ArticlePloS one2013
Role of recently migrated monocytes in cigarette smoke-induced lung inflammation in different strain of mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 32 citations in OpenAlex.
- Transcriptomic analysis reveals distinct effects of cigarette smoke on murine airspace and bone-marrow derived macrophages.Respiratory research · 2024Article
- MMP9 SNP and MMP SNP-SNP interactions increase the risk for ischemic stroke in the Han Hakka population.Brain and behavior · 2022Article
- ISM1 protects lung homeostasis via cell-surface GRP78-mediated alveolar macrophage apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Non-heme iron overload impairs monocyte to macrophage differentiationFrontiers in immunology · 2022Article
- Role of Long Noncoding RNAs in Smoking-Induced Lung Cancer: An In Silico Study.Computational and mathematical methods in medicine · 2022Article
- Defective monocyte-derived macrophage phagocytosis is associated with exacerbation frequency in COPD.Respiratory research · 2021Article
- New Pharmacological Tools to Target Leukocyte Trafficking in Lung Disease.Frontiers in immunology · 2021Review
- Leukocyte Function in COPD: Clinical Relevance and Potential for Drug Therapy.International journal of chronic obstructive pulmonary disease · 2021Review
- PGELife science alliance · 2020Article
- UPLC-QTOF-MS-guided isolation of anti-COPD ginsenosides from wild ginseng.RSC advances · 2019Article
- Role of Macrophages in Acute Lung Injury and Chronic Fibrosis Induced by Pulmonary Toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2019Review
- Dysregulated Functions of Lung Macrophage Populations in COPD.Journal of immunology research · 2018Review
- Macrophage Depletion Protects against Cigarette Smoke-Induced Inflammatory Response in the Mouse Colon and Lung.Frontiers in physiology · 2018Article
- Time Course of the Phenotype of Blood and Bone Marrow Monocytes and Macrophages in the Lung after Cigarette Smoke Exposure In Vivo.International journal of molecular sciences · 2017Article
- MyeloidFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- Dusp3 deletion in mice promotes experimental lung tumour metastasis in a macrophage dependent manner.PloS one · 2017Article
- Resolvin D1 prevents smoking-induced emphysema and promotes lung tissue regeneration.International journal of chronic obstructive pulmonary disease · 2016Article
- Targeted Disruption of Ig-Hepta/Gpr116 Causes Emphysema-like Symptoms That Are Associated with Alveolar Macrophage Activation.The Journal of biological chemistry · 2015Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigates the role of proinflammatory monocytes recruited from blood circulation and recovered in bronchoalveolar lavage (BAL) fluid in mediating the lung damage in a model of acute cigarette smoke (CS)-induced lung inflammation in two strains of mice with different susceptibility to develop emphysema (susceptible -C57BL/6J and non susceptible -129S2/SvHsd). Exposure to whole-body CS for 3 consecutive research cigarettes in one single day induced acute inflammation in the lung of mice. Analysis of BAL fluid showed more influx of recently migrated monocytes at 72 h after CS-exposition in susceptible compared to non susceptible mice. It correlated with an increase in MMP-12 and TNF-α protein levels in the lung tissue, and with an increment of NF-κB translocation to the nucleus measured by electrophoretic mobility shift assay in C57BL/6J mice. To determine the functional role of these proinflammatory monocytes in mediating CS-induced airway inflammation, alveolar macrophages and blood monocytes were transiently removed by pretreatment with intratracheal and intravenous liposome-encapsulated CL2MDP, given 2 and 4 days prior to CS exposure and their repopulation was studied. Monocytes/macrophages were maximally depleted 48 h after last liposome application and subsequently recently migrated monocytes reappeared in BAL fluid of susceptible mice at 72 h after CS exposure. Recently migrated monocytes influx to the lung correlated with an increase in the MMP-12 protein level in the lung tissue, indicating that the increase in proinflammatory monocytes is associated with a major tissue damaging. Therefore our data confirm that the recruitment of proinflammatory recently migrated monocytes from the blood are responsible for the increase in MMP-12 and has an important role in the pathogenesis of lung disease induced by acute lung inflammation. These results could contribute to understanding the different susceptibility to CS of these strains of mice.
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