Beneficial effects of Red Light-Emitting Diode treatment in experimental model of acute lung injury induced by sepsis

Sci Rep. 2017 Oct 4;7(1):12670. doi: 10.1038/s41598-017-13117-5.

Abstract

Sepsis is a severe disease with a high mortality index and it is responsible for the development of acute lung injury (ALI). We evaluated the effects of light-emitting diode (LED) on ALI induced by sepsis. Balb-c mice were injected with lipopolysaccharide or saline and then irradiated or not with red LED on their tracheas and lungs for 150 s, 2 and 6 h after LPS injections. The parameters were investigated 24 h after the LPS injections. Red LED treatment reduced neutrophil influx and the levels of interleukins 1β, 17 A and, tumor necrosis factor-α; in addition to enhanced levels of interferon γ in the bronchoalveolar fluid. Moreover, red LED treatment enhanced the RNAm levels of IL-10 and IFN-γ. It also partially reduced the elevated oxidative burst and enhanced apoptosis, but it did not alter the translocation of nuclear factor κB, the expression of toll-like receptor 4 (TLR4), as well as, oedema or mucus production in their lung tissues. Together, our data has shown the beneficial effects of short treatment with LED on ALI that are caused by gram negative bacterial infections. It is suggested that LED applications are an inexpensive and non-invasive additional treatment for sepsis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / etiology
  • Acute Lung Injury / therapy*
  • Animals
  • Bronchoalveolar Lavage Fluid
  • Disease Models, Animal
  • Gene Expression Regulation / radiation effects
  • Humans
  • Interleukin-17 / genetics
  • Interleukin-1beta / genetics
  • Light*
  • Lung / metabolism
  • Lung / pathology
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B / genetics
  • Sepsis / chemically induced
  • Sepsis / complications
  • Sepsis / therapy*
  • Signal Transduction / radiation effects
  • Toll-Like Receptor 4 / genetics
  • Tumor Necrosis Factor-alpha / genetics

Substances

  • Interleukin-17
  • Interleukin-1beta
  • NF-kappa B
  • Tlr4 protein, mouse
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha