Characteristics and potential role of M2 macrophages in COPD
Alveolar macrophage
Pathogenesis
CD68
DOI:
10.2147/copd.s147144
Publication Date:
2017-10-18T02:18:21Z
AUTHORS (4)
ABSTRACT
Background: COPD is a multi-pathogenesis disease mainly caused by smoking. A further understanding of the mechanism smoking-related might contribute to preventions and treatments this in early stages. This study was designed identify characteristics M2 macrophages for better about their potential role. Materials methods: models were built C57BL/6 mouse cigarette smoke (CS) exposure combined with intraperitoneal injection extract (CSE). The modeling efficiency evaluated lung function hematoxylin eosin (H&E) staining. number different macrophage phenotypes detected immunohistochemical staining (IHS) CD206, CD86 CD68 on tissue paraffin section. RAW264.7 cells polarized toward phenotype interleukin IL-4 confirmed flow cytometer. gene expression levels TGF-βRII, Smad2, Smad3 Smad7 CSE-treated real-time reverse transcription polymerase chain reaction (RT-PCR). TGF-β/Smad pathway-related makers (TGF-βRII, p-Smad2, p-Smad3, TGF-β) alveolar two consecutive section IHS. Results: model well established, which test H&E whole ratio M2/M1 are both increased ( p <0.05). level CD206 + IL-4-stimulated up 93.4%, all enhanced <0.05) CES-treated macrophages, RT-PCR. protein markers group. Conclusion: found an deposition pathway vitro vivo, induced CSE and/or CS exposure, indicating that through changing pathway. Keywords: COPD, macrophage,
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