The damage is caused by macrophages . There are t

The damage is caused by macrophages . There are two types M1 and M2, a switch is ccr5 receptor, specifically ccl5, which leronlimab can block. So it can turn the M2 which is causing the lung damage, creating fibrosis back to M1, which doesn't.





https://www.hindawi.com/journals/mi/2018/1264913/

The Role of Macrophages in the Pathogenesis of ALI/ARDS

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Notably, macrophages play a dual role of proinflammation and anti-inflammation based on the microenvironment in different pathological stages. In the acute phase of ALI/ARDS, resident alveolar macrophages, typically expressing the alternatively activated phenotype (M2), shift into the classically activated phenotype (M1) and release various potent proinflammatory mediators. In the later phase, the M1 phenotype of activated resident and recruited macrophages shifts back to the M2 phenotype for eliminating apoptotic cells and participating in fibrosis. In this review, we summarize the main subsets of macrophages and the associated signaling pathways in three different pathological phases of ALI/ARDS. According to the current literature, regulating the function of macrophages and monocytes might be a promising therapeutic strategy against ALI/ARDS.

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Pulmonary fibrosis, a late complication of ALI/ARDS, is marked by fibroblast proliferation and excessive deposition of extracellular matrix [80]. M2 phenotype cells are involved in regulating the fibrotic responses in the lungs [81, 82]. Persistence of M2 macrophages at the injury sites is a hallmark of the development of fibrosis , and the steady expression of IL-4 and IL-13 can promote collagen deposition through TGF-β and arginase 1 pathways [83, 84]. Wakayama et al. [85] have demonstrated that dental pulp stem cells can ameliorate bleomycin-induced lung injury and fibrosis by inducing anti-inflammatory M2-like lung macrophages

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