Bacteriology of the conjunctiva in pre-cataract surgery patients with occluded nasolacrimal ducts and the operation outcomes in Japanese patients.

BACKGROUND: Contamination of the conjunctiva in association with nasolacrimal duct obstruction is by all accounts a risk factor for infectious endophthalmitis post-cataract surgery. METHODS: All patients who underwent cataract day surgery routinely received nasolacrimal duct syringing with normal saline at the Wakayama Medical University Hospital, Japan, from 2011 to 2013. The microorganisms isolated from conjunctival swab samples of patients with occluded nasolacrimal ducts and their susceptibility to antibiotics, as well as the operation outcomes in all the patients were retrospectively investigated. RESULTS: Nasolacrimal duct obstruction was observed in 125 eyes of 90 patients (3.3%; 42 eyes of 30 male individuals, and 83 eyes of 60 female individuals) from a total of 3754 eyes of 2384 patients by using irrigation samples of nasolacrimal ducts. The mean age of the subjects with duct obstruction was 79 ± 8.5 years.. In bacterial cultures of swabs from these 125 individuals, microbial growth was detected in 56 samples (i.e. 44.8%). Coagulase-negative Staphylococcus was detected in 28 eyes, and Corynebacterium species was detected in 17 eyes. Staphylococcus aureus, excluding methicillin-resistant S. aureus was detected in seven eyes with nasolacrimal duct obstruction. Methicillin-resistant S. aureus was isolated in two eyes with nasolacrimal duct obstruction. Each case was treated with topical antibiotics based on the results of antibiotic sensitivity tests. After culturing of cotton swab samples from the conjunctiva, and using direct micrography of bacteria every 2 or 3 days after starting treatment, and once the results were negative (consecutively tested three times), the patients received cataract surgery. In the current case series, bacteria were not detected in conjunctival swabs obtained consecutively three times for 3 weeks after starting topical antibiotics in 118 eyes from 125 eyes (94.4%), and later in the remaining patients. No patient required dacryocystorhinostomy to eliminate bacterial contamination in the conjunctiva following topical antibiotic therapy. No patient developed infectious endophthalmitis at least 1-year post-cataract surgery. CONCLUSIONS: All the patients receiving cataract day surgery underwent the operation after the elimination of conjunctival microorganism contamination in association with nasolacrimal duct obstruction by using appropriate topical antibiotics.

Endogenous osteopontin involvement in laser-induced choroidal neovascularization in mice.

PURPOSE: To evaluate the effects of the lack of osteopontin (OPN) and the administration of anti-OPN antibody on inflammation and vascular endothelial growth factor (VEGF) expression in choroidal tissue and on the development of choroidal neovascularization (CNV) after retinal photocoagulation in mice. METHODS: CNV was induced in one eye each of 20 C57BL/6-background OPN-deficient mice or 20 wild-type littermates. In another series of experiments, CNV was induced in 40 C57BL/6 mice treated with intraperitoneal administration of 400 µg anti-OPN (SLAYGLR) neutralizing antibody or control IgG. Four laser spots were prepared in each eye. At day 14, the size of the CNV was evaluated by high-resolution angiography with fluorescein isothiocyanate (FITC)-dextran. Six wild-type or six knockout mice also received photocoagulation and processed for histology. mRNA expression of OPN, VEGF, and F4/80 macrophage antigen in laser-irradiated choroidal tissues was analyzed at day 3 in wild-type or knockout mice as well as in wild-type mice treated with anti-OPN antibody or control antibody. RESULTS: Photocoagulation upregulated OPN expression in choroidal tissue. Histology did not uncover the effects of the lack of OPN on the healing of laser injury in choroid. The lack of OPN or systemic administration of anti-OPN antibody suppressed mRNA expression of VEGF and macrophage invasion in choroidal tissue. FITC-dextran angiography showed that lacking OPN or systemic anti-OPN antibody reduced the size of laser-induced CNV. CONCLUSIONS: OPN is upregulated in laser-irradiated choroidal tissue. Endogenous OPN is required for macrophage inflammation and VEGF expression in choroidal tissue and for CNV development after retinal photocoagulation in mice.

Impaired angiogenic response in the corneas of mice lacking osteopontin.

PURPOSE: To investigate the effects of loss of osteopontin (OPN) in the development of neovascularization in corneal stroma in mice. Cell culture study was also conducted to clarify the effects of OPN in transforming growth factor (TGF) beta1-driven cell signaling and expression of vascular endothelial growth factor (VEGF). METHODS: Ocular fibroblasts from wild-type and OPN-null mice were used to study the role of OPN in TGFbeta1 signal and VEGF expression. The effect of the absence of OPN on corneal neovascularization was evaluated in mice. RESULTS: In ocular fibroblast culture, loss of OPN attenuated TGFbeta1 signals (Smad3 and p38) and reduced expression of VEGF. Loss of OPN attenuated neovascularization in corneal stroma in mice. CONCLUSIONS: OPN is involved in VEGF expression in cultured fibroblasts and is required for neovascularization in corneal stroma in vivo.

Endogenous TNFalpha suppression of neovascularization in corneal stroma in mice.

PURPOSE: To examine the role of tumor necrosis factor alpha (TNFalpha) in stromal neovascularization in injured cornea in vivo and in cytokine-enhanced vessel-like endothelial cell tube formation in vitro. METHODS: An in vitro model of angiogenesis was used to examine the roles of TNFalpha on tube formation by human umbilical vein endothelial cells (HUVECs) cocultured with fibroblasts on induction by transforming growth factor beta1 (TGFbeta1) and vascular endothelial growth factor (VEGF). Central cauterization was used to induce stromal neovascularization in corneas of wild-type (WT) and TNFalpha-null (Tnfalpha(-/-)) mice. At 7, 14, or 21 days of injury, experimental mice were killed, and the eyes were enucleated and subjected to histologic and immunohistochemical examination and real-time reverse transcription-polymerase chain reaction. RESULTS: HUVECs formed a vessel-like tube structure on the fibroblast feeder layer. Adding TGFbeta1, VEGF, or both augmented vessel-like tube formation by HUVECs cocultured with fibroblasts. Adding TNFalpha (5 ng/mL) completely abolished the formation of tube-like structures despite the presence or absence of TGFbeta1 or VEGF in coculture. In vivo, cauterization of the central cornea induced the formation of CD31(+) new vessels surrounding the limbus in WT mice. More prominent central stromal neovascularization accompanied by increased expression of TGFbeta1 and VEGF was found in Tnfalpha(-/-) mice compared with WT mice. CONCLUSIONS: In addition to inhibiting TGFbeta1 and VEGF expression by fibroblasts, endogenous TNFalpha may counter the induction effects of TGFbeta1 and VEGF on vascular endothelial cells and may block neovascularization.