Attenuation of the inflammatory response and polarization of macrophages by photobiomodulation

Lasers Med Sci. 2020 Sep;35(7):1509-1518. doi: 10.1007/s10103-019-02941-y. Epub 2020 Feb 17.


In spinal cord injury (SCI), inflammation is a major mediator of damage and loss of function and is regulated primarily by the bone marrow-derived macrophages (BMDMs). Photobiomodulation (PBM) or low-level light stimulation is known to have anti-inflammatory effects and has previously been used in the treatment of SCI, although its precise cellular mechanisms remain unclear. In the present study, the effect of PBM at 810 nm on classically activated BMDMs was evaluated to investigate the mechanisms underlying its anti-inflammatory effects. BMDMs were cultured and irradiated (810 nm, 2 mW/cm2) following stimulation with lipopolysaccharide and interferon-γ. CCK-8 assay, 2',7'-dichlorofluorescein diacetate assay, and ELISA and western blot analysis were performed to measure cell viability, reactive oxygen species production, and inflammatory marker production, respectively. PBM irradiation of classically activated macrophages significantly increased the cell viability and inhibited reactive oxygen species generation. PBM suppressed the expression of a marker of classically activated macrophages, inducible nitric oxide synthase; decreased the mRNA expression and secretion of pro-inflammatory cytokines, tumor necrosis factor alpha, and interleukin-1 beta; and increased the secretion of monocyte chemotactic protein 1. Exposure to PBM likewise significantly reduced the expression and phosphorylation of NF-κB p65 in classically activated BMDMs. Taken together, these results suggest that PBM can successfully modulate inflammation and polarization in classically activated BMDMs. The present study provides a theoretical basis to support wider clinical application of PBM in the treatment of SCI.

Keywords: Inflammation; Macrophage; Photobiomodulation; Polarization; Spinal cord injury.

MeSH terms

  • Animals
  • Cell Polarity* / radiation effects
  • Cell Survival / radiation effects
  • Chemokines / genetics
  • Chemokines / metabolism
  • Gene Expression Regulation / radiation effects
  • Inflammation / radiotherapy*
  • Macrophage Activation / radiation effects
  • Macrophages / pathology*
  • Macrophages / radiation effects
  • Mice, Inbred BALB C
  • Phosphorylation / radiation effects
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reactive Oxygen Species / metabolism
  • Transcription Factor RelA / metabolism


  • Chemokines
  • RNA, Messenger
  • Reactive Oxygen Species
  • Transcription Factor RelA