Biosynthesis of prostaglandins in pathogenic and nonpathogenic strains of Acanthamoeba spp.

Hadas, E.; Mazur, T.

doi:10.1007/s004360050250

Cited by 42 publications

(45 citation statements)

References 10 publications

(11 reference statements)

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“…The Acanthamoeba trophozoites secrete a variety of proteases with nonspecific collagenolytic activity to facilitate the invasion and degradation of stroma. These include serine proteases, cysteine proteases, metalloproteinases, elastase, collagenolytic enzyme, phospholipase A and a novel plasminogen activator [24,27,58]. Studies have shown the direct role of extracellular proteases in Acanthamoeba keratitis by co-incubating corneal epithelial cells with Acanthamoeba conditioned medium, which resulted in host cell cytotoxicity [65].…”

Section: Stromal Invasionmentioning

confidence: 99%

Pathogenesis of microbial keratitis

Lakhundi

Siddiqui

Khan

2017

Microbial Pathogenesis

171

121

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Microbial keratitis is a sight-threatening ocular infection caused by bacteria, fungi, and protist pathogens. Epithelial defects and injuries are key predisposing factors making the eye susceptible to corneal pathogens. Among bacterial pathogens, the most common agents responsible for keratitis include Staphylococcus aureus, Pseudomonas aeruginosa, Streptococcus pneumonia and Serratia species. Fungal agents of corneal infections include both filamentous as well as yeast, including Fusarium, Aspergillus, Phaeohyphomycetes, Curvularia, Paecilomyces, Scedosporium and Candida species, while in protists, Acanthamoeba spp. are responsible for causing ocular disease. Clinical features include redness, pain, tearing, blur vision and inflammation but symptoms vary depending on the causative agent. The underlying molecular mechanisms associated with microbial pathogenesis include virulence factors as well as the host factors that aid in the progression of keratitis, resulting in damage to the ocular tissue. The treatment therefore should focus not only on the elimination of the culprit but also on the neutralization of virulence factors to minimize the damage, in addition to repairing the damaged tissue. A complete understanding of the pathogenesis of microbial keratitis will lead to the rational development of therapeutic interventions. This is a timely review of our current understanding of the advances made in this field in a comprehensible manner. Coupled with the recently available genome sequence information and high throughput genomics technology, and the availability of innovative approaches, this will stimulate interest in this field.

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Section: Stromal Invasionmentioning

confidence: 99%

Pathogenesis of microbial keratitis

Lakhundi

Siddiqui

Khan

2017

Microbial Pathogenesis

171

121

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“…Amebic proteolytic enzymes include serine proteases (11,28,29), contact-dependent metalloproteases (17), elastases (9), cysteine proteases (11), and cytotoxic proteinases, induced by mannose-mediated adhesion (21). The use of gelatin gels has shown the presence of several proteolytic enzymes secreted by the amebae in medium conditioned by cultured amebae (1).…”

Section: Discussionmentioning

confidence: 99%

Induction of Morphological and Electrophysiological Changes in Hamster Cornea after In Vitro Interaction with Trophozoites of Acanthamoeba spp

Omaña‐Molina¹,

Navarro-Garcı́a²,

González‐Robles³

et al. 2004

Infect Immun

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Acanthamoeba castellani and Acanthamoeba polyphaga are free-living amebae that cause keratitis and granulomatous encephalitis in humans. We have analyzed the early morphological and electrophysiological changes occurring during the in vitro interaction of cultured amebae with intact or physically damaged corneas obtained from hamsters. Both species of Acanthamoeba produced similar cytopathic changes, as seen by light microscopy and scanning electron microscopy. After adhesion to the epithelial surface, trophozoites formed clumps and migrated toward the cell borders, causing the separation of adjacent cells at 1 h of coculture. At later stages (2 to 4 h), some amebae were found under desquamating epithelial cells whereas others were seen associated with damaged cells or forming amebostome-like structures to ingest detached epithelial cells. Control corneas incubated in culture medium conditioned with amebae showed a cytoplasmic vacuolization and blurring of the epithelial-stromal junction. The early stages of corneal epithelial damage caused by amebae were also analyzed by measuring the transepithelial resistance changes in corneas mounted in Ussing chambers. Both species of Acanthamoeba caused a rapid decrease in electrical resistance. The present observations demonstrate that under in vitro conditions, Acanthamoeba trophozoites rapidly cause significant damage to the corneal epithelium. Furthermore, in our experimental model, previous physical damage to the corneas was not a prerequisite for the development of amebic corneal ulcerations.

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“…Both pathogenic and nonpathogenic Acanthamoeba species endogenously produce a variety of prostaglandins, including PGE 2 , PGD 2 , and PGF 2␣ (48). However, pathogenic species produce more PGF 2␣ than nonpathogenic species.…”

Section: Protozoal Infectionsmentioning

confidence: 99%

Production of Eicosanoids and Other Oxylipins by Pathogenic Eukaryotic Microbes

2003

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Oxylipins are oxygenated metabolites of fatty acids. Eicosanoids are a subset of oxylipins and include the prostaglandins and leukotrienes, which are potent regulators of host immune responses. Host cells are one source of eicosanoids and oxylipins during infection; however, another potential source of eicosanoids is the pathogen itself. A broad range of pathogenic fungi, protozoa, and helminths produce eicosanoids and other oxylipins by novel synthesis pathways. Why do these organisms produce oxylipins? Accumulating data suggest that phase change and differentiation in these organisms are controlled by oxylipins, including prostaglandins and lipoxygenase products. The precise role of pathogen-derived eicosanoids in pathogenesis remains to be determined, but the potential link between pathogen eicosanoids and the development of TH2 responses in the host is intriguing. Mammalian prostaglandins and leukotrienes have been studied extensively, and these molecules can modulate Th1 versus Th2 immune responses, chemokine production, phagocytosis, lymphocyte proliferation, and leukocyte chemotaxis. Thus, eicosanoids and oxylipins (host or microbe) may be mediators of a direct host-pathogen “cross-talk” that promotes chronic infection and hypersensitivity disease, common features of infection by eukaryotic pathogens

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Biosynthesis of prostaglandins in pathogenic and nonpathogenic strains of Acanthamoeba spp.

Cited by 42 publications

References 10 publications

Pathogenesis of microbial keratitis

Pathogenesis of microbial keratitis

Induction of Morphological and Electrophysiological Changes in Hamster Cornea after In Vitro Interaction with Trophozoites of Acanthamoeba spp

Production of Eicosanoids and Other Oxylipins by Pathogenic Eukaryotic Microbes

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