Abstract
This mini-review summarizes the current evidence for the role of macrophage activation and polarization in inflammation and immune response pertinent to interstitial lung disease, specifically pulmonary fibrosis. In the fibrosing lung, the production and function of inflammatory and fibrogenic mediators involved in the disease development have been reported to be regulated by the effects of polarized M1/M2 macrophage populations. The M1 and M2 macrophage phenotypes were suggested to correspond with the pro-inflammatory and pro-fibrogenic signatures, respectively. These responses towards tissue injury followed by the development and progression of lung fibrosis are further regulated by macrophage-derived microRNAs (miRNAs). Besides cellular miRNAs, extracellular exosomal-miRNAs derived from M2 macrophages have also been proposed to promote the progression of pulmonary fibrosis. In a future perspective, harnessing the noncoding miRNAs with a key role in the macrophage polarization is, therefore, suggested as a promising therapeutic strategy for this debilitating disease.
Highlights
Pulmonary fibrosis (PF) is a progressive, irreversible and lethal lung disease and has remained a challenge for clinicians and researchers
The pro-inflammatory and profibrotic cytokines involved in PF promote inflammation and irreversible damage to lung architecture with the loss of alveolar-capillary barrier basal membrane leading to persistent fibrosis [4]
During the development processes of tissue injury and inflammatory reaction and their subsequent progression to PF, Alveolar macrophages (AM) and interstitial macrophages (IM) are polarized to different cell phenotypes - M1 and M2 macrophages, respectively [16, 25]
Summary
Pulmonary fibrosis (PF) is a progressive, irreversible and lethal lung disease and has remained a challenge for clinicians and researchers. During the development processes of tissue injury and inflammatory reaction and their subsequent progression to PF, AM and IM are polarized to different cell phenotypes - M1 and M2 macrophages, respectively [16, 25]. The enhanced M2 macrophage polarization has been suggested to inhibit the inflammatory reaction and/or directly regulate the development and progression of fibrotic lung diseases through the production of chemokines, MMPs, tissue inhibitor of metalloproteinases (TIMPs), and fibronectin as well as, the capability of M2 to differentiate into fibrocyte-like cells that express collagen [27,28,29,30].
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