ArticleAmerican journal of respiratory cell and molecular biology2011
Cigarette smoke inhibits engulfment of apoptotic cells by macrophages through inhibition of actin rearrangement.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Modeling the Exposome in Murine Cardiovascular Disease.JACC. Basic to translational science · 2026Review
- Neutrophil Heterogeneity in Airway Inflammatory Diseases.Inflammation · 2025Review
- Heterogeneity of Lung Phagocytes and Clearance of Apoptotic Cells in Lung Injury and Repair.Seminars in respiratory and critical care medicine · 2025Review
- Prevalence and Associated Factors of Latent Tuberculosis Infection Among Healthcare Workers in a Mexican Tertiary Care Hospital.Diseases (Basel, Switzerland) · 2025Article
- Efferocytosis and Respiratory Disease.International journal of molecular sciences · 2023Review
- No smoke without fire: the impact of cigarette smoking on the immune control of tuberculosis.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Nrf2 Is Required for Optimal Alveolar-Macrophage-Mediated Apoptotic Neutrophil Clearance after Oxidant Injury.Antioxidants (Basel, Switzerland) · 2022Article
- RIP3-dependent necroptosis contributes to the pathogenesis of chronic obstructive pulmonary disease.JCI insight · 2021Article
- Chronic cigarette smoke exposure and pneumococcal infection induce oropharyngeal microbiota dysbiosis and contribute to long-lasting lung damage in mice.Microbial genomics · 2020Article
- Lung Macrophage Functional Properties in Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2020Review
- E-cigarettes: Effects in phagocytosis and cytokines response against Mycobacterium tuberculosis.PloS one · 2020Article
- Regulation of Apoptotic Cell Clearance During Resolution of Inflammation.Frontiers in pharmacology · 2019Review
- Epidemiologic Evidence of and Potential Mechanisms by Which Second-Hand Smoke Causes Predisposition to Latent and Active Tuberculosis.Immune network · 2018Review
- Dysregulated Functions of Lung Macrophage Populations in COPD.Journal of immunology research · 2018Review
- Mechanisms and modulation of microvesicle uptake in a model of alveolar cell communication.The Journal of biological chemistry · 2017Article
- Increased expression of Siglec-9 in chronic obstructive pulmonary disease.Scientific reports · 2017Article
- A longitudinal modelling study estimates acute symptoms of community acquired pneumonia recover to baseline by 10 days.The European respiratory journal · 2017Observational
- Cigarette smoke attenuates phagocytic ability of macrophages through down-regulating Milk fat globule-EGF factor 8 (MFG-E8) expressions.Scientific reports · 2017Article
- MFG-E8, a clearance glycoprotein of apoptotic cells, as a new marker of disease severity in chronic obstructive pulmonary disease.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2015Article
- Second-hand cigarette smoke impairs bacterial phagocytosis in macrophages by modulating CFTR dependent lipid-rafts.PloS one · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Exposure to cigarette smoke (CS) was shown to impair the capacity of macrophages to clear bacteria and apoptotic cells. Here, we show that both the exposure of macrophages to cigarette smoke extract (CSE) in vitro and an acute single exposure to CS in vivo impair the macrophage clearance of apoptotic polymorphonuclear leukocytes (PMNs). Upon longer periods of exposure to smoke in vivo (4-12 weeks), the impaired capacity of macrophages to clear apoptotic cells persisted after the cessation of smoking, with slow recovery to normality observed 4 weeks later. With respect to the mechanism by which CS impairs the macrophage uptake of apoptotic PMNs, we did not detect altered surface expression of receptors associated with apoptotic cell clearance. We did observe the impaired phosphorylation of the guanine nucleotide exchange factor Vav1 and the downstream inhibition of Ras-related C3 botulinum toxin substrate 1 (Rac1) activation. Consistent with these findings, CS impaired the macrophage cytoskeletal changes observed after stimulation with apoptotic cells. A loss of actin occurred at the leading edge, manifested as impaired ruffling of the cell membrane and a decreased capacity to engulf apoptotic cells. The inability to clear PMNs would lead to a greater release of destructive PMN products, and would diminish the reparative phenotype induced by the macrophage clearance of apoptotic cells.
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Registered trials
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