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Related Experiment Video

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Method for the Assessment of Effects of a Range of Wavelengths and Intensities of Red/near-infrared Light Therapy on Oxidative Stress In Vitro
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Low level laser therapy reduces acute lung inflammation without impairing lung function.

Vivian Cury1, Thais Martins de Lima1, Carla Maximo Prado2

  • 1University of São Paulo, School of Medicine, Emergency Medicine Department, Av. Dr. Arnaldo, 455, Sala 3189, São Paulo - SP, Brazil.

Journal of Biophotonics
|September 19, 2015
PubMed
Summary

Low level laser therapy (LLLT) effectively reduced inflammation and inflammatory cell influx in acute lung injury (ALI) mouse models. This treatment improved lung condition without negatively impacting pulmonary function or mechanical properties.

Keywords:
acute lung injurylow level laser therapylung functionphotobiomodulation

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Area of Science:

  • Biomedical Engineering
  • Pulmonary Medicine
  • Photomedicine

Background:

  • Acute lung injury (ALI) involves severe inflammation and dysfunction in the lungs.
  • Low level laser therapy (LLLT) shows potential for managing inflammatory conditions and promoting tissue repair.
  • Its efficacy in treating internal organ injuries, like ALI, requires further investigation.

Purpose of the Study:

  • To investigate the therapeutic effects of LLLT on lipopolysaccharide (LPS)-induced ALI in a mouse model.
  • To assess LLLT's impact on inflammatory cell infiltration and mediator secretion in the lungs.
  • To evaluate LLLT's influence on lung mechanical properties during ALI.

Main Methods:

  • C57BL/6 mice were induced with ALI using intratracheal lipopolysaccharide (LPS).
  • Groups received LLLT (660 nm, 10 J/cm²) or were sham-treated.
  • Inflammatory cell counts, cytokine/chemokine levels (TNF-α, IL-1β, IL-6, MCP-1), and lung mechanics (resistance, elastance) were measured.

Main Results:

  • LPS instillation significantly increased inflammatory cell infiltration in lung tissues.
  • Elevated levels of pro-inflammatory cytokines and chemokines were observed post-LPS exposure.
  • LLLT treatment markedly reduced inflammatory cell influx and mediator secretion.
  • LLLT did not alter lung resistance or elastance, preserving mechanical properties.

Conclusions:

  • LLLT effectively mitigates the inflammatory response in LPS-induced acute lung injury.
  • The therapy reduces inflammatory cell infiltration and mediator release without compromising lung function.
  • LLLT presents a promising, non-invasive therapeutic strategy for managing ALI.