Tags

Type your tag names separated by a space and hit enter

Choroidal neovascularization enhanced by Chlamydia pneumoniae via Toll-like receptor 2 in the retinal pigment epithelium.
Invest Ophthalmol Vis Sci. 2010 Sep; 51(9):4694-702.IO

Abstract

PURPOSE

Choroidal neovascularization (CNV) is directly related to visual loss in persons with age-related macular degeneration (AMD) and other macular disorders. Chlamydia pneumoniae, a prokaryotic pathogen that causes chronic inflammation, is recognized as a risk factor for cardiovascular diseases. In this study, the authors investigated the association between C. pneumoniae infection and AMD using a laser-induced CNV model in mice.

METHODS

C57BL/6 mice, myeloid differentiation factor (MyD) 88 knockout (KO) mice, Toll-like receptor (TLR) 2 KO mice, and TLR4 KO mice were used. Experimental CNV was induced by rupturing the Bruch's membrane by laser photocoagulation (PC). Seven days after PC, the eyes were enucleated and the areas of CNV were measured in choroidal flat mounts. Cytokine gene expression by quantitative real-time PCR in the primary cultured retinal pigment epithelium (RPE) cells was also examined.

RESULTS

Vitreous injection of the C. pneumoniae antigen increased the size of CNV. Although lipopolysaccharide stimulation can induce multiple cytokines, cultured mouse RPE cells from C57BL/6 mice expressed IL-6 and VEGF, but not TNF-alpha mRNA, in response to C. pneumoniae antigen. RPE cells from either MyD88 KO mice or TLR2 KO mice did not respond to the C. pneumoniae antigen. TLR2 KO mice did not augment the size increase of experimental CNV by C. pneumoniae antigen in vivo.

CONCLUSIONS

C. pneumoniae can trigger inflammatory responses in the eye and promote experimental CNV in a TLR2-dependent manner. These data provide experimental evidence to imply persistent C. pneumoniae infection is a risk factor for AMD.

Authors+Show Affiliations

Department of Ophthalmology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20393111

Citation

Fujimoto, Takeshi, et al. "Choroidal Neovascularization Enhanced By Chlamydia Pneumoniae Via Toll-like Receptor 2 in the Retinal Pigment Epithelium." Investigative Ophthalmology & Visual Science, vol. 51, no. 9, 2010, pp. 4694-702.
Fujimoto T, Sonoda KH, Hijioka K, et al. Choroidal neovascularization enhanced by Chlamydia pneumoniae via Toll-like receptor 2 in the retinal pigment epithelium. Invest Ophthalmol Vis Sci. 2010;51(9):4694-702.
Fujimoto, T., Sonoda, K. H., Hijioka, K., Sato, K., Takeda, A., Hasegawa, E., Oshima, Y., & Ishibashi, T. (2010). Choroidal neovascularization enhanced by Chlamydia pneumoniae via Toll-like receptor 2 in the retinal pigment epithelium. Investigative Ophthalmology & Visual Science, 51(9), 4694-702. https://doi.org/10.1167/iovs.09-4464
Fujimoto T, et al. Choroidal Neovascularization Enhanced By Chlamydia Pneumoniae Via Toll-like Receptor 2 in the Retinal Pigment Epithelium. Invest Ophthalmol Vis Sci. 2010;51(9):4694-702. PubMed PMID: 20393111.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Choroidal neovascularization enhanced by Chlamydia pneumoniae via Toll-like receptor 2 in the retinal pigment epithelium. AU - Fujimoto,Takeshi, AU - Sonoda,Koh-Hei, AU - Hijioka,Kuniaki, AU - Sato,Kohta, AU - Takeda,Atsunobu, AU - Hasegawa,Eiichi, AU - Oshima,Yuji, AU - Ishibashi,Tatsuro, Y1 - 2010/04/14/ PY - 2010/4/16/entrez PY - 2010/4/16/pubmed PY - 2010/10/5/medline SP - 4694 EP - 702 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 51 IS - 9 N2 - PURPOSE: Choroidal neovascularization (CNV) is directly related to visual loss in persons with age-related macular degeneration (AMD) and other macular disorders. Chlamydia pneumoniae, a prokaryotic pathogen that causes chronic inflammation, is recognized as a risk factor for cardiovascular diseases. In this study, the authors investigated the association between C. pneumoniae infection and AMD using a laser-induced CNV model in mice. METHODS: C57BL/6 mice, myeloid differentiation factor (MyD) 88 knockout (KO) mice, Toll-like receptor (TLR) 2 KO mice, and TLR4 KO mice were used. Experimental CNV was induced by rupturing the Bruch's membrane by laser photocoagulation (PC). Seven days after PC, the eyes were enucleated and the areas of CNV were measured in choroidal flat mounts. Cytokine gene expression by quantitative real-time PCR in the primary cultured retinal pigment epithelium (RPE) cells was also examined. RESULTS: Vitreous injection of the C. pneumoniae antigen increased the size of CNV. Although lipopolysaccharide stimulation can induce multiple cytokines, cultured mouse RPE cells from C57BL/6 mice expressed IL-6 and VEGF, but not TNF-alpha mRNA, in response to C. pneumoniae antigen. RPE cells from either MyD88 KO mice or TLR2 KO mice did not respond to the C. pneumoniae antigen. TLR2 KO mice did not augment the size increase of experimental CNV by C. pneumoniae antigen in vivo. CONCLUSIONS: C. pneumoniae can trigger inflammatory responses in the eye and promote experimental CNV in a TLR2-dependent manner. These data provide experimental evidence to imply persistent C. pneumoniae infection is a risk factor for AMD. SN - 1552-5783 UR - https://www.unboundmedicine.com/medline/citation/20393111/Choroidal_neovascularization_enhanced_by_Chlamydia_pneumoniae_via_Toll_like_receptor_2_in_the_retinal_pigment_epithelium_ L2 - https://iovs.arvojournals.org/article.aspx?doi=10.1167/iovs.09-4464 DB - PRIME DP - Unbound Medicine ER -