EXPRESSION AND DISTRIBUTION OF CELL-MEMBRANE COMPLEMENT REGULATORY GLYCOPROTEINS ALONG THE HUMAN RESPIRATORY-TRACT

Citation
S. Varsano et al., EXPRESSION AND DISTRIBUTION OF CELL-MEMBRANE COMPLEMENT REGULATORY GLYCOPROTEINS ALONG THE HUMAN RESPIRATORY-TRACT, American journal of respiratory and critical care medicine, 152(3), 1995, pp. 1087-1093
Citations number
29
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
152
Issue
3
Year of publication
1995
Pages
1087 - 1093
Database
ISI
SICI code
1073-449X(1995)152:3<1087:EADOCC>2.0.ZU;2-F
Abstract
Complement in the human respiratory tract protects the host from invad ing microorganisms and from other inhaled insults. However, complement may also lyse the host's respiratory tract cells, leading to tissue i njury. In many extrapulmonic tissues, cells express cell-membrane comp lement regulatory glycoproteins that protect the cells from complement -induced lysis. To determine whether these glycoproteins are expressed in human respiratory tract tissue, we studied tissue biopsies of heal thy and diseased human respiratory tract from nose to alveoli for the presence of four cell-membrane complement regulatory glycoproteins (me mbrane cofactor protein [MCP], decay-accelerating factor [DAF], CD59, and complement receptor type 1 [CR1]) using an immunoperoxidase techni que. In addition, to establish a model for in vitro studies of these g lycoproteins in respiratory cells, we studied whether they are express ed in cultured nasal epithelial cells, using the same technique. Altog ether, 26 tissue specimens from 22 patients were studied. We found tha t normal human respiratory tract from nose to alveoli express MCP, DAF , and CD59, but not CR1, and that this expression increases in inflamm ation and in lung cancer. In addition, expression in nasal epithelial cells is retained under cell culture conditions. These findings sugges t that human respiratory tract tissue may regulate complement activati on on its surface in order to avoid self-injury. We propose that imbal ances in the mechanism that regulates cell-membrane complement may pre dispose the respiratory tract to tissue injury and disease, and that i atrogenic modulation of such imbalances may help to prevent these adve rse consequences.