RT Journal Article
SR Electronic
T1 Toll-like receptor 3 activation drives the inflammatory response in oxygen-induced retinopathy in rats
JF British Journal of Ophthalmology
JO Br J Ophthalmol
FD BMJ Publishing Group Ltd.
SP 125
OP 132
DO 10.1136/bjophthalmol-2014-305690
VO 99
IS 1
A1 Min Cai
A1 Xuedong Zhang
A1 Yingyuan Li
A1 Haiyan Xu
YR 2015
UL http://bjo.bmj.com/content/99/1/125.abstract
AB Aims Ischaemia is one of the most important causes of blindness. The purpose of this study was to investigate the potential role and mechanisms by which toll-like receptor 3 (TLR3) influences the progression of the inflammatory response in a rat model of oxygen-induced retinopathy (OIR). Methods OIR rat models were successfully established and received single intravitreal injections of polyinosine-polycytidylic acid (poly (I:C)) and anti-TLR3 antibody, respectively, on postnatal day 17 (P17). Pathological retinal neovascularisation was evaluated by haematoxylin and eosin staining and immunohistochemistry with Isolectin B4 FITC (fluorescein isothyocyanate). Retinal expressions of TLR3 and nuclear factor kappa B (NF-κB) were measured using real-time PCR, immunohistochemistry and western blot. Furthermore, interleukin-6 (IL-6) and tumour necrosis factor α (TNFα) expression levels were assessed with real-time PCR and ELISA. Results Both gene and protein expression levels of TLR3 and NF-κB were significantly elevated in the retinas of OIR rats compared to the controls. Increased IL-6 and TNFα expression levels were also observed in the retinas of OIR rats. Furthermore, TLR3 signalling pathway components, including NF-κB and IL-6/TNFα, were markedly upregulated upon stimulation with poly(I:C). In addition, the pre-treatment of TLR3 neutralising antibody in OIR models significantly decreased TLR3 and NF-κB expressions, as well as related inflammatory factors IL-6/TNFα expression. Conclusions Our results suggest that upregulation of the TLR3 signalling pathway is involved in the pro-inflammatory response in OIR rat retinas.