Functional characteristics of human alveolar macrophages in lung cancer

Clerici, N.; Leyva-Cobián, Francisco; Reboiras, S; Mercado, P. Lázaro de

doi:10.1007/bf02713660

Cited by 5 publications

(1 citation statement)

References 15 publications

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“…Non-smokers' AM had a higher expression of CD11a, CD54 and CD71 than smokers' AM. On the other hand, receptors mediating adhesion (CD11b, CD11c) and phagocytosis (CD16) were unaltered (in agreement with reports from others [6,14,15,25] ), or even increased (CD11c) in smokers' AM. The findings suggest that smokers' AM may have adapted to a long history of phagocytosis, and therefore have reached a more final stage of maturation, displaying above all the adhesion and phagocyte receptors while having less receptors reflecting accessory functions.…”

Section: Discussionsupporting

confidence: 91%

Chronic smoke exposure alters the phenotype pattern and the metabolic response in human alveolar macrophages

Sköld

Lundahl

Halldén

et al. 1996

Clinical and Experimental Immunology

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SUMMARYSmoking induces a chronic inflammatory process in the lower respiratory tract, where the alveolar macrophages (AM) are the main phagocytes. In the present study, the expressions of different membrane glycoproteins (CD11abc, CD71, CD54, CD14 and CD16) were determined by flow cytometry in AM from smokers and non-smokers after quenching of the intracellular autofluorescence. The metabolic activity of the AM was quantified as a functional test. The expressions of CD11a, CD54 and CD71 were higher in non-smokers' AM than in smokers'. The expressions of CD11b and CD16 were similar between the groups, while the CD11c was higher in smokers' AM compared with nonsmokers'. The expression of CD14 was weak in both groups, therefore there was no clear-cut difference between the background and positively labelled cell populations. The metabolic response after in vitro stimulation with the phorbol ester phorbol myristate acetate (PMA) was higher in non-smokers' than in smokers' AM. Our results indicate that chronic exposure to tobacco smoke influences both the expression of AM membrane antigens and the metabolic activity. AM from non-smokers express a phenotype more related to cell proliferation and an accessory function. In contrast, receptors reflecting adhesion and phagocytosis were unaltered or even increased in smokers' AM. The findings suggest a functional change in the AM population after chronic smoke exposure.

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Section: Discussionsupporting

confidence: 91%

Chronic smoke exposure alters the phenotype pattern and the metabolic response in human alveolar macrophages

Sköld

Lundahl

Halldén

et al. 1996

Clinical and Experimental Immunology

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Reduction in HLA-DR antigen density on alveolar macrophages of smokers

Pankow

Neumann

Rüschoff

et al. 1991

Lung

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Alveolar macrophage cytotoxic activity is inhibited by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a carcinogenic component of cigarette smoke

Proulx

Paré²,

Bissonnette

2006

Cancer Immunol Immunother

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4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is a carcinogenic compound of cigarette smoke that generates electrophilic intermediates capable of damaging DNA. Recently, we have shown that NNK can modulate mediator production by alveolar macrophages (AM) and bronchial and alveolar epithelial cells, suggesting that cigarette smoke can alter lung immune response. Thus, we investigated the effect of NNK and cigarette smoke extract (CSE) on AM capacity to eliminate tumoral cells. Rat AM cell line, NR8383, was treated with NNK (500 microM) or CSE (3%) and stimulated with lipopolysaccharide (10 ng/ml). The release of cytotoxic mediators, tumor necrosis factor (TNF) and reactive oxygen species (ROS), was measured in cell-free supernatants using ELISA and superoxide anion production. TNF- and ROS-dependent cytotoxicity were studied using a (51)Chromium-release assay and WEHI-164 and P-815 cell lines. Treatment of AM with NNK and CSE for 18 h significantly inhibited AM TNF release. CSE exposure resulted in a significant increase of ROS production, whereas NNK did not. TNF-dependent cytotoxic activity of NR8383 and freshly isolated rat AM was significantly inhibited after treatment with NNK and CSE. Interestingly, although ROS production was stimulated by CSE and not affected by NNK, CSE inhibited AM ROS-dependent cytotoxicity. These results suggest that NNK may be one of the cigarette smoke components responsible for the reduction of pulmonary cytotoxicity. Thus, NNK may have a double pro-carcinogenic effect by contributing to DNA adduct formation and inhibiting AM cytotoxicity against tumoral cells.

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Functional characteristics of human alveolar macrophages in lung cancer

Cited by 5 publications

References 15 publications

Chronic smoke exposure alters the phenotype pattern and the metabolic response in human alveolar macrophages

Chronic smoke exposure alters the phenotype pattern and the metabolic response in human alveolar macrophages

Reduction in HLA-DR antigen density on alveolar macrophages of smokers

Alveolar macrophage cytotoxic activity is inhibited by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a carcinogenic component of cigarette smoke

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