Acanthamoeba castellanii: Characterization of an Adhesin Molecule

Kennett, Mary J.; Hook, Reuel R.; Franklin, Craig L.; Riley, Lela K.

doi:10.1006/expr.1999.4417

Cited by 23 publications

(16 citation statements)

References 27 publications

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“…The initial adhesion to the target cell could be mediated by specific receptors such as those described by other investigators (15,16,38,48). Cao et al (5) showed that mannosemediated adhesion of amebae to the target cells also contributes to induction of the cytopathic effect produced by the parasite.…”

Section: Discussionmentioning

confidence: 88%

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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Section: Discussionmentioning

confidence: 88%

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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“…Studies in which monoclonal antibodies were shown to be reactive with different surface membrane epitopes suggest the presence of more than one adhesion molecule on the ameba surface (212). Kennett et al (212) proposed that an adhesion molecule distinct from the 136-kDa mannose-binding protein, or an adhesion molecule composed of two different subunits, plays a role in attachment of amebae to host cells. Gordon et al (160), using binding assays, reported that Acanthamoeba binds preferentially to collagen IV, laminin, and fibronectin.…”

Section: Virulence Factorsmentioning

confidence: 99%

Acanthamoebaspp. as Agents of Disease in Humans

2003

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Acanthamoeba spp. are free-living amebae that inhabit a variety of air, soil, and water environments. However, these amebae can also act as opportunistic as well as nonopportunistic pathogens. They are the causative agents of granulomatous amebic encephalitis and amebic keratitis and have been associated with cutaneous lesions and sinusitis. Immuno compromised individuals, including AIDS patients, are particularly susceptible to infections with Acanthamoeba. The immune defense mechanisms that operate against Acanthamoeba have not been well characterized, but it has been proposed that both innate and acquired immunity play a role. The ameba's life cycle includes an active feeding trophozoite stage and a dormant cyst stage. Trophozoites feed on bacteria, yeast, and algae. However, both trophozoites and cysts can retain viable bacteria and may serve as reservoirs for bacteria with human pathogenic potential. Diagnosis of infection includes direct microscopy of wet mounts of cerebrospinal fluid or stained smears of cerebrospinal fluid sediment, light or electron microscopy of tissues, in vitro cultivation of Acanthamoeba, and histological assessment of frozen or paraffin-embedded sections of brain or cutaneous lesion biopsy material. Immunocytochemistry, chemifluorescent dye staining, PCR, and analysis of DNA sequence variation also have been employed for laboratory diagnosis. Treatment of Acanthamoeba infections has met with mixed results. However, chlorhexidine gluconate, alone or in combination with propamidene isethionate, is effective in some patients. Furthermore, effective treatment is complicated since patients may present with underlying disease and Acanthamoeba infection may not be recognized. Since an increase in the number of cases of Acanthamoeba infections has occurred worldwide, these protozoa have become increasingly important as agents of human disease

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“…Similarly, Kennett (Kennett et al 1999) reported that mannose and mannan do not affect the binding of monoclonal antibodies to Acanthamoeba membrane extracts. Our results suggested that the binding of IgA to amoebae does not involve interactions between saccharides in the molecule of IgA and adhesins (mannose binding protein) on the surface of the parasite.…”

Section: Discussionmentioning

confidence: 94%

Human IgA inhibits adherence ofAcanthamoeba polyphagato epithelial cells and contact lenses

et al. 2004

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Specific anti-Acanthamoeba IgA antibodies have been detected in the serum and tears of patients and healthy individuals. However, the role of human secretory IgA antibodies in inhibiting the adherence of Acanthamoeba had not been previously investigated. Therefore, the purpose of this study was to purify secretory IgA from human colostrum and analyze its effect on the adherence of Acanthamoeba trophozoites to contact lenses and Madin-Darby canine kidney (MDCK) cells. IgA antibodies to Acanthamoeba polyphaga in colostrum of healthy women as well as in saliva and serum of healthy subjects were analyzed by ELISA and Western blot analysis. In serum, saliva, and colostrum, we detected IgA antibodies that recognized several antigens of A. polyphaga. In addition, colostrum and IgA antibodies purified from it inhibited adherence of A. polyphaga trophozoites to contact lenses and MDCK cells. These results suggest that IgA antibodies may participate in the resistance to the amoebic infection, probably by inhibiting the adherence of the trophozoites to contact lenses and corneal epithelial cells.

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Acanthamoeba castellanii: Characterization of an Adhesin Molecule

Cited by 23 publications

References 27 publications

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

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

Acanthamoebaspp. as Agents of Disease in Humans

Human IgA inhibits adherence ofAcanthamoeba polyphagato epithelial cells and contact lenses

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