ArticleScientific reports2017
Commensal microbiota maintains alveolar macrophages with a low level of CCL24 production to generate anti-metastatic tumor activity.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 42 citations in OpenAlex.
- Regulatory network architecture constrains inflammatory responses in tissue-resident alveolar macrophages.bioRxiv : the preprint server for biology · 2026Article
- Respiratory microbiome-host interaction on lung carcinogenesis, immunity, and immunotherapy.Frontiers in immunology · 2025Review
- Article
- Tissue-Resident Macrophages in Cancer: Friend or Foe?Cancer medicine · 2024Review
- UGRP1-modulated MARCOImmunity & ageing : I & A · 2023Article
- Airway microbiome-immune crosstalk in chronic obstructive pulmonary disease.Frontiers in immunology · 2022Review
- The lung, the niche, and the microbe: Exploring the lung microbiome in cancer and immunity.Frontiers in immunology · 2022Review
- Lower Airway Dysbiosis Affects Lung Cancer Progression.Cancer discovery · 2021Article
- CCL24 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021Article
- The Role of Respiratory Microbiota in Lung Cancer.International journal of biological sciences · 2021Review
- Exploration of the sputum methylome and omics deconvolution by quadratic programming in molecular profiling of asthma and COPD: the road to sputum omics 2.0.Respiratory research · 2020Article
- M2-like, dermal macrophages are maintained via IL-4/CCL24-mediated cooperative interaction with eosinophils in cutaneous leishmaniasis.Science immunology · 2020Article
- Review
- The Host Microbiota Contributes to Early Protection Against Lung Colonization byFrontiers in immunology · 2018Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microbiota maintains host tissue homeostasis and influences tissue-resident macrophages. However, the mechanisms by which commensal bacteria in regulating the alveolar macrophages remain unclear. Here, by using an antibiotic-treated (Abt) mouse model, we found commensal bacteria depletion induced lower frequencies and numbers of alveolar macrophages. This effect was accompanied by the altered levels of genes involved in several biological pathways, including M2 macrophage polarization, as determined by gene expression analysis. Alveolar macrophages from the Abt mice had higher protein and gene levels of Arg1, CCL24, IL-13, IL-10, IL-6 and IL-1β, which could be recovered to normal levels by reconstructing commensal bacteria in the upper respiratory of Abt mice. Moreover, alveolar macrophages performed significant enhancement of M2 functions, especially CCL24 secretion, in the Abt mice challenged with B16/F10 melanoma. Adoptive transfer of normal alveolar macrophages or antibody neutralization of CCL24 significantly recovered the decrease of γδT17 cells and rescued the defect anti-tumor response of Abt mice, indicating the elevated amount of alveolar macrophage-derived CCL24 inhibited γδT cell mediated anti-tumor response. In conclusion, we demonstrated the ability of commensal bacteria to maintain alveolar macrophages with a low level of CCL24 production, which was necessary for the normal anti-tumor response in the lung.
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