Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

cDNA clones for bovine retinal S-antigen (48K protein) have been isolated and sequenced. Secondary structure prediction for the deduced amino acid sequence suggest that the protein has predominantly beta-conformation with a helical region at the C-terminus. Local regions of sequence similarity with alpha-transducin have been observed, including the sites subject to ADP-ribosylation by pertussis and cholera toxins. Thirty-nine tryptic peptides and ten CNBr peptides of native S-antigen were purified and partially sequenced, showing good agreement with the sequence deduced from the cDNA analysis. The locations of two monoclonal epitopes have been determined by different methods. Furthermore, one synthetic peptide corresponding to the determined amino acid sequence was found to be highly pathogenic for the induction of experimental autoimmune uveitis (EAU). Native S-antigen has further been shown to be glycosylated, which has implications for its antigenicity.
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PMID:The structure of bovine retinal S-antigen: sequence analysis and identification of monoclonal antibody epitopes and uveitogenic site. 244 31

The effect of pertussis toxin (PT) on experimental autoimmune uveoretinitis (EAU) induced by immunization with S-antigen was examined in rats. Intravenous administration of PT (2 micrograms/rat) initiated the development of EAU in rats that had been made resistant to the induction of EAU by immunization with S-antigen and complete Freund's adjuvant (CFA). The capacity of PT to promote EAU was also demonstrated by a marked augmentation of the inflammation in EAU eyes of rats susceptible to the induction of EAU. PT was most effective when it was given from the day before to the day after immunization with S-antigen. However the induction of EAU was promoted by the injection of PT even 7 days before and 14 days after immunization. The clinical and histopathological findings of the EAU produced by the additional PT treatment were described and the mechanisms by which PT augmented the induction of EAU were discussed.
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PMID:Experimental autoimmune uveoretinitis (EAU) in rats: abrogation of resistance to the induction and augmentation of the inflammation by pertussis toxin. 278 90

Microgram quantities bovine IRBP (interphotoreceptor retinoid binding protein) injected in Freund's complete adjuvant induced severe autoimmune uveoretinitis and pinealitis in Lewis rats. At low doses the onset was accelerated and intensified by co-injection of Hemophilus pertussis bacteria. Wistar, BN and PVG rats were less susceptible, while the eyes of athymic, nude rats did not respond. The disease developed similar to but faster than S-antigen-induced uveoretinitis, while its onset was one day earlier and the reactions were slightly more severe. As distinct from these two types of uveoretinitis, opsin (in much higher doses) caused milder reactions in the anterior segment, while retinitis dominated. In each type of inflammation the photoreceptor cell layer was totally destroyed. All three ocular diseases were inhibited by cyclosporine treatment, which indicates that T cell-dependent mechanisms are essential for the development.
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PMID:Induction of experimental autoimmune uveoretinitis and pinealitis by IRBP. Comparison to uveoretinitis induced by S-antigen and opsin. 293 89

In an extension of our previous studies, experimental autoimmune uveoretinitis (EAU) was induced in Lewis rats by injection of very high doses of bovine opsin. The induced reaction consisted predominantly of a mild posterior retinitis. Varying the amount of injected opsin between 300 and 1,000 micrograms did not influence this result, provided that the antigen was injected in Freund's complete adjuvant. Pathogenicity of opsin appeared to be lower than that of interphotoreceptor retinoid binding protein (IRBP) or S-antigen, while EAU induced by the latter antigens was much more dose-dependent than EAU induced by opsin. An increase of the dose strongly accelerated the onset and increased the incidence of EAU from low to moderate. However, severe inflammation and high incidence were only obtained by co-injection of Hemophilus pertussis bacteria. This adjuvant especially increased cellular immune responses to opsin as measured by lymphocyte transformation. No marked effects on humoral responses were detected by ELISA, using different types of opsin preparations. Development of opsin-induced EAU was inhibited by ciclosporin, a suppressor of certain specific T cell functions. Ciclosporin injections lowered the antibody response of the rats and eliminated measurable lymphocyte transformation in vitro. Induction of opsin-EAU therefore appears to be T-cell-dependent. The effect of pertussis adjuvant may be explained by enhancement of the T cell responses to opsin and by increasing the permeability of the blood-retina barriers. Other properties of the adjuvant may be of importance as well. A relationship between change in molecular conformation and uveitogenicity of opsin is discussed.
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PMID:Immunological and immunopathological aspects of opsin-induced uveoretinitis. 295 58

S-Antigen is a major soluble protein of the retina and pineal. It is capable of inducing experimental autoimmune uveitis (EAU) in laboratory animals and also seems to play an important role in the visual cycle. The results of partial cDNA sequence analysis reveal interesting homologies with alpha-transducin, a GTP-binding protein of retina and other purine nucleotide-binding proteins. In particular S-antigen shows over 50% identity to the proposed pertussis toxin ADP-ribosylation site of alpha-transducin. It also contains the Gly-X-X-X-X-Gly-Lys pattern common to phosphoryl binding sites. A possible relationship between S-antigen and purine nucleotide-binding proteins is discussed. There is also evidence for a repetitious beta-structure in the C-terminal half of S-antigen, with a monoclonal antibody epitope in a helical region at the C-terminus.
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PMID:Sequence analysis of bovine retinal S-antigen. Relationships with alpha-transducin and G-proteins. 308 Mar 38

The S-antigen (alias 48K protein or arrestin) of bovine rod photoreceptors contains two stretches of amino acid sequence homologous to the ADP-ribosylation sites of the alpha subunit of transducin (Ta). We have found that cholera toxin transfers the ADP-ribosyl group from NAD to purified bovine S-antigen as well as to S-antigen in rod outer segment membranes, while Bordetella pertussis toxin is unable to catalyze the transfer reaction efficiently. Under the same conditions, both toxins catalyzed ADP-ribosylation of Ta in rod outer segments. The ADP-ribosylation of S-antigen by cholera toxin indicates that S-antigen not only exhibits sequence homology with the ADP-ribosylation sites of Ta, but it must also resemble Ta in the tertiary structure of the domain which determines the susceptibility of S-antigen to the catalytic action of cholera toxin. These results suggest that S-antigen may function as a competitor of Ta in some stage of the cGMP cascade of visual transduction.
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PMID:ADP-ribosylation of bovine S-antigen by cholera toxin. 319 Jun 95

Experimental autoimmune uveoretinitis (EAU), an intraocular inflammatory disease, is induced in experimental animals by immunization with a retinal specific antigen, S-antigen (S-Ag), emulsified in complete Freund's adjuvant (CFA). The induction of EAU is enhanced by treating S-Ag-immunized animals with Bordetella pertussis. This study examined the effects of a purified component of B. pertussis, pertussis toxin (Ptx), on EAU induction as well as the mode of action of this toxin. Treatment of Lewis rats with Ptx concurrent with S-Ag and CFA enhanced EAU induction as shown by an earlier onset of disease, increased severity of ocular changes, and the reduction of the threshold amount of S-Ag needed for EAU induction. Treatment with Ptx selectively enhanced delayed-type hypersensitivity responses to S-Ag but did not affect specific antibody production. The mode of action of Ptx was analyzed by using the adoptive transfer of EAU by sensitized lymphocytes. Ptx treatment of donor rats enhanced the capacity of lymphocytes to transfer EAU. However, Ptx treatment of recipient rats on the day of cell transfer resulted in a delay in the onset of disease. These results indicate that Ptx enhances the immunopathogenic processes of EAU by enhancing lymphocyte activation and/or increasing their pathogenic activities.
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PMID:The effects of pertussis toxin on the induction and transfer of experimental autoimmune uveoretinitis. 348 70

Rats immunized with microgram amounts of interphotoreceptor retinoid-binding protein (IRBP), a glycoprotein which localizes specifically in the eye and pineal gland, developed uveoretinitis and pinealitis. The severity and onset of changes were found to be dose-related and to be enhanced by B. pertussis bacteria. In general, the inflammatory changes induced by IRBP resembled those provoked by S-antigen (S-Ag), but significant differences were noted between the two diseases. The possible usefulness of the new experimental autoimmune disease is discussed.
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PMID:Uveoretinitis and pinealitis induced by immunization with interphotoreceptor retinoid-binding protein. 348 97

Experimental autoimmune uveoretinitis (EAU) is an ocular autoimmune disease induced in rats by immunization with retinal S-antigen. Athymic nude rats (rnu/rnu) have been previously shown to be refractory to EAU induction and antibody production to S-antigen, while heterozygous (rnu/+) are good responders. Increasing the antigen dose and adding pertussis adjuvant produced ocular disease in some nude rats, and antibody response in most of them. Specific IgE antibodies were demonstrated by ELI-SA only in the serum of nude rats presenting the disease. However, most immunized nude rats had evidence of mast cell sensitization to S-antigen (direct degranulation test) and of circulating specific IgE detected by passive sensitization of normal mast cells (indirect degranulation test). This positive response could be explained by an incomplete depletion of the different T lymphocyte subsets.
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PMID:Experimental autoimmune uveoretinitis in athymic rats: specific IgE response to retinal S-antigen and disease. 387 39

Experimental autoimmune retinitis has been induced in Lewis rats by injection of opsin in mycobacterial adjuvant and Hemophilus pertussis adjuvant. Clinical, histopathological and immunological parameters of the disease are reported. Two types of opsin were prepared from purified bovine retina outer segments, one type in Triton X-100 and the other in lithium dodecyl sulfate. Both preparations were free from S-antigen. Dodecyl sulfate-denaturated-opsin displayed lower antigenicity and pathogenicity than Triton-opsin. Triton-opsin (250 micrograms) induced moderate to severe non-granulomatous uveitis (predominantly retinitis) in 70% of the Lewis rats at the end of the second week after injection. The photoreceptor cell layer was destructed within a few days. This group displayed high responses to opsin in the lymphocyte transformation test. In view of observed histological features, the possible early involvement of vasoactive factors is discussed. Low opsin doses (50 or 100 micrograms) seldomly induced severe retinitis, while the incidence of mild pathology was low. Lewis rats appeared to be more susceptible for the development of experimental autoimmune retinitis than Wistar rats.
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PMID:Opsin-induced experimental autoimmune retinitis in rats. 624 Nov 36


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