Pneumocystis cariniiinduces ICAM-1 expression in lung epithelial cells through a TNF-α-mediated mechanism

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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 withP.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-α (TNF-α) release from macrophages or thatP.carinii directly stimulated ICAM-1 expression. Alveolar macrophages were incubated withP.carinii, and the medium was added to A549 epithelial cells. Treatment of macrophages withP.carinii enhanced A549 ICAM-1, which was inhibited with antibody to TNF-α. 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 withP.carinii-exposed macrophages. Thus ICAM-1 is enhanced in lung epithelium duringP.carinii infection, in part, through TNF-α-mediated mechanisms.

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