2003·Clinical and Diagnostic Laboratory Immunology·Mark E LasburyChao-Hung Lee
Mar 11, 2000·American Journal of Physiology. Lung Cellular and Molecular Physiology·C MadjdpourB Beck-Schimmer
May 15, 2001·American Journal of Physiology. Lung Cellular and Molecular Physiology·N FukudaM A Matthay
Feb 20, 2007·American Journal of Physiology. Lung Cellular and Molecular Physiology·Jing WangTerry W Wright

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