Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022568 (keratitis)
 5,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Interaction of leucocytes with human corneal endothelial cells (HCECs) can be observed in several clinicopathological conditions, such as uveitis, keratitis, and corneal graft rejection. Since leucocyte-endothelial cell interactions involve various adhesion receptors we have analysed the expression and distribution pattern of the neural cell adhesion molecule (NCAM), the intercellular adhesion molecule-1 (ICAM-1), the vascular cell adhesion molecule-1 (VCAM-1), the endothelial leucocyte adhesion molecule-1 (ELAM-1), and the cluster of differentiation antigen-44 (CD44) on flat preparations of normal and organ-cultured HCECs. NCAM and ICAM were constitutively expressed on HCECs whereas VCAM-1, ELAM-1, and CD44 were absent from normal HCECs. However flat mounts of HCECs from organ-culture preserved corneas showed a mosaic-like distribution pattern of VCAM-1 and ELAM-1 positive cells and garland-like clusters of CD44 positive cells. We suggest that modulation of ELAM-1, VCAM-1, and CD44 expression on HCECs may contribute to the regulation of leucocytes-HCECs interaction in the case of anterior segment inflammation.
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PMID:In situ immunohistochemical analysis of cell adhesion molecules on human corneal endothelial cells. 138 76

Acanthamoeba castellanii is a free-living protozoan that causes keratitis in humans and has been associated with pneumonia and granulomatous amebic encephalitis in dogs, sheep, and other species. Adherence of the Acanthamoeba to epithelial cells is critical to the pathogenesis of this disease. In this study, several mouse monoclonal antibodies (MAb) generated to whole Acanthamoeba trophozoites identified surface membrane epitopes by ELISA and IFA. Nine antibodies inhibited adherence of [(35)S]-methionine-labeled Acanthamoeba trophozoites to hamster corneal epithelial cells by 27-90%. Sodium periodate treatment, but not proteinase K digestion, of whole Acanthamoeba destroyed epitopes recognized by adherence-inhibiting antibodies such as MAb 7H6, suggesting that the adherence epitopes are carbohydrates. Other antibodies, MAb 2A8 for example, recognized surface membrane peptide epitopes that were proteinase K sensitive and sodium periodate resistant. Purified MAb 2A8 was used in an antigen-capture ELISA with peroxidase-labeled MAb 7H6 and demonstrated that the carbohydrate adhesion molecule was linked to the peptide recognized by MAb 2A8. Both MAbs 7H6 and 2A8 recognized a >207-kDa band on a Western blot of eluant from a MAb 2A8 immunoaffinity column, confirming that MAb 7H6 and MAb 2A8 recognize different epitopes on the same adherence molecule. MAbs 7H6 and 2A8 also identified the adhesion molecule in soluble Acanthamoeba membrane preparations and MAb 2A8 immunoaffinity column eluant by ELISA and Western blot. Neither of these antibodies were inhibited from binding to whole trophozoites nor membrane extracts by mannose or mannan in competitive binding assays. When our Acanthamoeba membrane preparations were electrophoresed and immunoblotted with alpha-d-mannosylated-biotin albumin, no bands were recognized in the >207 kDa range by our adherence-associated antibodies. These results suggest that the Acanthamoeba adhesin is not identical to the mannose binding protein of Acanthamoeba but rather is a distinct surface membrane glycoprotein.
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PMID:Acanthamoeba castellanii: characterization of an adhesin molecule. 1040 57

Although the absence of Substance P (SP), a neurotransmitter in the trigeminal nerve, has been speculated as a cause for developing neurotrophic keratitis, its exact pathogenesis is still not clarified. In a previous report, we showed with electron microscopic examination that epithelial cell attachment was weakened in denervated corneas. In this study, SV40-transformed human corneal epithelial cells (HCE-Ts) were used to explore the molecular mechanisms responsible for mediating regulation of E-cadherin expression in response to Substance P receptor stimulation. Expression of the mRNAs for specific SP receptors, neurokinin (NK)-1R, NK-2R, and NK-3R, was demonstrated with RT-PCR. The cells were treated with various concentrations of SP in vitro, and the expression of an adhesion molecule E-cadherin was analyzed by immunofluorescence, immunoblotting, and enzyme-linked immunosorbent assay (ELISA) using an anti-E-cadherin antibody. E-cadherin expression was increased by SP in a dose-dependent manner both in the cytosolic fraction and in the cell membrane fraction. This increase in E-cadherin expression was completely inhibited by Calphostin C (PKC inhibitor) and KN-62 (CaMK inhibitor), but not by H-89 (PKA inhibitor), indicating that SP-induced E-cadherin expression involves the activation of protein kinase C (PKC) and calmodulin kinase (CaMK). SP did not affect cell proliferation at all. All these findings indicate that SP induced E-cadherin expression through PKC and CaMK activation and suggest that a lack of SP may account in part for the pathogenesis of neurotrophic keratitis.
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PMID:Substance P-induced cadherin expression and its signal transduction in a cloned human corneal epithelial cell line. 1062 82

Pseudomonas aeruginosa and Staphylococcus aureus are the two dominant Gram-negative and -positive species, respectively, isolated from patients with contact lens-related bacterial keratitis. The clinical features of bacterial keratitis vary, such that timely differential diagnosis can be challenging, which may cause a delay in diagnosis resulting in poorer outcome. This review aims to explore the current understanding of clinical and immunological features associated with contact lens-related P. aeruginosa and S. aureus keratitis based on currently available evidence. Firstly, the review characterises contact lens-related P. aeruginosa and S. aureus keratitis, based on clinical features and prognostic factors. Secondly, the review describes the primary immune response associated with a bacterial infection in in-vivo non-scratch contact lens-wearing animal models, colonised by bacteria on contact lens and topical administration of bacteria on the cornea. Finally, the review discusses the role of macrophage inflammatory protein-2 (MIP-2) and intercellular adhesion molecule (ICAM-1) in neutrophil recruitment based on both in-vivo scratch models of bacterial keratitis and bacterial challenged in cell culture models.
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PMID:Understanding clinical and immunological features associated with Pseudomonas and Staphylococcus keratitis. 3330 56