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K.-H. Sonoda, T. Fujimoto, Y. Oshima, K. Hijioka, E. Hasegawa, T. Ishibashi; The Possible Role of Chlamydia Pneumoniae Infection in the Formation of Choroidal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2009;50(13):4288.
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Choroidal neovascularization (CNV) is directly related to visual loss in age-related macular degeneration (AMD) and other macular disorders. The pathogenesis of AMD is complex and has still need to be elucidated. Chlamydia pneumoniae, a prokaryotic pathogen that causes chronic inflammation is come to be recognized as a risk factor of cardiovascular diseases. In this study, we investigated the association of C. pneumoniae infection and AMD using mouse laser-induced CNV model.
We used female 8-10 weeks C57BL/6 mice, Toll-like receptor (TLR) 2 knockout (KO) mice, and TLR4 KO mice. Experimental CNV was induced with rupturing in Bruch’s membrane by laser photocoagulation (PC). Seven days after PC, the eyes were enucleated and the areas of CNV were measured in the choroidal flat mounts. We also examined cytokine gene expression by quantitative real-time PCR in the primary cultured retinal pigment epithelium (RPE) cells.
Vitreous injection of the C. pneumoniae antigen induced the increasing size of CNV. We also found that primary mouse RPE cells expressed IL-6 and VEGF in response to C. pneumoniae antigen in vitro. Importantly, TLR2, but not TLR4, is essential for C. pneumoniae induced cytokine production from RPE cells. TLR2KO mice miss the size increase of experimental CNV due to C. pneumoniae antigen in vivo.
C. pneumoniae infection can be a risk factor for AMD and TLR2 is essential for this inflammatory signaling. Our data provide evidence of a link between infection and AMD.
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