Oxidative Metabolism of Alveolar Macrophages from Young Asymptomatic Cigarette Smokers

Hoidal, J. R.; Fox, Richard B.; LeMarbre, P.A.; Takiff, Howard; Repine, John E.

doi:10.1378/chest.77.2.270

Cited by 32 publications

(27 citation statements)

References 8 publications

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“…For example, with regard to adherence of macrophages from smokers, Mann [27][28][29] This may be due to differences between the subjects, including their smoking history, as well as between experimental methods.…”

Section: Discussionmentioning

confidence: 99%

Surface morphology and function of human pulmonary alveolar macrophages from smokers and non-smokers.

Ando¹,

Sugimoto²,

Nishi³

et al. 1984

Thorax

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Pulmonary alveolar macrophages were obtained by saline lavage from 23 healthy male volunteers-10 non-smokers and 13 cigarette smokers. Lavage produced three times as many alveolar macrophages in smokers than in non-smokers. When macrophages from smokers and from non-smokers were incubated in vitro, more cells from smokers adhered to glass, spread out, and showed enhanced nitroblue tetrazolium (NBT) reduction. The surface morphology of alveolar macrophages from smokers showed more with a plate like appearance and ridge like membrane surface, while the macrophages from non-smokers were predominantly spherical with ruffles. The proportions of cells which stained highly for , f galactosidase were 55% in smokers and 11% in non-smokers. Thus, in a resting state in vitro, alveolar macrophages from smokers were more active than those from non-smokers. When, however, macrophages from smokers and non-smokers were incubated with immunobeads and with opsonised or non-opsonised BCG, the phagocytic activity and stimulated NBT reduction of alveolar macrophages from smokers were similar to or somewhat less than those of non-smokers.Alveolar macrophages act as a main cellular defence for the lung against inhaled microorganisms and other particles.' Potential damage to these cells by cigarette smoke could lead to microbial infection and parenchymal damage, possibly mediated through excessive release of several reactive products of alveolar macrophages, including both oxidative agents and lysosomal enzymes.23 Many studies have therefore been directed at the function and biochemistry of alveolar macrophages but data on functional differences between alveolar macrophages from smokers and non-smokers have often been contradictory.4 Furthermore, few have described quantitative differences in both cellular morphology and function.The aims of the present study were (1) to evaluate the functional differences between alveolar macrophages from smokers and non-smokers with respect to adherence and spreading, phagocytosis, nitroblue Our results indicate that in the unstimulated condition alveolar macrophages from smokers appear more active than those from non-smokers in both surface morphology and function. Their responsiveness to foreign bodies or bacteria, however, was equivalent or somewhat inferior to that of nonsmokers when determined by phagocytosis and by NBT reduction, which reflects superoxide production by the cells.5 6 Methods SUBJECTSThe 23 healthy male volunteers were medical students or physicians in our university. Ten were nonsmokers and 13 were cigarette smokers. All the smokers had a history of more than five pack years, were currently smoking more than one pack per day, and had done so for more than one year before the study. The mean age of the non-smokers was 27-4 (range 23-37) years and that of the smokers was 27-2 (range 23-35) years. 850 on 12 May 2018 by guest. Protected by copyright.

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Section: Discussionmentioning

confidence: 99%

Surface morphology and function of human pulmonary alveolar macrophages from smokers and non-smokers.

Ando¹,

Sugimoto²,

Nishi³

et al. 1984

Thorax

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“…In the breath hydrogen peroxide and nitric oxide, direct measurements of oxidants generated by cigarette smoking, or released from inflammatory leukocytes and epithelial cells, have been shown to be increased in patients with both stable and acute COPD in the case of hydrogen peroxide (18) and in exacerbations of the condition in the case of nitric oxide (19). Alveolar leukocytes from smokers and patients with chronic bronchitis have increased ability to release oxygen radicals, compared with those from healthy controls (20). Xanthine/ xanthine oxidase, which generates superoxide anion, has also been shown to be increased in the bronchoalveolar lavage fluid from patients with COPD (21).…”

Section: Evidence Of Oxidative Stress In Smokers and Patients With Copdmentioning

confidence: 99%

Oxidants and Antioxidants as Therapeutic Targets in Chronic Obstructive Pulmonary Disease

MacNee

Rahman

1999

Am J Respir Crit Care Med

195

127

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There is now increasing evidence that an oxidant/antioxidant imbalance, in favor of oxidants, occurs in chronic obstructive pulmonary disease (COPD). Evidence is also accumulating that oxidative stress is a critical event in the pathogenesis of this condition. A large number of studies have demonstrated an increased oxidant burden and consequently increased markers of oxidative stress in the airspaces, breath, blood, and urine of smokers and of patients with COPD. There are several events related to oxidative stress, which are important in the pathogenesis of COPD. These include oxidative inactivation of antiproteinases, airspace epithelial injury, increased sequestration of neutrophils in the pulmonary microvasculature, and gene expression of proinflammatory mediators. Oxidative processes have a fundamental role in the inflammation of smokers and patients with COPD, through redox-sensitive transcription factors such as NF-kappaB and AP-1, which regulate the genes for proinflammatory mediators and protective mechanisms, such as antioxidant gene expression. In addition to the oxidative stress produced by cigarette smoking, dietary deficiency in antioxidants is related to the development of airflow limitation, and hence dietary supplementation may be a beneficial therapeutic intervention in this condition. The use of antioxidants with good bioavailability or molecules that have antioxidant enzyme activity may be treatments that not only protect against the direct injurious effects of oxidants, but may fundamentally alter the inflammatory events that are thought to play an important part in the pathogenesis of COPD. MacNee W, Rahman I. Oxidants and antioxidants as therapeutic targets in chronic obstructive pulmonary disease.

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“…Studies have also shown that macrophages from smokers have a significantly higher aryl hydrocarbon hydroxylase activity than similar cells from nonsmokers (33,34 These studies showed that there was no effect of cigarette smoke on uptake and metab? olism of PGF2a in isolated perfused rabbit lungs.…”

Section: Huber Et Al (26) Sug?mentioning

confidence: 99%

Effects of Cigarette Smoking on Metabolic Events in the Lung

Kitamura¹

1987

Environmental Health Perspectives

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Oxidative Metabolism of Alveolar Macrophages from Young Asymptomatic Cigarette Smokers

Cited by 32 publications

References 8 publications

Surface morphology and function of human pulmonary alveolar macrophages from smokers and non-smokers.

Surface morphology and function of human pulmonary alveolar macrophages from smokers and non-smokers.

Oxidants and Antioxidants as Therapeutic Targets in Chronic Obstructive Pulmonary Disease

Effects of Cigarette Smoking on Metabolic Events in the Lung

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