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

被引:9
作者
PESSINA, GP
PAULESU, L
CORRADESCHI, F
LUZZI, E
TANZINI, M
ALDINUCCI, C
DISTEFANO, A
BOCCI, V
机构
[1] UNIV SIENA,INST GEN PHYSIOL,VIA LATERINA 8,I-53100 SIENA,ITALY
[2] UNIV SIENA,DEPT MOLEC BIOL,I-53100 SIENA,ITALY
关键词
ALVEOLAR MACROPHAGES; CIGARETTE SMOKING; INFLAMMATION; INTERFERON; TUMOR NECROSIS FACTOR-ALPHA;
D O I
10.1155/S0962935193000602
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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 beta-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-degrees-C in a humidified atmosphere, released significantly high amounts of TNF-alpha. When challenged with lipopolysaccharide, alveolar macrophages of smoker rats released much more TNF-alpha but, in such a case, TNF-alpha 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-alpha. The results clearly demonstrated the activated state of alveolar macrophages and the resting state of peritoneal macrophages.
引用
收藏
页码:423 / 428
页数:6
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