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)

The single radial immunodiffusion technique was modified to determine tear complement component C3 with small sample volume. The C3 levels in the tears from 18 normal subjects and 42 patients with ocular diseases were determined using this method. In the normal subjects, the mean level of tear C3 was 5.12 mg per 100 ml. The physiological level of tear C3 was estimated to be less than 10 mg per 100 ml from the results in normal subjects and patients with noninflammatory ocular diseases. The cases of severe inflammatory diseases such as antiviral keratoconjunctivitis, herpetic keratitis and acute catarrhal conjunctivitis showed a high level of C3 in the tears. The C3 level was relatively low in the cases of mild inflammatory diseases such as allergic conjunctivitis. These results indicated that protein concentration of C3 in the tear was proportional to the severity of inflammation of the anterior ocular segment.
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PMID:Complement levels in human tears. 713 31

Purpose. Ulcerative keratitis due to Pseudomonas aeruginosa is a sight-threatening disease leading to loss of vision due to corneal inflammation. A human IgG1 monoclonal antibody (MAb F429) to the alginate capsule significantly reduces pathology and bacterial burdens in the cornea when applied topically starting 8 hours post-infection. The purpose of this study was to determine whether local polymorphonuclear neutrophils (PMN) recruitment and complement were important lipopolysaccharide co-factors in MAb F429-mediated reductions in P. aeruginosa tissue levels and corneal pathology. Methods. MyD88 knock-out mice unable to recruit PMN to tissues, mice depleted of PMNs, or mice depleted of complement component C3 were topically treated with MAb F429 starting 8 hours post-infection and evaluated for bacterial levels and corneal pathology 48 hours after infection with two P. aeruginosa isolates. Results. An inability to recruit PMN or systemic PMN depletion plus topical application of MAb F429 resulted in less pathology in the eye, but bacterial burdens were markedly increased in the cornea, brains, and spleens of these mice, indicative of systemic spread. Intraperitoneal injection of cobra venom factor (CVF) reduced C3 levels in the cornea approximately 40%, which did not change the beneficial effects of MAb F429. Both systemic injection and topical application of CVF reduced local C3 levels >60%, which eliminated MAb-mediated reductions in corneal pathology and bacterial levels. Conclusions. PMN recruitment and complement are both needed for maximal in vivo efficacy of MAb F429 in therapeutically treating P. aeruginosa keratitis, and attempts to reduce pathology by limiting PMN influx could have consequences leading to more extensive local and systemic infection.
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PMID:Role of neutrophils, MyD88-mediated neutrophil recruitment, and complement in antibody-mediated defense against Pseudomonas aeruginosa keratitis. 1989 65