Macrophages and Pulmonary Fibrosis
- PMID: 39779550
- DOI: 10.2174/0115665240286046240112112310
Macrophages and Pulmonary Fibrosis
Abstract
Most chronic respiratory diseases often lead to the clinical manifestation of pulmonary fibrosis. Inflammation and immune disorders are widely recognized as primary contributors to the onset of pulmonary fibrosis. Given that macrophages are predominantly responsible for inflammation and immune disorders, in this review, we first focused on the role of different subpopulations of macrophages in the lung and discussed the crosstalk between macrophages and other immune cells, such as neutrophils, regulatory T cells, NKT cells, and B lymphocytes during pulmonary fibrogenesis. Subsequently, we analyzed the interaction between macrophages and fibroblasts as a possible new research direction. Finally, we proposed that exosomes, which function as a means of communication between macrophages and target cells to maintain cellular homeostasis, are a strategy for targeting lung drugs in the future. By comprehending the mechanisms underlying the interplay between macrophages and other lung cells, we aim to enhance our understanding of pulmonary fibrosis, leading to improved diagnostics, preventative measures, and the potential development of macrophage-based therapeutics.
Keywords: B lymphocytes; NKT cells; exosomes.; fibroblasts; macrophages; neutrophils; pulmonary fibrosis; regulatory T cells.
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
Similar articles
-
Cell Cross-Talk in Alveolar Microenvironment: From Lung Injury to Fibrosis.Am J Respir Cell Mol Biol. 2024 Jul;71(1):30-42. doi: 10.1165/rcmb.2023-0426TR. Am J Respir Cell Mol Biol. 2024. PMID: 38579159 Free PMC article. Review.
-
CD4+T and CD8+T cells profile in lung inflammation and fibrosis: targets and potential therapeutic drugs.Front Immunol. 2025 May 9;16:1562892. doi: 10.3389/fimmu.2025.1562892. eCollection 2025. Front Immunol. 2025. PMID: 40433386 Free PMC article. Review.
-
Iron-laden macrophage-mediated paracrine profibrotic signaling induces lung fibroblast activation.Am J Physiol Cell Physiol. 2024 Oct 1;327(4):C979-C993. doi: 10.1152/ajpcell.00675.2023. Epub 2024 Aug 26. Am J Physiol Cell Physiol. 2024. PMID: 39183565
-
Roles of Macrophage Polarization and Macrophage-Derived miRNAs in Pulmonary Fibrosis.Front Immunol. 2021 Aug 13;12:678457. doi: 10.3389/fimmu.2021.678457. eCollection 2021. Front Immunol. 2021. PMID: 34489932 Free PMC article. Review.
-
M2 macrophage accumulation contributes to pulmonary fibrosis, vascular dilatation, and hypoxemia in rat hepatopulmonary syndrome.J Cell Physiol. 2021 Nov;236(11):7682-7697. doi: 10.1002/jcp.30420. Epub 2021 May 27. J Cell Physiol. 2021. PMID: 34041750
References
-
- Bissonnette E.Y.; Lauzon-Joset J.F.; Debley J.S.; Ziegler S.F.; Cross-talk between alveolar macrophages and lung epithelial cells is essential to maintain lung homeostasis. Front Immunol 2020,11,583042 - DOI
Publication types
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources
Medical