Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.4.3 (phospholipase C)
 18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Biochemical features and sensitivity to chemotherapeutic agents of 190 strains of Staphylococcus isolated from pharinx and conjunctiva of ophtalmological patients and staff were studied. Each strain was investigated for: pigment, coagulase, hemolysis (alpha-toxin), phosphatase and penicillinase production and mannite fermentation. Twentyfour chemotherapeutic angents were used for sensitivity tests. The Authors emphasize that a positive coagulase test is the best laboratory evidence for pathogenicity of a given strain of Staphylococcus, and that the site of isolation of the examined strains is not related with their biochemical features and sensitivity to chemotherapeutic agents.
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PMID:[Study on 190 strains of "staphylococcus aureus" isolated in a department of ophthalmology (author's transl)]. 75 53

We sought to establish and immunocytochemically characterize primary cultures of human conjunctival epithelial (HCE) cells, and to determine the types of receptors coupled to adenylate cyclase (AC) and phospholipase C (PLC) present on them which may be stimulated following allergic or inflammatory provocation of the tissue. HCE cells possessed the key epithelial cell surface cytokeratins AE1, AE3 and AE5. Signal transduction studies (n > or = 3), using agonists and antagonists, revealed the presence of beta 2-adrenergic (isoproterenol EC50 = 5.2 nM), prostaglandin E2 (EC50 = 168 nM) and vasoactive intestinal peptide (EC50 = 0.69 nM) receptors positively coupled to AC in HCE cells. Bradykinin (EC50 = 0.83 nM), platelet activating factor (EC50 = 4.5 nM), leukotriene C4 (EC50 = 300 nM) and histamine1 (EC50 = 3.1 microM) receptors were coupled to PLC (n = 3 for each). These data suggest that HCE cells in vivo may represent target cells for mast cell mediators and certain neurotransmitters which are released into the tear-film upon allergic provocation of the conjunctiva.
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PMID:Pharmacological analysis of mast cell mediator and neurotransmitter receptors coupled to adenylate cyclase and phospholipase C on immunocytochemically-defined human conjunctival epithelial cells. 926 68

Purified gamma-toxin is known to have a proinflammatory effect in the rabbit vitreous humor. To assess the biological role of the gamma-toxin, when expressed in vivo by Staphylococcus aureus strain Newman, the vitreous humor of rabbit eye was used as an infection model. A gamma-toxin-deficient mutant of strain Newman was constructed by allelic replacement. S. aureus Newman wild-type, its hlg-deficient derivative strain (N65) and the strain N65 complemented with the wild-type hlg+ gene were injected into the vitreous humor of rabbit eye. All three strains produced a strong proinflammatory effect in the eye conjunctiva, posterior and anterior chambers, suggesting a role for another unidentified proinflammatory component of strain Newman distinct from the gamma-toxin. These components are not the leucocidin of Panton-Valentine, beta-toxin or alpha-toxin which are not produced by this strain. Only the hlg-deficient mutant lacked the ability to cause inflammation in the eyelid, whereas the two Hlg-producing strains gave strong inflammation. These data suggest that in vivo, strain Newman produces as yet unidentified proinflammatory molecules and that the in vivo-produced HlgA, HlgB and HlgC molecules expressed by the gamma-toxin locus, contribute in part to the inflammatory process observed in vivo in the rabbit eye.
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PMID:Assessment of the role of gamma-toxin in experimental endophthalmitis using a hlg-deficient mutant of Staphylococcus aureus. 953 95

Conjunctival goblet cells secrete mucus in response to cholinergic (muscarinic) agonists, but the underlying signaling pathways activated in this tissue are not well understood. Cholinergic agonists usually activate phospholipase C to produce inositol 1,4,5 trisphosphate and diacylglycerol. Inositol 1,4,5 trisphosphate increases the intracellular Ca(2+)concentration ([Ca2(+)](i)) while diacylglycerol activates protein kinase C (PKC). PKC and Ca(2+), either by itself or with calmodulin, activate cellular functions. Goblet cell glycoprotein secretion, our index of mucin secretion, was measured from pieces of rat conjunctiva with an enzyme-linked lectin assay using the lectin Ulex europaeus agglutinin I (UEA-I). UEA-I selectively recognizes high molecular weight glycoproteins secreted by the goblet cells. Increasing the [Ca(+)](i)with the Ca(2+)ionophore ionomycin stimulated glycoprotein secretion from conjunctival goblet cells. Cholinergic agonist-induced secretion was completely blocked by chelation of extracellular Ca(2+)and by the Ca(2+)/calmodulin-dependent protein kinase inhibitors KN93 and W7 as well as their inactive analogs KN92 and W5. Activation of classical and novel PKC isozymes by phorbol 12-myristate 13-acetate and phorbol 12,13-dibutyrate stimulated goblet cell glycoprotein secretion. When ionomycin and PMA were added simultaneously, secretion was additive. PKC isozymes were identified by Western blotting analyses with antibodies specific to nine of the 11 PKC isozymes (PKCgamma and zeta were not tested). All nine PKC isozymes were identified in the conjunctival epithelium. The cellular location of the PKC isozymes was determined by immunofluorescence microscopy. Goblet cells contained the classical PKC isozymes PKCalpha, -betaI and -betaII, the novel PKC isozymes PKCepsilon, -theta;, and - mu, and the atypical PKC isozyme PKCzeta. We were unable to determine if PKC activation is required for cholinergic-agonist induced secretion because the PKC inhibitors chelerythrine and staurosporine alone greatly increased secretion. We conclude that Ca(2+)plays a major role in cholinergic agonist-induced conjunctival goblet cell secretion, but this agonist appears not to use Ca(2+)/calmodulin-dependent protein kinases. We also conclude that activated PKC can stimulate goblet cell secretion and that seven different PKC isoforms are present in the goblet cells.
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PMID:Regulation of conjunctival goblet cell secretion by Ca(2+)and protein kinase C. 1109 14

The effects of serotonin [5-hydroxytryptamine (5-HT)] on the transepithelial electrical properties of the short-circuited rabbit conjunctiva were examined. With this epithelium, the short-circuit current (I(sc)) measures Cl(-) secretion plus an amiloride-resistant Na(+) absorptive process. Apical addition of 5-HT (10 microM) elicited a prompt I(sc) reduction from 14.2 +/- 1.2 to 10.9 +/- 1.2 microA/cm(2) and increased transepithelial resistance from 0.89 +/- 0.05 to 1.03 +/- 0.06 kOmega. cm(2) (means +/- SE, n = 21, P<0.05). Similar changes were obtained with conjunctivae bathed without Na(+) in the apical bath, as well as with conjunctivae preexposed to bumetanide with the Cl(-)-dependent I(sc) sustained by the parallel activities of basolateral Na(+)/H(+) and Cl(-)/HCO(3)(-) exchangers. In contrast, the 5-HT-evoked effects were attenuated by the absence of Cl(-) (DeltaI(sc) = -0.5 +/- 0.2, n = 5), suggesting that reduced Cl(-) conductance(s) is an effect of 5-HT exposure. In amphotericin B-treated conjunctiva and in the presence of a transepithelial K(+) gradient, 5-HT addition reduced K(+) diffusion across the preparation by 13% and increased transepithelial resistance by 4% (n = 6, P < 0.05), indicating that an inhibition in K(+) conductance(s) was also detectable. Significant electrical responses also occurred under physiological conditions when 5-HT was introduced to epithelia pretreated with adrenergic agonists or protein kinase C, phospholipase C, phosphodiesterase, or adenylyl cyclase inhibitors or after perturbation of Ca(2+) homeostasis. Briefly, the conjunctiva harbors the only known Cl(-)-secreting epithelium in which 5-HT evokes Cl(-) transport inhibition; receptor subtype and signal transduction mechanism were not determined.
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PMID:Serotonin-elicited inhibition of Cl(-) secretion in the rabbit conjunctival epithelium. 1117 78

Staphylococcus aureus is a major pathogen of the eye able to infect the tear duct, eyelid, conjunctiva, cornea, anterior and posterior chambers, and the vitreous chamber. Of these infections, those involving the cornea (keratitis) or the inner chambers of the eye (endophthalmitis) are the most threatening because of their potential to cause a loss in visual acuity or even blindness. Each of these ocular sites is protected by the constitutive expression of a variety of antimicrobial factors and these defenses are augmented by a protective host response to the organism. Such infections often involve a predisposing factor that weakens the defenses, such as the use of contact lenses prior to the development of bacterial keratitis or, for endophthalmitis, the trauma caused by cataract surgery or intravitreal injection. The structural carbohydrates of the bacterial surface induce an inflammatory response able to reduce the bacterial load, but contribute to the tissue damage. A variety of bacterial secreted proteins including alpha-toxin, beta-toxin, gamma-toxin, Panton-Valentine leukocidin and other two-component leukocidins mediate tissue damage and contribute to the induction of the inflammatory response. Quantitative animal models of keratitis and endophthalmitis have provided insights into the S. aureus virulence and host factors active in limiting such infections.
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PMID:The Pathogenesis of Staphylococcus aureus Eye Infections. 2932 Apr 51