More and more research is focusing on the biomarkers found in tears as this interesting abstract discusses sPLA@-IIa which is a biomarker for inflammatory diseases in humans and is found in high levels in tears. IOVS is publishing what we have seen to be the first report of its involvement in ocular surface inflammation and also revealed lower goblet cell density in the conjunctiva.
IOVS.ORG Investigative Ophthalmology & Visual Science
http://www.iovs.org/cgi/content/abstract/iovs.10-6350v1
Abstract
Purpose. sPLA2-IIa is a biomarker for many inflammatory diseases in humans and is found at high levels in human tears. However, its role in ocular surface inflammation remains unclear. An experimentally-induced BALB/c mouse dry eye (DE) model was utilized to elucidate the role of sPLA2-IIa in ocular surface inflammation.
Methods. BALB/c mice were subcutaneously injected with scopolamine and placed in a daytime air-drying device for 5 to 10 days. Control mice received no treatment. DE status was evaluated with tear production by the Pheno-Red Thread method. Tear inflammatory cytokines were quantified by multiplex immunoassays. Ocular surface inflammation and sPLA2-IIa expression were examined by immune-staining and quantitative (q)RT2-PCR. Conjunctiva (CNJ) of the mice was cultured for prostaglandin E2 (PGE2) production induced by sPLA2-IIa with various amount of sPLA2-IIa inhibitor, S-3319
Results. Treated mice produced less tears and heavier corneal (CN) fluorescein staining than the un-treated controls (p<0.001). They also revealed lower goblet cell density (p<0.001) with greater inflammatory cell infiltration within the conjunctiva, and higher concentration of tear inflammatory cytokines than the controls. Moreover, treated mice showed heavier sPLA2-IIa immune-staining than the controls in the CNJ epithelium, but not in the CN epithelium or the lacrimal gland (LG). Treated mice exhibited up-regulated sPLA2-IIa and cytokine gene transcription. Furthermore, CNJ cultures treated with sPLA2-IIa inhibitor showed significantly reduced sPLA2-IIa-induced inflammation.
Conclusions. This is the first report regarding sPLA2-IIa in the regulation of ocular surface inflammation. The findings may therefore lead to new therapeutic strategies for ocular surface inflammation, such as DE disease.
http://www.iovs.org/cgi/content/abstract/iovs.10-6350v1
