CHRONIC CIGARETTE-SMOKING ENHANCES SPONTANEOUS RELEASE OF TUMOR-NECROSIS-FACTOR-ALPHA FROM ALVEOLAR MACROPHAGES OF RATS

Citation
Gp. Pessina et al., CHRONIC CIGARETTE-SMOKING ENHANCES SPONTANEOUS RELEASE OF TUMOR-NECROSIS-FACTOR-ALPHA FROM ALVEOLAR MACROPHAGES OF RATS, Mediators of inflammation, 2(6), 1993, pp. 423-428
Citations number
35
Categorie Soggetti
Cytology & Histology",Biology
Journal title
ISSN journal
09629351
Volume
2
Issue
6
Year of publication
1993
Pages
423 - 428
Database
ISI
SICI code
0962-9351(1993)2:6<423:CCESRO>2.0.ZU;2-0
Abstract
SOME biological effects of chronic cigarette smoking (two cigarettes f or 2 h, daily for 4 months) in rats were evaluated. During the smoking period, body weight of smoker rats was always significantly lower tha n that of control rats. Immediately after the last smoking session the carboxyhaemoglobin concentration in the blood was about 8.5% and the polymorphonuclear cells in the bronchoalveolar fluid increased signifi cantly. At the same time, enzymatic analyses on the supernatants of br onchoalveolar fluid revealed a significant increase of beta-glucuronid ase in the smoker group. Alveolar macrophages, collected 0, 8 and 24 h after the last smoking session, significantly increased the generatio n of superoxide anion and, after incubation for 24 h at 37-degrees-C i n a humidified atmosphere, released significantly high amounts of TNF- alpha. When challenged with lipopolysaccharide, alveolar macrophages o f smoker rats released much more TNF-alpha but, in such a case, TNF-al pha release was about one half of that observed in the control group. Peritoneal macrophages of both control and smoker rats were unable eit her to generate high levels of superoxide anion or to release signific ant amounts of TNF-alpha. The results clearly demonstrated the activat ed state of alveolar macrophages and the resting state of peritoneal m acrophages.