Journal
INFECTION AND IMMUNITY
Volume 73, Issue 2, Pages 1061-1068Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.73.2.1061-1068.2005
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Funding
- NEI NIH HHS [R01 EY009756, EY 09756] Funding Source: Medline
- NIAID NIH HHS [T32 AI007520, AI 07520] Funding Source: Medline
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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 remarkable, rare. The pathogenesis of Acanthamoeba keratitis is a complex, sequential process. Here we show that Acanthamoeba keratitis is profoundly affected by mannosylated proteins on the ocular surface, which stimulate the amoebae to elaborate a 133-kDa pathogenic protease. The mannose-induced protease (MIP133) mediates apoptosis of the corneal epithelium-facilitates corneal invasion, and degrades the corneal stroma. We show that contact lens wear upregulates manosylated proteins on the corneal epithelium, stimulates MIP133 secretion, and exacerbates corneal disease. Corynebacterium xerosis, a constituent of the ocular flora, contains large amounts of mannose and is associated with Acanthamoeba keratitis. The present results show that amoebae exposed to C xerosis produce increased amounts of MIP133 and more severe corneal disease. Oral immunization with MIP133 mitigates Acanthamoeba keratitis and demonstrates the feasibility of antidisease vaccines for pathogens that resist immune elimination.
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