ArticleImmunology2016
Genetic background affects the expansion of macrophage subsets in the lungs of Mycobacterium tuberculosis-infected hosts.
Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- The Sialomucin CD43 Drives Tuberculosis Immunopathology Across Different Host Genetic Backgrounds.Inflammation · 2026Article
- A narrative review of the controversy on the risk of mycobacterial infections with immune checkpoint inhibitor use: does Goldilocks have the answer?Journal of thoracic disease · 2024Review
- Strain specific differences in vitamin D3 response: impact on gut homeostasis.Frontiers in immunology · 2024Article
- Baseline gene expression in BALB/c and C57BL/6 peritoneal macrophages influences but does not dictate their functional phenotypes.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Biliatresone induces cholangiopathy in C57BL/6J neonates.Scientific reports · 2023Article
- Establishment of head and neck squamous cell carcinoma mouse models for cetuximab resistance and sensitivity.Cancer drug resistance (Alhambra, Calif.) · 2023Article
- Ohmyungsamycin promotes M1-like inflammatory responses to enhance host defence againstVirulence · 2022Article
- Obesity-Induced Dysbiosis Exacerbates IFN-γ Production and Pulmonary Inflammation in theCells · 2021Article
- Different Innate Immune Responses in BALB/c and C57BL/6 Strains following Corneal Transplantation.Journal of innate immunity · 2021Article
- Extracellular Matrix Protein Tenascin C Increases Phagocytosis Mediated by CD47 Loss of Function in Glioblastoma.Cancer research · 2019Article
- Stimulation of bovine monocyte-derived macrophages with lipopolysaccharide, interferon-ɣ, Interleukin-4 or Interleukin-13 does not induce detectable changes in nitric oxide or arginase activity.BMC veterinary research · 2019Article
- Characterization of immune cell subtypes in three commonly used mouse strains reveals gender and strain-specific variations.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Genetic Polymorphisms ofBioMed research international · 2018Article
- Protective immunity against tuberculosis: what does it look like and how do we find it?Current opinion in immunology · 2017Review
- Identification of compounds that decrease numbers ofJournal of leukocyte biology · 2017Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
M1 macrophages are more effective in the induction of the inflammatory response and clearance of Mycobacterium tuberculosis than M2 macrophages. Infected C57BL/6 mice generate a stronger cellular immune response compared with BALB/c mice. We hypothesized that infected C57BL/6 mice would exhibit a higher frequency and function of M1 macrophages than infected BALB/c mice. Our findings show a higher ratio of macrophages to M2 macrophages in the lungs of chronically infected C57BL/6 mice compared with BALB/c mice. However, there was no difference in the functional ability of M1 and M2 macrophages for the two strains in vitro. In vivo, a deleterious role for M2 macrophages was confirmed by M2 cell transfer, which rendered the infected C57BL/6, but not the BALB/c mice, more susceptible and resulted in mild lung inflammation compared with C57BL/6 mice that did not undergo cell transfer. M1 cell transfer induced a higher inflammatory response, although not protective, in infected BALB/c mice compared with their counterparts that did not undergo cell transfer. These findings demonstrate that an inflammation mediated by M1 macrophages may not induce bacterial tolerance because protection depends on the host genetic background, which drives the magnitude of the inflammatory response against M. tuberculosis in the pulmonary microenvironment. The contribution of our findings is that although M1 macrophage is an effector leucocyte with microbicidal machinery, its dominant role depends on the balance of M1 and M2 subsets, which is driven by the host genetic background.
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