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Pulmonary fibrosis is an irreversible and progressive disease affecting the lungs, and the etiology remains poorly understood. This disease can be lethal and currently has no specific clinical therapeutic regimen. Macrophages, the most common type of immune cell in the lungs, have been reported to play a key role in the pathogenesis of fibrotic disease. The lung macrophage population is mostly composed of alveolar macrophages and interstitial macrophages, both of which have not been thoroughly studied in the pathogenesis of lung fibrosis. Interstitial macrophages have recently been recognised for their participation in lung fibrosis due to new technology arising from a combination of bioinformatics and single-cell RNA sequencing analysis. This paper reviews recent developments regarding lung macrophage classification and summarizes the origin and replenishment of interstitial macrophages and their function in pulmonary fibrosis.
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http://dx.doi.org/10.3389/fimmu.2022.923235 | DOI Listing |
STAR Protoc
September 2025
Macrophage Lab, Department of Microbiology and Immunology, and Institute of Endemic Disease, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, Republic of Korea; Cancer Researc
Interstitial macrophages increase significantly during lung metastasis and may contribute to tumor dissemination. However, isolating them is challenging due to their localization within lung tissue and phenotypic overlap with other immune cells. Here, we present a protocol for isolating and characterizing murine interstitial macrophages.
View Article and Find Full Text PDFAlveolar macrophages (AMs) are the first immune cells to encounter Mycobacterium tuberculosis (Mtb) in the lungs, but they frequently fail to eliminate this causative agent of tuberculosis (TB), allowing Mtb to persist or replicate. Interstitial macrophages (IMs) are recruited to restrict Mtb growth and limit immune evasion. While IMs have been implicated in the control of acute Mtb infection, their role during latent tuberculosis infection (LTBI) has not yet been explored.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
July 2025
Department of Geriatrics, Hospital of Chengdu University of Traditional Chinese Medicine Chengdu 610072, China.
Idiopathic pulmonary fibrosis(IPF) is a chronic progressive interstitial lung disease characterized by a complex pathogenesis and limited treatment options. Although studies have indicated that lipid metabolism dysregulation is associated with the progression of IPF, the core regulatory mechanisms remain unclear. By integrating RNA sequencing data from the GEO database, we identified four key genes related to lipid metabolism: peroxisome proliferator-activated receptor gamma(PPARG), secreted phosphoprotein 1(SPP1), caspase 3(CASP3), and platelet endothelial cell adhesion molecule 1(PECAM1).
View Article and Find Full Text PDFInt Immunopharmacol
September 2025
Department of Cuiying Biomedical Research Center, Lanzhou University Second Hospital, Lanzhou, China; Department of Rheumatology, Lanzhou University Second Hospital, Lanzhou, China; Gansu Province Clinical Research Center for Rheumatology, Lanzhou, Gansu, China. Electronic address:
Background: Previous studies by our research group have demonstrated that neutrophil extracellular traps (NETs) play a pathogenic role in myositis-associated interstitial lung disease (IIM-ILD). Based on this, we hypothesized that NETs may contribute to the pathogenesis of IIM-ILD by regulating macrophage polarization and pyroptosis.
Methods: Pathological studies were conducted using lung biopsy samples from a dermatomyositis-associated interstitial lung disease (DM-ILD) patient and lung tissues from experimental autoimmune myositis (EAM) mice.
A case report of pulmonary sarcoidosis with fibrosis after COVID-19 is presented. Morphologic and immunohistochemical analysis of lung biopsies for Sars-Cov2 nucleocapsid and adhesion proteins was performed. Virus proteins were detected in alveolar macrophages, second-order pneumocytes and bronchiolar epithelium, also in granuloma-associated macrophages, multinucleated Pirogov-Langhans cells, indicating Sars-Cov2 persistence.
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