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Biomedical subjects

A M Silverstein

Publications and source records attributed to A M Silverstein.

At least 73 records · Page 4Linked to original sources
PubMed1983

Conjunctival immunity: compared effects of ocular or intestinal immunization in rats.

The ability to induce a conjunctival antitoxin response by conjunctival or enteric administration of cholera toxin antigen was studied in rats. Repeated enteric immunization caused a vigorous jejunal antitoxin response, but none in the conjunctiva. Enteric immunization did, however, prime for a conjunctival antitoxin response to locally applied antigen, as did direct ocular administration of cholera toxin. Vigorous conjunctival antitoxin responses occurred only after ocular challenge, and were localized to the challenged eye. These results agree with the notions that (1) specific memory cells migrate to the conjunctiva after enteric immunization, or arise locally after ocular immunization; and (2) specific antibody-producing plasma cells arise almost entirely within the immunized conjunctiva, and few if any migrate to the conjunctiva from distant mucosae or from the conjunctiva of the immunized eye to that of the nonimmunized eye.

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PubMed1982

Sindbis virus-induced ocular immunopathology.

The intraocular injection of the Sindbis virus in adult BALB/c mice produces a uveoretinitis with little or no central nervous system involvement. Ocular disease starts on the third day after infection and presents as a mild to moderate iridocyclitis and retinitis, usually accompanied by typical severe dysplastic changes of the retina. The inflammatory infiltrate consists almost exclusively of lymphocytes and histiocytes. Immunosuppression of the mouse with cyclophosphamide on the day after infection markedly reduces or eliminates completely the inflammatory response, suggesting that the virus itself is not cytopathogenic. In the normal host, the virus replicates within the eye for several days but is then completely eliminated by day 8 after infection. In the immunosuppressed animal, virus titers reach greater levels than in the normal animal and then fall, in step with the developing inflammatory response. It would appear that the immunologic mechanisms responsible for clearance of the viral infection from the eye also mediate the ocular disease.

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PubMed1982

An animal model of trachoma II. The importance of repeated reinfection.

An animal model of chronic cicatrizing trachoma has been produced by repeated ocular inoculation with Chlamydia trachomatis serotype E, a genitally transmitted strain. We have now produced a chronic follicular conjunctivitis on cynomolgus monkeys by repeated inoculation with C. trachomatis serotype A, which has been isolated from an area of endemic trachoma. This disease was similar in all respects to that which followed infection with the serotype E strain. Cynomolgus monkeys inoculated with a single dose of serotype E of C. trachomatis strain developed an acute, self-limited follicular conjunctivitis, which was intense for 4 weeks and then slowly subsided. The organism could be reisolated only during the first 4 weeks after inoculation. On reinoculation at 15 and 30 weeks after the initial infections, these animals demonstrated only a mild and transitory clinical response, and the agent could be recovered for only up to 14 days after inoculation. In contrast, repeated weekly reinoculation with either serotype led to a chronic progressive clinical response in these animals, although after the first 6 weeks the agent was isolated only occasionally. This chronic disease was shown not to be due to hypersensitivity to the egg yolk components in which the organism was grown. These data suggest that the serotype of the chlamydial organism may not be as important in determining the clinical course of disease as is the frequency or persistence of exposure to the chlamydial agent. Although a single inoculum produced an acute follicular conjunctivitis, repeated inoculation is needed to produce the chronic disease characteristic of trachoma in this animal model.

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PubMed1982

Mechanisms of allograft rejection of corneal endothelium.

The local intraocular graft-vs.-host (GVH) reaction, involving the destruction of the corneal endothelial cells of the rabbit host by sensitized donor lymphoid cells, has been used to study the mechanism of corneal allograft rejection. Pretreatment of donor cells with a specific mouse monoclonal hybridoma anti-T cell antibody and complement suppresses the destructive reaction, suggesting that a cellular-immune mechanism is primarily involved. Pretreatment of donor cells with mitomycin-C completely abolishes the local GVH reaction, indicating that the effector lymphocytes must undergo mitosis within the eye before they can engage in target cell destruction. Finally, studies of the local GVH reaction in irradiated leukopenic recipients or in preinflamed rabbit eyes suggest that host leukocytes may contribute nonspecifically to enhance the destructive process. These studies show that the local ocular GVH reaction may provide a useful model for the study of the mechanisms involved in the rejection of corneal allografts.

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PubMed1982

Desquamation of corneal endothelial cells.

The process of wound healing of rabbit corneal endothelium involves the desquamation of significant numbers of endothelial cells, which may be found floating freely in the aqueous. It is suggested that this may be a general phenomenon of corneal endothelial wound healing, which accompanies the release of endothelial-cell attachments to Descemet's membrane and to neighboring cells during mitosis, allowing some of the cells to "fall of" into the anterior chamber. The possibility is discussed that such endothelial desquamation may contribute to had sensitization to he histocompatibility antigens of penetrating corneal grafts.

Animals↗
PubMed1981

Secretory component of IgA: a marker for differentiation of ocular epithelium.

Secretory component (SC) was studied by indirect immunofluorescence of the ocular surface epithelium. We find that conjunctival epithelium produces this component, and that it is absent in the corneal epithelium. Conjunctival epithelium loses its SC staining within 1 to 2 days as it grows over a denuded corneal stroma. This implies a very rapid turn-off of the SC gene and rapid export of the gene product previously formed. However, conjunctival flap epithelium does not change its characteristic structure or functions. Vascularization of corneas resurfaced by conjunctival epithelium usually leads to a rapid reversal of both morphological and biochemical characteristics in the surface epithelium, as judged by the reappearance of goblet cells and positive staining for SC. Vascularization of normal corneas leaves the epithelium unchanged, so that neither goblet cells nor SC appear. Thus metaplasia of conjunctival to corneal epithelium is incomplete, permitting reversion to type under certain conditions.

Animals↗
PubMed1981

Perpetuation of inflammation in uveitis.

A large number of different and predominantly non-specific mechanisms has evolved to amplify and to perpetuate inflammatory reactions. Which of these mechanisms enters into play depends upon the nature of the primary insult. Thus, pyogenic bacteria call forth polymorphonuclear leucocytes, which release enzymes and other pharmacologically active substances to enhance the response. Other organisms elicit a predominantly monocytic response, whose active monokines contribute further to the infiltration and activation of inflammatory cells. Those stimuli involving antigens act primarily upon lymphocytes, whose lymphokines contribute significantly to the amplification and perpetuation of inflammation. This paper will present examples of these and other mechanisms that enhance and prolong the inflammatory response, with special emphasis on those that contribute to immunopathological disease.

Animals↗
PubMed1981

An animal model for cicatrizing trachoma.

An animal model of cicatrizing trachoma was developed in cynomolgus monkeys. This model is consistent with our hypothesis that repeated ocular inoculation of Chlamydia trachomatis, BOUR strain, mimics the repeated reinfection that occurs naturally in endemic human trachoma. A chronic follicular conjunctivitis developed, and scarring later appeared in the superior tarsal conjunctiva. The organism was reisolated after the infection and was also demonstrated cytologically. Specific antichlamydial antibodies of both the IgM and IgG types appeared in the sera of the monkeys. Histopathologic examination of conjunctiva showed a marked lymphocytic response and the presence of germinal centers; areas of conjunctival scar tissue were also examined. Efforts to produce a similar model in rhesus monkeys were less successful.

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PubMed1979

Characterization of prolactin binding by membrane preparations from rat liver.

Binding sites for prolactin were identified in a plasma-membrane-enriched fraction isolated from livers of mature female rats. 125I-labelled sheep prolactin prepared by the lactoperoxidase procedure retained the same molecular integrity and binding affinity as the native hormone at physiological pH. The receptors bound prolactin from different species, whereas non-lactogenic hormones were not bound. The binding of 125I-labelled sheep prolactin was activated equally by bivalent and univalent cations, bivalent cations exerting their maximal effect at much lower concentrations. The association of 125I-labelled sheep prolactin with the receptor was a time- and temperature-dependent process. Partial dissociation was detected. The binding of 125I-labelled sheep prolactin was strongly influenced by pH, with an optimum observed at pH 6.5. Receptor activity was destroyed by Pronase and phospholipase C, whereas neuraminidase increased binding. Treatment of the membranes by ribonuclease and deoxyribonuclease did not affect the binding. Binding of 125I-labelled sheep prolactin was inhibited by p-chloromercuribenzoic acid, dithiothreitol and by brief exposure to high temperatures. Scatchard analysis of the binding of 125I-labelled sheep prolactin to receptors indicated that prolactin has a high affinity for its receptor. Binding of prolactin to liver membranes showed some properties different from those observed with mammary cells. Binding by these tissues differed in pH optimum, in effects of ions, and in response to neuraminidase.

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