PURPOSE: To clarify the effect of Pseudomonas aeruginosa culture filtrates on the association with, invasion into, and cytotoxicity against cloned cells from murine corneal epithelial cells and KB cells. METHODS: Simian virus 40-transformed murine corneal epithelial (MCE) cells were established. Murine corneal epithelial cells and KB cells were infected with a protease-positive strain, IID1117 (Pa IID1117), and a protease-negative strain, IID1130 (Pa IID1130) of P. aeruginosa, and then tested for association and invasion of Pa IID1117. The cytotoxicity test was performed by incubating the cells with culture filtrate. RESULTS: Association of Pa IID1117 with KB cells pretreated with Pa IID1130 was significantly promoted. After pretreatment with culture filtrate, invasion was more effective into MCE cells than into KB cells. When infecting bacteria (Pa IID1117) were pretreated with protease inhibitor, invasion of the bacteria into MCE cells and KB cells clearly decreased. The cellular damage induced by the culture filtrate of Pa IID1130 was greater than the damage by that of Pa IID1117. CONCLUSION: These results suggest that association of P. aeruginosa with MCE cells and KB cells was influenced by the culture filtrates other than proteases, and that invasion of P. aeruginosa into MCE cells and KB cells was promoted by protease.

Animals↗

PubMedDate not supplied

Cyclic 3',5'-guanosine monophosphate synthesis induced by atrial natriuretic peptide, C-type natriuretic peptide, and nitric oxide in the rat retina.

This study was undertaken to determine whether pathways exist in the rat retina for atrial natriuretic peptide (ANP)-, C-type natriuretic peptide (CNP)-, and nitric oxide (NO)- cyclic 3', 5'-guanosine monophosphate (cGMP). Exposure of the retina to ANP (10(-7) mol/L), CNP (10(-7) mol/L), S-nitroso-N-acetylpenicillamine (10(-5) mol/L, SNAP; a NO donor), A23187 (10(-5)mol/L; a Ca2+ ionophore), and carbachol (10(-3) mol/L) caused 1.45 approximately 1.67-fold increases in cGMP content (P < .01). The increase in cGMP content induced by A23187 was blocked by 2-4-carboxyphenyl . 4455-tetramethyl imidazoline 1-oxyl 3-oxide (10(-3) mol/ L, carboxy-PTIO; a NO scavenger). Both carboxy-PTIO (10(-3) mol/L) and NG-nitro-L-arginine (10(-3) mol/L, L-NNA: a NO synthase inhibitor) blocked the increase in cGMP content induced by carbachol. Atropine (10(-50 mol/L; a muscarinic receptor antagonist) also blocked the cGMP increase induced by carbachol. These data demonstrate that ANP-, CNP-, and NO-cGMP pathways exist in the rat retina and that the NO-cGMP pathway may be linked to the activation of the muscarinic receptor.

Animals↗

PubMedDate not supplied

Expression of stress-response protein 60 in lens epithelial cells in atopic cataract.

PURPOSE: To clarify the pathogenesis of atopic cataract, especially to determine if there is any relationship between autoimmunity and atopic cataract. METHODS: We investigated the lens epithelia obtained at surgery from 12 patients (12 eyes) with atopic cataract: from 8 patients (8 eyes) with nonatopic cataract (5 with senile cataract, 2 with juvenile cataract, and one with secondary cataract due to anterior uveitis); and from 4 autopsy eyes as controls. RESULTS: Histopathological findings in the lens epithelial cells from atopic and nonatopic cataract patients were essentially the same: atrophy of the cells, presence of the superimposed cells, migration of cells into the lens cortex, cytoplasmic vacuolation, and loss of cells. In an immunohistochemical study, the expression of stress-response protein 60 (srp 60), srp 27, and srp 72 was examined in the lens epithelial cells. In atopic cataract specimens, 71%-87% of the lens epithelial cells were stained with the antibody against srp 60, but the cells in nonatopic cataract and control specimens were not stained. CONCLUSIONS: Srp 27 and srp 72 were not expressed in any observed epithelial cells. The expression of srp 60 may reflect a protective mechanism of the epithelial cells against injury triggered by immunorelated agents. These findings suggest that the pathogenesis of degeneration of the lens epithelial cells in patients with atopic cataract may be related to autoimmunity.

Adult↗

PubMedDate not supplied

Expression of stress-response protein 60 in iritis associated with experimental autoimmune encephalomyelitis.

PURPOSE: To study the expression of stress-response proteins in the inflamed iris of rats with experimental autoimmune encephalomyelitis (EAE). METHODS: EAE was induced in Lewis rats by immunization with homogenized spinal cord of the guinea pig emulsified in complete Freund's adjuvant (CFA) (group EAE). Control rats included those immunized with only CFA (group CFA) and those that were untreated (group Normal). Immunohistochemical study for the localization of stress-response protein (srp) 27, srp 60, srp 72, ubiquitin, and alphaB-crystallin was performed. RESULTS: All rats in group EAE developed iritis, whereas none of the rats in group CFA and group Normal developed iritis. No expression of ubiquitin, alphaB-crystallin, srp 27, srp 60, or srp 72 was seen in the epithelium of the iris in group CFA rats. In the eyes of rats in group EAE, srp 60 was expressed in the epithelium of the iris in 20 of 22 (90.9%), ubiquitin in 4 of 22 (18.2%), and alphaB-crystallin in 3 of 22 (13.6%). In the group Normal rats, only ubiquitin was expressed in the epithelium of the iris in 1 of 6 (16.7%) eyes examined. CONCLUSIONS: These results suggest that srp 60 may be a potential uveitogenic antigen in the iris in EAE.

Animals↗

PubMedDate not supplied

[Testicular feminization: report of two cases in the same family (author's transl)].

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Androgen-Insensitivity Syndrome↗