3.9 Article

Effects of 810-nm Laser on Murine Bone-Marrow-Derived Dendritic Cells

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PHOTOMEDICINE AND LASER SURGERY
卷 29, 期 6, 页码 383-389

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MARY ANN LIEBERT, INC
DOI: 10.1089/pho.2010.2837

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  1. NIH [R01AI050875]
  2. Center for Integration of Medicine and Innovative Technology [DAMD17-02-2-0006]
  3. CDMRP Program in TBI [W81XWH-09-1-0514]
  4. Air Force Office of Scientific Research [FA9950-04-1-0079]

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Objective: The purpose of this study was to Investigate the effect of 810-nm low level laser therapy (LLLT) on dendritic cells (DC) in vitro. Background data: LLLT can enhance wound healing and increase cell proliferation and survival, and is used to treat inflammatory conditions. However there are reports that LLLT can stimulate leukocytes and could therefore be pro-inflammatory. Recently, DC have been found to play an important role in inflammation and immune response. Methods: Murine bone-marrow-derived DC were isolated, stimulated with lipopolysaccharide (LPS) or CpG oligodeoxynucleotide and treated with 810-nm laser, using fluences of 0.3, 3, and 30 J/cm(2) delivered at irradiances of 1, 10, and 100mW/cm(2) respectively. Confocal microscopy, flow cytometry for DC markers, viability using propidium iodide, enzyme-linked immunosorbent assays (ELISA) for secreted interleukin-12 (IL-12), and bioluminescence measurements in cells transduced with a reporter for toll-like receptor (TLR)-9/nuclear factor kappa B (NF-kappa B) activation, were performed. Results: LLLT changed the morphology of LPS-stimulated DC, increased their viability, and altered the balance of DC activation markers (major histocompatibility complex [MHC] class 2 up and CD86 down). LLLT reduced IL-12 secretion from DC stimulated by either LPS or CpG. LLLT reduced NF-kappa B activation in reporter cells stimulated with CpG. There was no obvious light dose response observed. Conclusions: Taken together, these data suggest that 810-nm LLLT has an anti-inflammatory effect on activated DC, possibly mediated by cyclic adenosine monophosphate (cAMP) and reduced NF-kappa B signaling.

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