Low level laser therapy (LLLT): Attenuation of cholinergic hyperreactivity, β2-adrenergic hyporesponsiveness and TNF-α mRNA expression in rat bronchi segments in E. coli lipopolysaccharide-induced airway inflammation by a NF-κB dependent mechanism
Version of Record online: 13 JAN 2009
Copyright © 2009 Wiley-Liss, Inc.
Lasers in Surgery and Medicine
Volume 41, Issue 1, pages 68–74, January 2009
How to Cite
Mafra de Lima, F., Costa, M.S., Albertini, R., Silva, J.A. and Aimbire, F. (2009), Low level laser therapy (LLLT): Attenuation of cholinergic hyperreactivity, β2-adrenergic hyporesponsiveness and TNF-α mRNA expression in rat bronchi segments in E. coli lipopolysaccharide-induced airway inflammation by a NF-κB dependent mechanism. Lasers Surg. Med., 41: 68–74. doi: 10.1002/lsm.20735
- Issue online: 13 JAN 2009
- Version of Record online: 13 JAN 2009
- Manuscript Accepted: 13 NOV 2008
- low level laser therapy;
- airway inflammation;
Background and Objectives
It is unknown if the decreased ability to relax airways smooth muscles in asthma and other inflammatory disorders, such as acute respiratory distress syndrome (ARDS), can be influenced by low level laser therapy (LLLT) irradiation. In this context, the present work was developed in order to investigate if LLLT could reduce dysfunction in inflamed bronchi smooth muscles (BSM) in rats.
Study Design/Materials and Methods
A controlled ex vivo study was developed where bronchi from Wistar rat were dissected and mounted in an organ bath apparatus with or without a TNF-α.
LLLT administered perpendicularly to a point in the middle of the dissected bronchi with a wavelength of 655 nm and a dose of 2.6 J/cm2, partially decreased BSM hyperreactivity to cholinergic agonist, restored BSM relaxation to isoproterenol and reduced the TNF-α mRNA expression. An NF-κB antagonist (BMS205820) blocked the LLLT effect on dysfunction in inflamed BSM.
The results obtained in this work indicate that the LLLT effect on alterations in responsiveness of airway smooth muscles observed in TNF-α-induced experimental acute lung inflammation seems to be dependent of NF-κB activation. Lasers Surg. Med. 41:68–74, 2009. © 2008 Wiley-Liss, Inc.