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)

A 70 year-old-man with recurrent herpetic keratitis had a meningo-encephalitis with transient left hemiplegia and disorders of consciousness. EEG disclosed periodic slow waves on the right temporal region. Isotope and CT scans showed focal abnormalities in the same region. Antibodies to herpes simplex virus were demonstrated by complement fixation in serum and specific antiherpes IgG and IgM by immunofluorescence assay in serum and CSF. A year later the patient had a status epilepticus. CT scan showed a large right temporal hypodense area. CSF was abnormal with pleiocytosis, increased protein and IgG levels. High titers of antiherpes IgG persisted in serum and CSF. Neuropsychological tests did not demonstrate any memory impairment. The occurrence of persistent inflammation after herpes simplex encephalitis is discussed. The unusual benign course without antiviral therapy, may be related to the reactivation of a latent infection with an efficient immunological response. The unilateral temporal necrosis may explain the absence of amnestic sequelae.
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PMID:[Acute necrotizing herpetic encephalitis with a spontaneously improving clinical course]. 669 26

T-cell responses to pathogenic free-living amoebae, Acanthamoeba sp., were analyzed in healthy Japanese individuals. Of 20 healthy subjects, 10 (50%) showed significant proliferative responses of peripheral blood mononuclear cells to the soluble amoebic antigens in vitro. The antigens used were not mitogenic, and no evidence of amoebic superantigens was available. We established human T-cell clones reactive to Acanthamoeba, all of which were CD3- and CD4-positive, CD8-negative, and TCR-alpha beta-positive. We isolated two strains of Acanthamoeba from two patients, one from a patient with meningoencephalitis (CSF strain) and the other from a patient with keratitis (K strain). Of 13 clones, 11 were reactive to the K-strain as well as to the CSF-strain antigen under human leukocyte antigen (HLA)-DR restriction, whereas the other two were specific for the K-strain antigen. All but one clone tested showed TH1-equivalent functions because these cells produced interferon (IFN)-gamma in response to the amoebic antigen but produced no detectable level of interleukin 4 (IL-4). These results suggest that immunocompetent hosts might have acquired protective immunity mediated by Acanthamoeba-specific T-cells during natural sensitization.
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PMID:Acanthamoeba-specific human T-cell clones isolated from healthy individuals. 785 19

HSV-1 topical infection on the murine cornea can induce herpetic stromal keratitis (HSK), a T cell-mediated inflammatory response that results in blindness. To begin to decipher the molecular interactions involved in this infection, extracts of infected corneas were assayed for the presence of seven different cytokines by ELISA. The most prominent cytokines detected were IL-1 alpha and IL-6. Both were elevated by day 2 after infection, reached peak levels of 82 and 538 pg/cornea, respectively, at day 10, and then diminished over the next 10 days. In contrast, TNF-alpha concentrations were not elevated over that seen in uninfected corneas at any time during the 20-day observation period. IFN-gamma and granulocyte-macrophage CSF corneal concentrations were below the sensitivity of the assay. We investigated whether passive transfer of antibody to viral glycoprotein D, which prevents HSK, influenced the production of IL-1 alpha and IL-6. It was found that corneal concentrations of IL-1 alpha were reduced threefold and IL-6 was undetectable at day 10 in the antibody-treated hosts. The levels of IL-10 and IL-4 in uninfected control and antibody-treated hosts were also monitored. Neither of these two regulatory cytokines was associated with HSK development or effective antibody therapy. Naive corneas cultured in vitro spontaneously produced IL-1 and IL-6, indicating that cells resident in the cornea had the ability to synthesize these proinflammatory cytokines. Collectively, our results imply that IL-1 alpha and IL-6 may be important contributors to the development of HSK pathogenesis.
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PMID:Cytokine expression in vivo during murine herpetic stromal keratitis. Effect of protective antibody therapy. 839 96