Am. J. Respir. Crit. Care Med., Vol 152, No. 3, Sep 1995, 1087-1093.
Expression and distribution of cell-membrane complement regulatory glycoproteins along the human respiratory tract
S Varsano, I Frolkis and D Ophir
Department of Pulmonary Medicine, Sapir Medical Center, Meir General Hospital, Kfar Sava, Israel.
Complement in the human respiratory tract protects the host from invading
microorganisms and from other inhaled insults. However, complement may also
lyse the host's respiratory tract cells, leading to tissue injury. In many
extrapulmonic tissues, cells express cell- membrane complement 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 healthy and diseased human
respiratory tract from nose to alveoli for the presence of four
cell-membrane complement regulatory glycoproteins (membrane cofactor
protein [MCP], decay-accelerating factor [DAF], CD59, and complement
receptor type 1 [CR1]) using an immunoperoxidase technique. In addition, to
establish a model for in vitro studies of these glycoproteins in
respiratory cells, we studied whether they are expressed in cultured nasal
epithelial cells, using the same technique. Altogether, 26 tissue specimens
from 22 patients were studied. We found that normal human respiratory tract
from nose to alveoli express MCP, DAF, and CD59, but not CR1, and that this
expression increases in inflammation and in lung cancer. In addition,
expression in nasal epithelial cells is retained under cell culture
conditions. These findings suggest that human respiratory tract tissue may
regulate complement activation on its surface in order to avoid
self-injury. We propose that imbalances in the mechanism that regulates
cell-membrane complement may predispose the respiratory tract to tissue
injury and disease, and that iatrogenic modulation of such imbalances may
help to prevent these adverse consequences.