ArticleJournal of leukocyte biology2010
Differential polarization of alveolar macrophages and bone marrow-derived monocytes following chemically and pathogen-induced chronic lung inflammation.
Article in Journal of leukocyte biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 117 citations in OpenAlex.
- Temporal upregulation of TREM2 parallel to M2 macrophage marker expression in tuberculosis: implications for macrophage polarization regulation.Frontiers in cellular and infection microbiology · 2026Article
- Current landscape of the immunoproteasome: implications for disease and therapy.Cell death discovery · 2025Review
- Engineered Endosymbionts that Modulate Primary Macrophage Function and Attenuate Tumor Growth by Shifting the Tumor Microenvironment.ACS applied bio materials · 2025Article
- The Role of Inflammation in the Pathogenesis of Comorbidity of Chronic Obstructive Pulmonary Disease and Pulmonary Tuberculosis.International journal of molecular sciences · 2025Review
- Metabolic reprogramming of macrophages in chronic obstructive pulmonary disease.Frontiers in immunology · 2025Review
- Article
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- Immune cell composition of the bronchoalveolar lavage fluid in healthy and respiratory diseased dromedary camels.BMC veterinary research · 2022Article
- Heterogeneous macrophages contribute to the pathology of disc herniation induced radiculopathy.The spine journal : official journal of the North American Spine Society · 2022Article
- Isolation and Analysis of Macrophage Subsets from the Mouse and Human Lung.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Tumor-Associated Macrophages: Reasons to Be Cheerful, Reasons to Be Fearful.Experientia supplementum (2012) · 2022Article
- Nrf2 Regulates Anti-InflammatoryAntioxidants (Basel, Switzerland) · 2021Article
- Fatty acid oxidation of alternatively activated macrophages prevents foam cell formation, but Mycobacterium tuberculosis counteracts this process via HIF-1α activation.PLoS pathogens · 2020Article
- HIV and the tuberculosis "set point": how HIV impairs alveolar macrophage responses to tuberculosis and sets the stage for progressive disease.Retrovirology · 2020Review
- Susceptibility to Intracellular Infections: Contributions of TNF to Immune Defense.Frontiers in microbiology · 2020Review
- Differential expression and predictive value of monocyte scavenger receptor CD163 in populations with different tuberculosis infection statuses.BMC infectious diseases · 2019Article
- Single cell RNA sequencing identifies unique inflammatory airspace macrophage subsets.JCI insight · 2019Article
- A Quantitative Approach to SIV Functional Latency in Brain Macrophages.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019Review
- Polarization of Human Monocyte-Derived Cells With Vitamin D Promotes Control ofFrontiers in immunology · 2019Article
- A Gene Expression Classifier from Whole Blood Distinguishes Benign from Malignant Lung Nodules Detected by Low-Dose CT.Cancer research · 2019Article
9 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Alveolar macrophages and BDMCs undergo sequential biochemical changes during the chronic inflammatory response to chemically induced lung carcinogenesis in mice. Herein, we examine two chronic lung inflammation models-repeated exposure to BHT and infection with Mycobacterium tuberculosis-to establish whether similar macrophage phenotype changes occur in non-neoplastic pulmonary disease. Exposure to BHT or M. tuberculosis results in pulmonary inflammation characterized by an influx of macrophages, followed by systemic effects on the BM and other organs. In both models, pulmonary IFN-gamma and IL-4 production coincided with altered polarization of alveolar macrophages. Soon after BHT administration or M. tuberculosis infection, IFN-gamma content in BALF increased, and BAL macrophages became classically (M1) polarized, as characterized by increased expression of iNOS. As inflammation progressed in both models, the amount of BALF IFN-gamma content and BAL macrophage iNOS expression decreased, and BALF IL-4 content and macrophage arginase I expression rose, indicating alternative/M2 polarization. Macrophages present in M. tuberculosis-induced granulomas remained M1-polarized, implying that these two pulmonary macrophage populations, alveolar and granuloma-associated, are exposed to different activating cytokines. BDMCs from BHT-treated mice displayed polarization profiles similar to alveolar macrophages, but BDMCs in M. tuberculosis-infected mice did not become polarized. Thus, only alveolar macrophages in these two models of chronic lung disease exhibit a similar progression of polarization changes; polarization of BDMCs was specific to BHT-induced pulmonary inflammation, and polarization of granuloma macrophages was specific to the M. tuberculosis infection.
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