Glenn A. Warr

Induction of aryl hydrocarbon hydroxylase in human pulmonary alveolar macrophages and peripheral lymphocytes by cigarette tars

Cigarette smoking is associated with alterations in pulmonary alveolar macrophages (PAMs), including increased cytoplasmic inclusions and induction of the aryl hydrocarbon hydroxylase (AHH) system. Nonpigmented PAMs from nonsmokers were able to ingest and accumulate pigment from lysed PAMs of smokers, however, this pigment did not induce AHH activity in either PAMs or peripheral lymphocytes. In contrast, the cigarette tars significantly induced AHH levels in PAMs and in peripheral lymphocytes from either nonsmokers or smokers. This provides further evidence that components in cigarette smoke can explain the in vivo induction of AHH documented in cells from smokers.

Concanavalin-A agglutination of human pulmonary alveolar macrophages from nonsmokers and cigarette smokers: A comparison

Abstract Incubation of pulmonary alveolar macrophages (PAMs) from nonsmokers in phosphate buffered saline (PBS) leads to minimal auto-agglutination of these cells, while smokers PAMs incubated in medium remained individually dispersed in suspension. Incubation with the lectin concanavalin A (Con-A) induced agglutination of PAMs from cigarette smokers, while PAMs from nonsmokers were not further agglutinated. After trypsin treatment, both nonsmoker and smoker PAMs agglutinated in the presence of Con-A. Both PAM populations bound the same amount of 125I-Con-A. Low temperatures (4°C), α-methylmannose, and pre-fixation of smoker PAMs with glutaraldehyde prevented Con-A induced cell agglutination. Candida bound to PAMs by Con-A were similarly distributed on the surfaces of nonsmoker and smoker cells.