Access to eBooks is limited to institutions that have purchased or currently subscribe to the SPIE eBooks program. eBooks are not available via an individual subscription. SPIE books (print and digital) may be purchased individually on SPIE.Org.

Contact your librarian to recommend SPIE eBooks for your organization.

4.1 Inflammation

Lim and co-workers found that 635-nm light irradiation at low power can lead to an anti-inflammatory effect by inhibiting prostaglandin E2 (PGE2) production and cyclo-oxygenase 1 and 2 (COX-1 and COX-2) mRNA expression. The light irradiation was able to decrease intracellular ROS, which mediates the expression of calcium-dependent phospholipase A2 (cPLA2), secretory phospholipase A2 (sPLA2), and COX-2, as well as inhibiting the release of PGE2.

PGE2 synthesis is dependent on NF-κB modulation of the cellular signaling mechanism. NF-κB is found in the cytosol in its dimeric form of NF-κB/IκB (the latter is an inhibitory protein). Pro-inflammatory stimuli, such as LPS, can activate the NF-κB upstream signaling regulator IκB kinase (IKK), which is responsible for the phosphorylation and degradation of IκB. The free NF-κB is translocated to the nucleus and induces the expression of pro-inflammatory genes. Lim demonstrated that 635-nm light irradiation suppresses the release of PGE2, possibly through a mechanism related to the inhibition of the NF-κB pathway. It did not affect the phosphorylation of IκB, IKK, and NF-κB in HSP27-silenced human gingival fibroblasts (hGFs), suggesting that NF-κB modulation by 635-nm light through HSP27 is required for the down-regulation of pro-inflammatory gene expression in these fibroblasts.

Online access to SPIE eBooks is limited to subscribing institutions.

Back to Top