Abstract
Objective: This study investigated the effect of low-intensity laser irradiation (LILI) on pro-inflammatory cytokines
involved in wound healing processes in diabetes and hypoxia. Background data: Diabetes is associated
with impaired wound healing and a prolonged inflammatory phase. Pro-inflammatory cytokines such as interleukin
(IL)-1b, tumor necrosis factor (TNF)-a and IL-6 are elevated in diabetes. LILI has been reported to
accelerate wound healing and decrease inflammatory cytokines. Methods: A human skin fibroblast cell line
(WS1) was used in vitro. Cells were exposed to various insults, namely, wounding, and a diabetic or hypoxic
environment. Experimental cells were exposed to an energy density of 5 J/cm2 using a continuous wave 636-nm
diode laser at an average power of 95mW, an illuminated area of 9.05 cm2, and an irradiance of 11 mW/cm2
(irradiation time, 476 sec). The effect of laser irradiation on cytokine expression was examined at 1 or 24 h postirradiation.
Cellular morphology, viability, proliferation, and cytokine expression (IL-1b, IL-6, and TNF-a) were
investigated. Translocation of nuclear factor – kappa B (NF-kB) was also determined. Results: There was a
higher rate of migration in irradiated wounded cultures, and irradiated hypoxic cells showed an improvement in
cellular morphology. All cell models showed an increase in proliferation. Normal wounded cells showed a
decrease in apoptosis, TNF-a, and IL-1b. Diabetic wounded cells showed an increase in viability and a decrease
in apoptosis and IL-1b, whereas hypoxic cells showed an increase in viability and IL-6, and a decrease in
apoptosis and TNF-a. NF-kB was translocated into the nucleus post-irradiation. Conclusions: Phototherapy
resulted in hastened wound closure, increased proliferation, and normalization of cellular function. The decrease
in the different pro-inflammatory cytokines and NF-kB translocation was model and time dependent. Overall,
laser irradiation resulted in a reduction in inflammatory cytokines and directed cells into the cell survival
pathway.