acanthamoeba keratitis/protease

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Proteases as markers for differentiation of pathogenic and nonpathogenic species of Acanthamoeba.

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Acanthamoeba keratitis is a vision-threatening infection caused by pathogenic species of the genus Acanthamoeba. Although not all Acanthamoeba spp. can cause keratitis, it is important to differentiate pathogenic species and isolates from nonpathogens. Since extracellular proteases may play a role

Serine-like proteolytic enzymes correlated with differential pathogenicity in patients with acute Acanthamoeba keratitis.

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Acute ocular infection due to free-living amoebae of the genus Acanthamoeba is characterized by severe pain, loss of corneal transparency and, eventually, blindness. Proteolytic enzymes secreted by trophozoites of virulent Acanthamoeba strains have an essential role in the mechanisms of

Role of contact lens wear, bacterial flora, and mannose-induced pathogenic protease in the pathogenesis of amoebic keratitis.

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The ocular surface is continuously exposed to potential pathogens, including free-living amoebae. Acanthamoeba species are among the most ubiquitous amoebae, yet Acanthamoeba keratitis is remarkably rare. The pathogenesis of Acanthamoeba keratitis is a complex, sequential process. Here we show that

Extracellular protease profile of Acanthamoeba after prolonged axenic culture and after interaction with MDCK cells.

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Free-living amoebae of the genus Acanthamoeba are causative agents of Acanthamoeba keratitis and amoebic encephalitis in humans, both of which are serious infections. The ability to produce proteases is one of the factors involved in the pathogenesis of Acanthamoeba infections. The aim of this study

Protease-activated receptor 2 (PAR2) is upregulated by Acanthamoeba plasminogen activator (aPA) and induces proinflammatory cytokine in human corneal epithelial cells.

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OBJECTIVE Acanthamoeba plasminogen activator (aPA) is a serine protease elaborated by Acanthamoeba trophozoites that facilitates the invasion of trophozoites to the host and contributes to the pathogenesis of Acanthamoeba keratitis (AK). The aim of this study was to explore if aPA stimulates

Strategies for the prevention of contact lens-related Acanthamoeba keratitis: a review.

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OBJECTIVE Acanthamoeba keratitis is a severe, often sight threatening, corneal infection which in Western countries is predominantly seen in daily wear of contact lenses. This review aims to summarise the pathobiology and epidemiology of contact lens-related Acanthamoeba keratitis, and to present

The pathogenesis of Acanthamoeba keratitis.

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Free-living amoebae of the genus Acanthamoeba produce a progressive, blinding infection of the corneal surface. The pathogenesis of Acanthamoeba keratitis involves parasite-mediated cytolysis and phagocytosis of corneal epithelial cells and induction of programmed cell death. Acanthamoeba spp.

The pathophysiology of Acanthamoeba keratitis.

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Acanthamoeba keratitis is a sight-threatening infection of the ocular surface that is produced by several free-living amebae of the genus Acanthamoeba. Infection is usually initiated by Acanthamoeba-contaminated contact lenses and produces exquisite pain and ulceration of the ocular surface. The

Molecular and physiological differentiation between pathogenic and nonpathogenic Acanthamoeba.

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In this study, 14 isolates of Acanthamoeba from both clinical and environmental sources belonging to seven different species were assayed for tolerance of high osmotic pressure, temperature tolerance, extracellular proteases, and cytopathic effects (CPE) on immortalized rabbit corneal epithelial

Characterization of a plasminogen activator produced by Acanthamoeba castellanii.

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Serine proteases play an important role in a diverse array of biological processes, including embryogenesis, metastasis, angiogenesis, thrombolysis and tissue invasion by certain parasites. The latter observation prompted us to explore the possibility that the tissue-invasive ocular parasite

Failure of Acanthamoeba castellanii to produce intraocular infections.

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OBJECTIVE This study examined possible mechanisms to explain why Acanthamoeba castellanii remains restricted to the cornea and rarely produces intraocular infections. The first hypothesis proposed that trophozoites cannot penetrate Descemet's membrane and the corneal endothelium to enter the

Amoebicidal Activity of Caffeine and Maslinic Acid by the Induction of Programmed Cell Death in Acanthamoeba.

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Free-living amoebae of the genus Acanthamoeba are the causal agents of a sight-threatening ulceration of the cornea called Acanthamoeba keratitis, as well as the rare but usually fatal disease granulomatous amoebic encephalitis. Although there are many therapeutic options for the treatment of

Acanthamoeba-cytopathic protein induces apoptosis and proinflammatory cytokines in human corneal epithelial cells by cPLA2α activation.

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OBJECTIVE We have shown that Acanthamoeba interacts with a mannosylated protein on corneal epithelial cells and stimulates trophozoites to secrete a mannose-induced 133 kDa protease (MIP-133), which facilitates corneal invasion and induces apoptosis. The mechanism of MIP-133-induced apoptosis is

Genotyping of potentially pathogenic Acanthamoeba strains isolated from nasal swabs of healthy individuals in Peru.

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Free Living Amoebae (FLA) of Acanthamoeba genus are widely distributed in the environment and can be found in the air, soil and water; and have also been isolated from air-conditioning units. In humans, they are causative agents of a sight-threating infection of the cornea, Acanthamoeba keratitis

Mannose induces the release of cytopathic factors from Acanthamoeba castellanii.

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Acanthamoeba keratitis is a chronic inflammatory disease of the cornea which is highly resistant to many antimicrobial agents. The pathogenic mechanisms of this disease are poorly understood. However, it is believed that the initial phases in the pathogenesis of Acanthamoeba keratitis involve

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