Effects of 810-nm Laser on Murine Bone-Marrow-Derived Dendritic Cells
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Hamblin-2011-Effects of 810-nm.pdf
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Author(s) • • •
Chen, Aaron Chih-Hao
Huang, Ying-Ying
Sharma, Sulbha K.
Hamblin, Michael R.
Date Issued
June 2011
Journal
Photomedicine and Laser Surgery
Publisher
Mary Ann Liebert, Inc.
Citation
Chen, Aaron C.-H. et al. “Effects of 810-nm Laser on Murine Bone-Marrow-Derived Dendritic Cells.” Photomedicine and Laser Surgery 29 (2011): 383-389. ©2011 Mary Ann Liebert, Inc.
Version
Final published version
Abstract
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/cm2 delivered at irradiances of 1, 10, and 100 mW/cm2 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-κB) 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-κB 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-κB signaling.
MIT Department
Harvard University--MIT Division of Health Sciences and Technology
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DOI of Published Version
https://doi.org/10.1089/pho.2010.2837