Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 141, Issue 8, Pages 2056-+Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2020.11.035
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Funding
- Ministry of Science and Technology, Taiwan [MOST106-2320-B-037-030 -MY3, MOST107-2314-B-037058, MOST108-2314-B-037-012, MOST109-2320-B-037-013]
- National Health Research Institutes, Taiwan [100A1-PDCO-03000001]
- Research Center for Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan (Higher Education Sprout Project by the Ministry of Education, Taiwan) [KMU-TC108A01]
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NIR can penetrate dermis and regulate skin cells and immune cells, providing significant anti-inflammatory effects. By inducing H3K4 hypermethylation and citrate synthase expression, NIR promotes M2 polarization in macrophages and results in the release of TGF beta 1.
Near-infrared (NIR) can penetrate the dermis. NIR is able to regulate cutaneous component cells and immune cells and shows significant anti-inflammatory therapeutic effects. However, the mechanisms of these effects are largely unknown. The purpose of this study is to elucidate NIR-induced molecular mechanisms on macrophages because macrophages play initial roles in directing immune responses by their M1 or M2 polarizations. Proteomic analysis revealed that NIR radiation enhanced the expression of mitochondrial respiratory gene citrate synthase. This increased citrate synthase expression was triggered by NIR-induced H3K4 hypermethylation on the citrate synthase gene promoter but not by heat, which led to macrophage M2 polarization and finally resulted in TGF beta 1 release from CD4(+) cells. These cellular effects were validated in human primary macrophages and abdominal NIR-irradiated mouse experiments. In a phorbol 12-myristate 13-acetate-induced inflammatory model on mouse ear, we confirmed that NIR irradiation induced significant anti-inflammatory effects through decreased M1 counts, reduced TNF-alpha, and increased CCL22 and/or TGF beta 1 levels.
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