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Alveolar macrophages from subjects with chronic obstructive pulmonary disease are deficient in their ability to phagocytose apoptotic airway epithelial cells
Abstract
Chronic obstructive pulmonary disease is a highly prevalent, complex disease, usually caused by cigarette smoke. It causes serious morbidity and mortality and costs the global community billions of dollars per year. While chronic inflammation, extracellular matrix destruction and increased airway epithelial cell apoptosis are reported in chronic obstructive pulmonary disease, the understanding of the basic pathogenesis of the disease is limited and there are no effective treatments. We hypothesized that the accumulation of apoptotic airway epithelial cells chronic obstructive pulmonary disease in could be due to defective phagocytic clearance by alveolar macrophages. There have been no previous studies of the phagocytic capacity of alveolar macrophages in chronic obstructive pulmonary disease using physiologically relevant apoptotic airway epithelial cells as phagocytic targets. We developed a phagocytosis assay whereby cultured 16HBE airway epithelial cells were induced to apoptosis with ultraviolet radiation and stained with mitotracker green. Alveolar macrophages from bronchoalveolar lavage from eight control and six chronic obstructive pulmonary disease subjects were analysed following 1.5 h incubation with apoptotic airway epithelial cells, then staining with macrophage marker anti CD33. CD33+/mitotracker green + events (i.e., alveolar macrophages which had phagocytosed apoptotic airway epithelial cells) were analysed using flow cytometry. Phagocytosis of polystyrene microbeads was investigated in parallel. A significantly reduced proportion of alveolar macrophages from chronic obstructive pulmonary disease subjects ingested apoptotic airway epithelial cells compared with controls (11.6 ± 4.1% for chronic obstructive pulmonary disease versus 25.6 ± 9.2% for control group). Importantly, the deficiency was not observed using polystyrene beads, suggesting that the failure to resolve epithelial damage in chronic obstructive pulmonary disease may result, at least partially, from specific defects in phagocytic ability of alveolar macrophages to ingest apoptotic airway epithelial cells.
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“Impaired phagocytosis and clearance of cellular debris by airway macrophages in COPD result in persistent inflammation (85, 104).”
From Aging and Lung Disease (2020) · cites this paper as [104]
In the citing paper
“Specifically, macrophages, which can produce multiple proinflammatory cytokines and secrete MMPs, are the most abundant cell type in the BAL fluid of COPD patients, and increased numbers correlate with disease severity (85, 86, 104).”
From Aging and Lung Disease (2020) · cites this paper as [104]
In the citing paper
“Due to reduced immunity, coexisting comorbidities, and age-associated functional limitations, the incidence of severe sepsis and septic shock increases in older individuals (104, 146).”
From Aging and Lung Disease (2020) · cites this paper as [104]
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“There is compelling evidence that alveolar macrophages from patients with COPD are less effective in the phagocytosis of apoptotic airway epithelial cells compared to controls (6).”
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Self-citationEffect of the inhaled PDE4 inhibitor CHF6001 on biomarkers of inflammation in COPD
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“cystic fibrosis, and is hypothesized to contribute to persistent inflammation.(29,34,35) For instance, airway macrophages from patients with severe asthma have reduced ability to efferocytose apoptotic cells, a function that can be increased approximately 3-fold by glucocorticoids.”
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“However, not only elevated tissue invasion but also impaired neutrophil clearance was implicated in the pathogenesis of COPD as alveolar macrophages exhibit a loss in phagocytic activity and cigarette smoke has directly been linked to reduced phagocytosis of apoptotic neutrophils [76, 77].”
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“Not only is the clearance of bacteria diminished in COPD cells but these macrophages also fail to clear apoptotic cells [20], leading”
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Butler, A., Walton, G., & Sapey, E. (2018) · COPD Journal of Chronic Obstructive Pulmonary Disease · doi:10.1080/15412555.2018.1476475 · Cited by 74
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BackgroundOpsonic Phagocytosis in Chronic Obstructive Pulmonary Disease Is Enhanced by Nrf2 Agonists
Bewley, M. A., Budd, R. C., Ryan, E. M., Cole, J., Collini, P., Marshall, J. L., Kolsum, U., Beech, G., Emes, R. D., Tcherniaeva, I., et al. (2018) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201705-0903oc · Cited by 73
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Acute respiratory distress syndrome is associated with impaired alveolar macrophage efferocytosis
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“COPD patients also have impaired AM efferocytosis(28) with overexpression of efferocytosis receptors CD206 and CD163 (29).”
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“BAL was performed as previously described (18).”
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Kazeros, A., Harvey, B., Carolan, B. J., Vanni, H., Krause, A., & Crystal, R. G. (2008) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2007-0306oc · Cited by 64
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Pappas, K., Papaioannou, A. Ι., Κostikas, Κ., & Tzanakis, Ν. (2013) · Cytokine · doi:10.1016/j.cyto.2013.09.010 · Cited by 71
“Of interest, the increased concentrations of apoptotic material and macrophage dysfunction persist in subjects with COPD, long after the cessation of smoking [89,106], whereas in smokers without COPD, these defects appear to resolve upon cessation of smoking.”
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“It has also been shown that neutrophil elastase cleaves the phosphatidylserine receptor on macrophages, resulting in impaired clearance of apoptotic cells [21].”
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“STAT1 is not activated (5, 6) and there is defective”
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Eosinophil Apoptosis and Clearance in Asthma
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“M. catarrhalis is also a common cause of OM in infants and children and causes an estimated 2–4 million exacerbations of COPD in adults annually in the USA (106).”
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“For instance, alveolar macrophages can promote resolution of lung injury by enhancing the clearance of apoptotic bodies (43), which suggests that recruitment of alveolar macrophages observed in syndecan-2 transgenic mice during the late phase of bleomycin-induced pulmonary fibrosis could enhance efferocytosis (44).”
BackgroundBarnawi, J., Tran, H. B., Jersmann, H. P. A., Pitson, S. M., Roscioli, E., Hodge, G. L., Meech, R., Haberberger, R. V., & Hodge, S. J. (2015) · PLoS ONE · doi:10.1371/journal.pone.0122771 · Cited by 59
“One of the major causes of this defect is thought to be a reduced ability of alveolar macrophages to phagocytose apoptotic cells and bacteria [3,32] which contributes to ongoing inflammation in lungs of these patients [8,33].”
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Self-citationThe impact of pulmonary diseases on the fate of inhaled medicines—A review
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“Furthermore, the alveolar macrophages of COPD patients have impaired bacterial (Haemophillus influenza, Escherichia coli, and Streptococcus pneumonia) phagocytosis [5,54], but the specific mechanism is not known.”
BackgroundMacrophage phagocytosis cracking the defect code in COPD
Jubrail, J., Kurian, N., & Niedergang, F. (2017) · Biomedical Journal · doi:10.1016/j.bj.2017.09.004 · Cited by 58
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BackgroundTNFα inhibits apoptotic cell clearance in the lung, exacerbating acute inflammation
Borges, V. M., Vandivier, R. W., McPhillips, K. A., Kench, J. A., Morimoto, K., Groshong, S. D., Richens, T. R., Graham, B. B., Muldrow, A. M., Heule, L. V., et al. (2009) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.90569.2008 · Cited by 56
“Conversely, defects in apoptotic cell clearance have been implicated in the pathogenesis of a number of chronic inflammatory lung diseases including chronic obstructive pulmonary disease, cystic fibrosis, bronchiectasis, and asthma (13, 14, 15, 17, 30, 31).”
BackgroundStatin-Regulated Efferocytosis in Physiological and Pathological Conditions
Tajbakhsh, A., Hayat, S. M. G., Askari, H., Savardashtaki, A., Pirro, M., Johnston, T. P., & Sahebkar, A. (2022) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2022.108282 · Cited by 57
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β1 Integrin regulates adult lung alveolar epithelial cell inflammation
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Therapeutic Role for Mannose-Binding Lectin in Cigarette Smoke–Induced Lung Inflammation?
Hodge, S. J., Matthews, G. M., Dean, M. M., Ahern, J., Djukic, M., Hodge, G. L., Jersmann, H. P. A., Holmes, M., & Reynolds, P. N. (2009) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2008-0486oc · Cited by 52
Self-citationSoriano, C., Mukaro, V. R., Hodge, G. L., Ahern, J., Holmes, M., Jersmann, H. P. A., Moffat, D. F. C., Meredith, D., Jurisevic, C. A., Reynolds, P. N., et al. (2012) · Lung Cancer · doi:10.1016/j.lungcan.2012.01.017 · Cited by 51
Self-citationState of the Art. Apoptosis and Cell Homeostasis in Chronic Obstructive Pulmonary Disease
Henson, P. M., Cosgrove, G. P., & Vandivier, R. W. (2006) · Proceedings of the American Thoracic Society · doi:10.1513/pats.200603-072ms · Cited by 51
“Macrophages lavaged from patients with COPD show evidence of decreased ingested apoptotic cells (8), and have been suggested to exhibit defective phagocytosis of microorganisms (19) or apoptotic 16HBE cells (20) in vitro.”
BackgroundCellular Regulation of the Inflammatory Response
Janssen, W. J., & Henson, P. M. (2011) · Toxicologic Pathology · doi:10.1177/0192623311428477 · Cited by 53
“Such a defect in apoptotic cell removal has been shown (Hodge et al. 2003, 2006, 2005, 2007; Morimoto, Janssen, Fessler, McPhillips, et al. 2006; Morimoto, Janssen, Fesser, Xiao, et al. 2006; Richens et al. 2009).”
BackgroundTheegarten, D., Sachse, K., Mentrup, B., Fey, K., Hotzel, H., & Anhenn, O. (2008) · Respiratory Research · doi:10.1186/1465-9921-9-14 · Cited by 49
“In current non-smokers with COPD MP show reduced capacity to ingest apoptotic airway epithelial cells as well [32].”
Cellular therapies for lung disease: A distant horizon
Moodley, Y. P., Manuelpillai, U., & Weiss, D. J. (2010) · Respirology · doi:10.1111/j.1440-1843.2010.01914.x · Cited by 49
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Defective monocyte-derived macrophage phagocytosis is associated with exacerbation frequency in COPD
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“However, macrophages from patients with COPD display defective phagocytosis of bacteria including Haemophilus influenzae and Streptococcus pneumoniae [2, 3], apoptotic cells [4] and fungal spores [5] and exhibit a pro-inflammatory secretory phenotype which drives inflammation in the lungs [6].”
BackgroundEosinophil and T cell markers predict functional decline in COPD patients
D'Armiento, J. M., Scharf, S. M., Roth, M. D., Connett, J. E., Ghio, A. J., Sternberg, D. I., Goldin, J. G., Louis, T. A., Mao, J. T., O’Connor, G. T., et al. (2009) · Respiratory Research · doi:10.1186/1465-9921-10-113 · Cited by 48
“These damaging effects are accentuated by the fact that pulmonary macrophages from COPD patients have a defect in their ability to phagocytose apoptotic cells in the lung[37].”
BackgroundHodge, S. J., Upham, J. W., Pizzutto, S. J., Petsky, H., Yerkovich, S. T., Baines, K. J., Gibson, P. G., Simpson, J. L., Buntain, H. M., Chen, A. C. –., et al. (2016) · CHEST Journal · doi:10.1016/j.chest.2015.10.066 · Cited by 48
Self-citationPhagocytosis of apoptotic eosinophils but not neutrophils by bronchial epithelial cells
Sexton, D. W., Al-Rabia, M. W., Blaylock, M. G., & Walsh, G. M. (2004) · Clinical & Experimental Allergy · doi:10.1111/j.1365-2222.2004.02054.x · Cited by 48
Winkler, A. R., Nocka, K. H., Sulahian, T. H., Kobzik, L., & Williams, C. M. M. (2008) · Experimental Lung Research · doi:10.1080/01902140802366261 · Cited by 47
“Because a deficiency in phagocytosis has been reported for the macrophages of COPD patients [62, 63], we also investigated the effect of acute smoke exposure on particle endocytosis by GMMØs using a novel confocal scanning cytometry method.”
MethodNeutrophil cannibalism – a back up when the macrophage clearance system is insufficient
Rydell-Törmänen, K., Uller, L., & Erjefält, J. S. (2006) · Respiratory Research · doi:10.1186/1465-9921-7-143 · Cited by 46
“A risk of impairment has been shown in several studies, for example in macrophages exposed to smoke or collected from COPD patients [27,28], and LPS stimulated alveolar macrophages from patients suffering from severe asthma [29].”
Alveolar-like Stem Cell–derived Myb − Macrophages Promote Recovery and Survival in Airway Disease
Litvack, M. L., Wigle, T. J., Lee, J., Wang, J., Ackerley, C. A., Grunebaum, E., & Post, M. (2016) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201509-1838oc · Cited by 46
E-cigarettes and health risks: more to the flavor than just the name
Ween, M. P., Moshensky, A., Thredgold, L. D., Bastian, N. A., Hamon, R., Badiei, A., Nguyen, P., Herewane, K., Jersmann, H. P. A., Bojanowski, C. M., et al. (2020) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00370.2020 · Cited by 46
Self-citationPalmieri, F., Koutsokera, A., Bernasconi, E., Junier, P., von Garnier, C., & Ubags, N. D. J. (2022) · Frontiers in Medicine · doi:10.3389/fmed.2022.832510 · Cited by 55
“In COPD patients, it has been demonstrated that alveolar macrophages exhibit reduced phagocytic capacity (30, 31).”
BackgroundBarnawi, J., Jersmann, H. P. A., Haberberger, R. V., Hodge, S. J., & Meech, R. (2016) · Respirology · doi:10.1111/resp.12949 · Cited by 45
Self-citationKotlyarov, S. N., & Котлярова, А. А. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22147634 · Cited by 50
Elastase/LPS-Exposed Mice Exhibit Impaired Innate Immune Responses to Bacterial Challenge
Ganesan, S., Faris, A. N., Comstock, A. T., Sonstein, J., Curtis, J. L., & Sajjan, U. S. (2011) · American Journal Of Pathology · doi:10.1016/j.ajpath.2011.09.029 · Cited by 44
COPD lung studies of Nrf2 expression and the effects of Nrf2 activators
Li, J., Baker, J. M., Higham, A., Shah, R. D., Montero, Á., Murray, C. M., Cooper, N., Lucas, C., Fox, C., Singh, D., et al. (2022) · Inflammopharmacology · doi:10.1007/s10787-022-00967-3 · Cited by 44
“In COPD, there is evidence of skewing towards a dysfunctional alveolar macrophage phenotype with reduced efferocytosis and phagocytosis in response to the local microenvironment (Hodge et al. 2003; Harvey et al. 2011; Dewhurst et al. 2017).”
BackgroundCai, X., Shi, Y., Dai, Y., Wang, F., Chen, X., & Li, X. (2022) · International Immunopharmacology · doi:10.1016/j.intimp.2022.108532 · Cited by 44
Preventing COPD exacerbations with macrolides: A review and budget impact analysis
Simoens, S., Laekeman, G., & Decramer, M. (2013) · Respiratory Medicine · doi:10.1016/j.rmed.2012.12.019 · Cited by 42
“First, alveolar macrophages of these patients are defective in phagocytosis of apoptotic cells.(20) Second, monocyte-derived macrophage phagocytosis of bacteria is also known to be defective in these patients.”
BackgroundTiwari, N., Marudamuthu, A. S., Tsukasaki, Y., Ikebe, M., Fu, J., & Shetty, S. (2016) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00290.2015 · Cited by 42
“Since lung inflammation has been implicated in both AEC apoptosis and senescence in response to chronic CS exposure (16), the identification of molecular mediators that trigger lung responses such as inflammation offers the potential for development of novel interventions.”
BackgroundCXCL16/CXCR6 is involved in LPS‐induced acute lung injury via P38 signalling
Tu, G.-W., Ju, M., Zheng, Y., Hao, G., Ma, G., Hou, J., Zhang, X., Luo, Z., & Lu, L. (2019) · Journal of Cellular and Molecular Medicine · doi:10.1111/jcmm.14419 · Cited by 42
Clearance of dying cells and autoimmunity
Michlewska, S., McColl, A., Rossi, A. G., Megson, I. L., & Dransfield, I. (2007) · Autoimmunity · doi:10.1080/08916930701357208 · Cited by 42
The aging lung: microenvironment, mechanisms, and diseases
Wang, Y., Huang, X., Luo, G., Xu, Y., Deng, X., Lin, Y., Wang, Z., Zhou, S., Wang, S., Chen, H., et al. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1383503 · Cited by 50
Resident Murine Alveolar and Peritoneal Macrophages Differ in Adhesion of Apoptotic Thymocytes
Hu, B., Jennings, J. H., Sonstein, J., Floros, J., Todt, J. C., Polak, T., & Curtis, J. L. (2003) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2003-0255oc · Cited by 41
“Human AMø also show reduced apoptotic cell ingestion (12).”
Korfei, M., MacKenzie, B., & Meiners, S. (2020) · European Respiratory Review · doi:10.1183/16000617.0126-2020 · Cited by 42
Impairment of phagocytosis of apoptotic cells and its role in chronic airway diseases
Krysko, O., Vandenabeele, P., Krysko, D. V., & Bachert, C. (2010) · APOPTOSIS · doi:10.1007/s10495-010-0504-x · Cited by 40
“Hodge and co-workers have elegantly shown in vitro that apoptotic cell clearance by alveolar macrophages (AMs) is impaired in COPD patients [14].”
BackgroundOxidative Stress Decreases Functional Airway Mannose Binding Lectin in COPD
Tran, H. B., Ahern, J., Hodge, G. L., Holt, P., Dean, M. M., Reynolds, P. N., & Hodge, S. J. (2014) · PLoS ONE · doi:10.1371/journal.pone.0098571 · Cited by 40
“Efferocytosis was assessed as previously reported [2,3] with minor modifications.”
Self-citationGroves, A. M., Gow, A. J., Massa, C. B., Hall, L., Laskin, J. D., & Laskin, D. L. (2013) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00027.2013 · Cited by 37
“Patients with COPD have been reported to have decreased pulmonary Sftpd levels (50); moreover, a single nucleotide polymorphism in Sftpd is associated with emphysema pathogenesis (25).”
BackgroundInfluentialTran, H. B., Jersmann, H. P. A., Truong, T. T., Hamon, R., Roscioli, E., Ween, M. P., Pitman, M. R., Pitson, S. M., Hodge, G. L., Reynolds, P. N., et al. (2017) · PLoS ONE · doi:10.1371/journal.pone.0179577 · Cited by 39
Self-citationBushfire smoke is pro-inflammatory and suppresses macrophage phagocytic function
Hamon, R., Tran, H. B., Roscioli, E., Ween, M. P., Jersmann, H. P. A., & Hodge, S. J. (2018) · Scientific Reports · doi:10.1038/s41598-018-31459-6 · Cited by 39
Self-citationExtracellular Vesicles from Airway Secretions: New Insights in Lung Diseases
Pastor, L., Vera, E., Marín, J. M., & Sánz-Rubio, D. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22020583 · Cited by 40
“Lungs of COPD patients also suffer an accelerated ageing produced by an abnormal accumulation of senescent structural cells [37].”
BackgroundMukaro, V., Bylund, J., Hodge, G., Holmes, M., Jersmann, H., Reynolds, P., & Hodge, S. (2013) · PLoS ONE · doi:10.1371/journal.pone.0056147 · Cited by 39
“MH-S macrophages were pre-treated with 50 mg/ml galectin-3 for 10 min before the addition of MitoTracker Green (MTG) labelled apoptotic epithelial cells.”
MethodInfluentialSelf-citationStolberg, V. R., McCubbrey, A. L., Freeman, C. M., Brown, J. P., Crudgington, S., Taitano, S. H., Saxton, B. L., Mancuso, P., & Curtis, J. L. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1402217 · Cited by 39
Beraprost sodium attenuates cigarette smoke extract-induced apoptosis in vascular endothelial cells
Chen, Y., Luo, H., Kang, N., Guan, C., Long, Y., Cao, J., Shen, Q., Li, J., Yang, M., Peng, H., et al. (2012) · Molecular Biology Reports · doi:10.1007/s11033-012-1924-1 · Cited by 38
Hacker, S., Lambers, C., Pollreisz, A., Höetzenecker, K., Lichtenauer, M., Mangold, A., Niederpold, T., Hacker, A., Láng, G., Dworschak, M., et al. (2009) · Journal of Clinical Laboratory Analysis · doi:10.1002/jcla.20348 · Cited by 37
“The remodeling process is a consequence of chronic apoptosis induction in lungs of patients with COPD or smokers (6,7).”
BackgroundTodt, J. C., Freeman, C. M., Brown, J. P., Sonstein, J., Ames, T. M., McCubbrey, A. L., Martínez, F. J., Chensue, S. W., Beck, J. M., & Curtis, J. L. (2013) · Respiratory Research · doi:10.1186/1465-9921-14-33 · Cited by 40
“This finding assumes increased significance based on the recognition of increased apoptotic cell death in emphysema [68] and decreased clearance of apoptotic cells by AMø of smokers [69-71], a defect postulated to foster lung injury and emphysema progression [71,72].”
BackgroundThe Mannose Receptor Is Involved in the Phagocytosis of Mycobacteria-Induced Apoptotic Cells
Garcia-Aguilar, T., Espinosa-Cueto, P., Magallanes-Puebla, A., & Mancilla, R. (2016) · Journal of Immunology Research · doi:10.1155/2016/3845247 · Cited by 41
“Increasing evidence suggests that the deficient removal of these cells could contribute to the progression of inflammation in these diseases [42–44].”
Targeting defective pulmonary innate immunity – A new therapeutic option?
Belchamber, K. B. R., & Donnelly, L. (2020) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2020.107500 · Cited by 37
Effects of corticosteroids on COPD lung macrophage phenotype and function
Higham, A., Scott, T. C., Li, J., Gaskell, R., Dikwa, A. B., Shah, R. D., Montero, Á., Lea, S., & Singh, D. (2020) · Clinical Science · doi:10.1042/cs20191202 · Cited by 39
Alteration of immunophenotype of human macrophages and monocytes after exposure to cigarette smoke
da Silva, C. O., Gicquel, T., Daniel, Y., Bártholo, T. P., Vène, É., Loyer, P., Pôrto, L. C., Lagente, V., & Victoni, T. (2020) · Scientific Reports · doi:10.1038/s41598-020-68753-1 · Cited by 37
Metadata
- Authors
- Hodge, S., Hodge, G., Scicchitano, R., Reynolds, P. N., & Holmes, M.
- Affiliations
- Royal Adelaide Hospital (AU)
- Women's and Children's Hospital (AU)
- Venue
- Immunology & Cell Biology
- Publisher
- Wiley
- Published
- 2003-08
- Volume
- 81
- Issue
- 4
- Pages
- 289-296
- ISSN
- 0004-945X (ISSN-L)
- 0818-9641
- 1440-1711
- OpenAlex
- W1980191732
- Cited by
- 440
- References
- 32
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 17 · 2023: 12 · 2022: 17 · 2021: 34 · 2020: 19 · 2019: 17 · 2018: 23 · 2017: 21 · 2016: 28 · 2015: 28 · 2014: 13 · 2013: 32 · 2012: 20
- FWCI
- 11.12
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Immunology and Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Funders
- Royal Adelaide Hospital
- Australian Lung Foundation
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Occupational and environmental lung diseases
- Keywords
- chronic obstructive pulmonary disease, alveolar macrophages, phagocytosis, cigarette smoke, 16HBE cells, MitoTracker Green, CD33, phagocytic defects
- MeSH terms
- Aged, Antibodies, Monoclonal, Bronchoalveolar Lavage Fluid, Cell Line, Transformed, Cell Survival, Epithelial Cells, Flow Cytometry, Humans, Phagocytosis, Macrophages, Alveolar, Apoptosis, Respiratory Mucosa, Pulmonary Disease, Chronic Obstructive
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