Disease relevance of Keratitis

• Interleukin 4 and T helper type 2 cells are required for development of experimental onchocercal keratitis (river blindness) [1].
• Ocular complications (limbitis, punctate keratitis, and uveitis) were also common in the DEC group, whereas in the flubendazole group they consisted only of one new punctate opacity at day 4 in one subject [2].
• Tyrosinemia type II (Richner-Hanhart syndrome, RHS) is a disease of autosomal recessive inheritance characterized by keratitis, palmoplantar hyperkeratosis, mental retardation, and elevated blood tyrosine levels [3].
• Vidarabine, acyclovir, ganciclovir, and foscarnet are used for systemic treatment of herpesvirus infections, while ophthalmic preparations of idoxuridine, trifluorothymidine, and vidarabine are available for herpes keratitis [4].
• Keratitis-ichthyosis-deafness syndrome (KID) is a rare ectodermal dysplasia characterized by vascularizing keratitis, profound sensorineural hearing loss (SNHL), and progressive erythrokeratoderma, a clinical triad that indicates a failure in development and differentiation of multiple stratifying epithelia [5].

High impact information on Keratitis

• Such mice demonstrate that eotaxin enhances the magnitude of the early (but not late) eosinophil recruitment after antigen challenge in models of asthma and stromal keratitis [6].
• Since angiogenesis appears to represent a vital step in the pathogenesis of herpetic stromal keratitis, these results indicate that targeting MMP-9 for inhibition should prove useful for the therapy of herpetic stromal keratitis [7].
• Chlorhexidine or polyhexamethylene biguanide for acanthamoeba keratitis [8].
• Keratitis from high doses intravenous cytarabine [9].
• Topical natamycin is usually the first choice for filamentous fungal keratitis, and topical amphotericin B is the first choice for yeast keratitis [10].

Chemical compound and disease context of Keratitis

• Neurotrophic keratitis was found in 81% of neonatally denervated animals; mortality rate due to HSV-1 infection was reduced from 80% in the controls to 24% in the capsaicin-treated group, and recovery of latent virus by cocultivation was reduced by 50% [11].
• A combination of acyclovir and dilute steroid drops appeared to be as effective as currently available treatments in the management of disciform keratitis [12].
• Acyclovir 3 percent ophthalmic ointment was compared with trifluorothymidine 2 percent ointment in a double-blind trial of 59 herpes keratitis patients [13].
• These studies indicate that cotherapy with ara-A and an adenosine deaminase inhibitor was a reasonable alternative therapy for keratitis due to mutants resistant to therapy with nucleoside analogs which require the virus-specified deoxypyrimidine kinase or DNA polymerase, while ara-A alone was not an effective alternative [14].
• We therefore conclude that antibody-mediated prevention of stromal keratitis and encephalitis does not require the obligatory participation of CD4+, CD8+, or asialo GM1+ cells [15].

Biological context of Keratitis

• Mutations in the human PAX6 gene produce various phenotypes, including aniridia, Peters' anomaly, autosomal dominant keratitis and familial foveal dysplasia [16].
• PURPOSE: Lipopolysaccharide (LPS) is one of the most powerful bacterial virulence factors in terms of proinflammatory properties and is likely to contribute to corneal bacterial keratitis [17].
• Histology and immunohistology of Igh-1-restricted herpes simplex keratitis in BALB/c congenic mice [18].
• We conclude that different pathogenic patterns of human HSV keratitis occur independent of genetic variation of the HSV UL6 (299-314) epitope [19].
• Kinetics of topically administered prednisolone acetate. Optimal concentration for treatment of inflammatory keratitis [20].

Anatomical context of Keratitis

• IL-17 expression in human herpetic stromal keratitis: modulatory effects on chemokine production by corneal fibroblasts [21].
• To characterize the underlying immune response, animal models have been developed that partially reproduce many of the clinical features of human onchocercal keratitis, Eric Pearlman here discusses how these studies have identified systemic and local immune responses associated with keratitis, including T helper-cell subset and cytokine responses [22].
• There was no inhibition of eosinophil and neutrophil migration to the corneas of E-selectin(-/-) mice, indicating that there is no direct role for this adhesion molecule in helminth-induced keratitis [23].
• Intracorneal injection of lipopolysaccharide (LPS) triggered infiltration of polymorphonuclear leukocytes (PMNs) to the cornea and induced severe keratitis [24].
• Cystic fibrosis transmembrane conductance regulator-mediated corneal epithelial cell ingestion of Pseudomonas aeruginosa is a key component in the pathogenesis of experimental murine keratitis [25].

Gene context of Keratitis

• Mutation of the PAX6 gene in patients with autosomal dominant keratitis [26].
• Clinically observable keratitis began 10 days postinoculation in susceptible C.AL-20 (Igh-1d) and moderately susceptible BALB/c (Igh-1a) mice, whereas HSV-1-resistant C.B-17 (Igh-1b) mice rarely developed disease [18].
• ICAM-1 was focally expressed on epithelial cells in corneas with chronic allograft rejection, herpetic stromal keratitis, zoster keratitis, chemical burns, atopic keratitis, fungal keratitis, and bacterial keratitis [27].
• Furthermore, our results indicate that MIP-1alpha plays a major role in herpes stromal keratitis development, whereas MCP-1 does not [28].
• Adenovirus keratitis: a role for interleukin-8 [29].

Analytical, diagnostic and therapeutic context of Keratitis

• This suggests that iontophoresis of acyclovir or ara-AMP either alone or in combination with intravenous administration of acyclovir may be of value in the treatment of HSV-1 stromal keratitis [30].
• Double-blind studies are now in progress to evaluate acyclovir in geographic and disciform keratitis [12].
• Topical administration of AC-SOD to the LPS-treated cornea markedly inhibited the infiltration of PMNs and suppressed the occurrence of keratitis [24].
• PURPOSE: To develop a topical inoculation model of Staphylococcus aureus keratitis in which scarification, contact lenses, and spermidine are used to inhibit the host defenses and to investigate the role of alpha-toxin in this infection [31].
• CONCLUSIONS: Due to their prolonged drug release properties, the ocular minitablets containing ciprofloxacin can be considered as a promising drug delivery system to be used in the treatment of ulcerative bacterial keratitis [32].

References