Irradiation with 780 nm diode laser attenuates inflammatory cytokines but upregulates nitric oxide in lipopolysaccharide-stimulated macrophages: Implications for the prevention of aneurysm progression
✍ Scribed by Lilach Gavish; Louise S. Perez; Petachia Reissman; S. David Gertz
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 425 KB
- Volume
- 40
- Category
- Article
- ISSN
- 0196-8092
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Background and Objectives
Low level laser irradiation (LLLI) has been shown to reduce inflammation in a variety of clinical situations. We have shown that LLLI (780 nm) increases aortic smooth muscle cell proliferation and matrix protein secretion and modulates activity and expression of matrix metalloproteinases. Inflammation is a major component of arteriosclerotic diseases including aneurysm. Macrophage recruitment and secretion of pro‐inflammatory cytokines and the vasodilator, nitric oxide (NO), are central to most immune responses in the arterial wall. The present study was designed to determine the effect of LLLI on cytokine gene expression and secretion as well as gene expression of inducible nitric oxide synthase (iNOS) and NO production in lipopolysaccharide (LPS)‐stimulated macrophages.
Study Design/Materials and Methods
Murine monocyte/macrophages (RAW 264.7) were irradiated with a 780 nm diode laser (2 mW/cm^2^, 2.2 J/cm^2^) during stimulation with LPS (0, 0.1, and 1 µg/ml). Gene expression of chemokines, cytokines, and iNOS were assessed by RT‐PCR. Secretion of interleukin (IL)‐1β and monocyte chemotactic protein (MCP)‐1 and NO were assessed by ELISA and the Griess reaction, respectively.
Results
LLLI reduced gene expression of MCP‐1, IL‐1α, IL‐10 (P<0.01), IL‐1β, and IL‐6 (P<0.05) when cells were stimulated by 1 µg/ml LPS. LLLI reduced LPS‐induced secretion of MCP‐1 over non‐irradiated cells by 17±5% and 13±5% at 12 hours (0.1 and 1 µg/ml LPS; P<0.01 and P = 0.05, respectively), and reduced IL‐1β by 22±5% and 25±9% at 24 hours (0.1 and 1 µg/ml LPS, P = 0.01 and P = 0.06, respectively). However, LLLI increased NO secretion after 12 hours (LLLI vs. Control: without LPS, 1.72±0.37 vs. 0.95±0.4 µM, P<0.05; 0.1 µg/ml LPS, 7.46±1.62 vs. 4.44±1.73 µM, P = 0.06; 1 µg/ml LPS, 10.91±3.53 vs. 6.88±1.52 µM, P<0.05).
Conclusions
These properties of LLLI, with its effects on smooth muscle cells reported previously, may be of profound therapeutic relevance for arterial diseases such as aneurysm where inflammatory processes and weakening of the matrix structure of the arterial wall are major pathologic components. Lesers Surg. Med. 40:371–378, 2008. © 2008 Wiley‐Liss, Inc.