Abstract
Some biological effects of chronic cigarette smoking (two cigarettes for 2 h, daily for 4 months) in rats were evaluated. During the smoking period, body weight of smoker rats was always significantly lower than 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 significantly. At the same time, enzymatic analyses on the supernatants of bronchoalveolar fluid revealed a significant increase of β-glucuronidase in the smoker group. Alveolar macrophages, collected 0, 8 and 24 h after the last smoking session, significantly increased the generation of superoxide anion and, after incubation for 24 h at 37° C in a humidified atmosphere, released significantly high amounts of TNF-α. When challenged with lipopolysaccharide, alveolar macrophages of smoker rats released much more TNF-α but, in such a case, TNF-α release was about one half of that observed in the control group. Peritoneal macrophages of both control and smoker rats were unable either to generate high levels of superoxide anion or to release significant amounts of TNF-α. The results clearly demonstrated the activated state of alveolar macrophages and the resting state of peritoneal macrophages.
Highlights
The lung represents a frequent site of inflammation because of its direct exposure to noxious agents, antigenic materials and invasion by microorganisms
polymorphonuclear cells (PMN) in the bronchoalveolar fluid (BAL) of smoker rats significantly increased in respect to air-sham exposed rats and, at the same time, peritoneal Mq in the peritoneal fluid (PF) decreased (Table 1)
Evaluation of COHb blood levels, immediately after the last smoking session, gave values of about 8.5% which compared well with those observed in guinea pig and in human cigarette smokers. 18J9 The total number of alveolar M4 collected from BAL of chronic smoker rats was unchanged compared with that of control rats or acute smoker rats, but PMN increased significantly in the BAL of smoker rats
Summary
The lung represents a frequent site of inflammation because of its direct exposure to noxious agents, antigenic materials and invasion by microorganisms. 2 The development of pulmonary inflammation is known to involve cellular events controlled by a variety of cytokines. These mediate interactions between macrophages (Mb), lymphocytes and granulocytes and represent an important event in the regulation of airway inflammation. 3’4 there is evidence that alveolar MqS, which are derived from blood monocytes, may mediate many of the harmful effects of smoking, exerting their activity at the inflammatory sites partly directly and partly through the action of tumour necrosis factor (TNF) and other immunological mediators. The locally regulated generation of TNF
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