keratitis/tyrosine

OBJECTIVE To determine if IL-17 regulates Mer tyrosine kinase-positive (MerTK+) cells in Pseudomonas aeruginosa keratitis. METHODS Interleukin 17 was tested in normal and infected cornea of susceptible C57BL/6 and resistant BALB/c mice. The latter were treated with recombinant mouse (rm) IL-17; both

One should henceforth systematically search for hypertyrosinemia which, too often, goes unrecognized for years, in patients presenting chronic keratitis associated with palmar and plantar hyperkeratosis. As a matter of fact, this highly crippling disease may be cured with an appropriate diet and the

Tyrosinemia type II (Richner-Hanhart syndrome, RHS) is a disorder of autosomal recessive inheritance characterized by keratitis, palmoplantar hyperkeratosis, mental retardation, and elevated blood tyrosine levels. The disease results from deficiency in hepatic tyrosine aminotransferase (TAT). We

Tyrosine-induced eye and skin lesions in man are an autosomal, recessive, inherited syndrome associated with tyrosinemia, tyrosinuria, and increased urinary excretion of tyrosine metabolites. Patients have mild to severe keratitis and erosive and hyperkeratotic lesions on the palms and soles. The

The authors report the cases of two unrelated children 16 and 5 years of age respectively, affected with hypertyrosinaemia type II. This condition is characterized by palmo-plantar hyperkeratosis associated with a herpetiform keratitis. The diagnosis is based on the finding of hypertyrosinaemia and

Richner-Hanhart syndrome (RHS, tyrosinemia type II) is a rare, autosomal recessive inborn error of tyrosine metabolism caused by tyrosine aminotransferase deficiency. It is characterized by photophobia due to keratitis, painful palmoplantar hyperkeratosis, variable mental retardation, and elevated

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. The disease results from deficiency in hepatic tyrosine aminotransferase (TAT;

Bilateral pseudo-dendritic keratitis in infancy can be due to tyrosinemia, a rare metabolic disorder. Ocular involvement may be the earliest presenting manifestation of this disease. Early diagnosis is essential because dietary modifications can result in complete reversal of the manifestations of

A boy of 3 2/12 years of age with Richner-Hanhart syndrome (plantar and palmar keratosis and chronic keratitis) was found to have hypertyrosinemia and to excrete the hydroxyacids derived from tyrosine. A diet poor in phenylalanine and tyrosine cured the skin and corneal lesions. Clinical and

Ulcerative keratitis is among the leading ocular bacterial infections, and Streptococcus aureus accounts for approximately 25% of cases in some surveys. Although S. aureus expresses numerous virulence factors, many of which are under the control of staphylococcal global regulatory genes, their

OBJECTIVE Herpes simplex virus type 1 (HSV-1) is a neurotrophic virus that can cause herpes stromal keratitis (HSK), a severe corneal inflammation that can lead to corneal scarring and blindness. This study identified neurologic changes that occur in HSV-1-infected corneas and related them to

Three children (6 eyes) with systemic tyrosinemia who presented with a diagnosis of herpes simplex keratitis are described. Two of the patients underwent extensive treatment for herpes simplex keratitis until their defects in tyrosine metabolism were discovered. All three children responded

The inability of epithelial cells from the cornea and other tissues to respond to LPS is reportedly due to low expression of the TLR4 co-receptor MD-2. We generated MD-2(-/-) bone marrow chimeras, and showed that MD-2 expression on non-myeloid cells was sufficient to mediate LPS-induced corneal

BACKGROUND Knock-in mice (gp130F759) with a Y759F point mutation in gp130, a signal transducing receptor subunit shared by members of the IL-6 cytokine family, show sustained activation of STAT3, enhanced acute-phase or immune responses, and autoimmune arthritis. We conducted a detailed analysis of

Herpes simplex virus 1 (HSV-1) Us3 protein kinase phosphorylates threonine at position 887 (Thr-887) in the cytoplasmic tail of envelope glycoprotein B (gB) in infected cells. This phosphorylation downregulates cell surface expression of gB and plays a role in viral pathogenesis in the mouse herpes