Am. J. Respir. Cell Mol. Biol., Volume 19, Number 4, October, 1998 537-542

RAPID COMMUNICATION
Expression of Fas (CD95) and FasL (CD95L) in Human Airway Epithelium

Kimm J. Hamann,^* Delbert R. Dorscheid,^* Franklin D. Ko, Amber E. Conforti, Anne I. Sperling, Klaus F. Rabe, and Steven R. White

Section of Pulmonary and Critical Care Medicine, Division of Biological Sciences, University of Chicago, Chicago, Illinois; and Krankenhaus Großhansdorf, Großhansdorf, Germany

The cell surface molecule Fas (CD95) is a member of the tumor necrosis factor receptor family. Ligation of the Fas receptor can lead to induction of apoptosis in inflammatory cells. It has been suggested that expression of the Fas receptor and its ligand (FasL) in airway epithelium may modulate the inflammatory response commonly found in asthmatic lungs. We examined Fas and FasL expression on primary human tissues, on bronchial epithelial cells in primary culture, and on the immortalized human airway epithelial cell line, 1HAE_o. Receptor and ligand expression were demonstrated using multiple antibodies and multiple techniques, including immunohistochemistry, flow cytometry, Western blots, and reverse transcription-polymerase chain reaction (RT-PCR). Immunohistochemical staining demonstrated that both columnar and basal cells of intact human lung tissues expressed cell surface Fas and FasL. In addition, both primary cultured and immortalized 1HAE_o cells expressed cell surface Fas and FasL, as demonstrated by flow cytometry; expression of Fas and FasL was confirmed at the transcription level using RT-PCR and, for additional confirmation of FasL, using Western blots. We demonstrate that both Fas and FasL are expressed by human airway epithelial cell subtypes. Expression of these molecules may play an important role in regulation of the inflammatory response.

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