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. 2023 Jan 16;9:9. doi: 10.1038/s41420-023-01310-7

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — The progression of ALI is influenced by alveolar and interstitial macrophage polarization. T helper 1-mediated production of IFNγ induces M1 polarization, with increased transcription of NF-κB, SOCS3, JNK and MAPK. M1 macrophages promote neutrophil recruitment either through phagocytosis and subsequent cell damage or through cytokine secretion and transcription factor activation. IL-4 and IL-13 polarize alveolar macrophages towards the M2 phenotype by regulating the transcription of JNK and c-Myc. M2 macrophages secrete cytokines that induce fibrosis or stimulate new cell regeneration. Both processes promote tissue repair. IFN interferon, TNF tissue necrosis factor, MyD88 myeloid differentiation primary response 88, NF-κB nuclear factor-kappaB, JNK c-Jun N-terminal kinase, AECII type II alveolar epithelial cell.