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.

• Klíčová slova
• M1/M2 polarization, MicroRNAs, exosomes, macrophage plasticity, pulmonary fibrosis,
• MeSH
• aktivace makrofágů genetika   imunologie   MeSH
• biologické markery MeSH
• biologické modely MeSH
• cytokiny metabolismus   MeSH
• exozómy metabolismus   MeSH
• lidé MeSH
• makrofágy imunologie   metabolismus   MeSH
• mediátory zánětu metabolismus   MeSH
• mikro RNA genetika   MeSH
• náchylnost k nemoci * MeSH
• plasticita buňky MeSH
• plicní fibróza etiologie   metabolismus   patologie   MeSH
• regulace genové exprese MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• biologické markery MeSH
• cytokiny MeSH
• mediátory zánětu MeSH
• mikro RNA MeSH