Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Anti-aortic antibodies were frequently detected from the sera of patients with aortitis syndrome. 2. Aortic antigens were demonstrated to exist mainly in the media. The antigenicity was inactivated by collagenase, trypsin and pepsin, but not by DNase-I. Analyses of aortic antigens were also made by ultracentrifugation and column chromatography. 3. Experimental arteritis could be produced in animals by isologous active immunization and heterologous passive immunization. 4. From these results, participation of antigen-antibody reaction in the development of the disease has been speculated. Possible role of streptococcal infection as one of the trigger mechanisms in antibody production has been suggested in combination with evidence indicating hypersensitivity of the patients to infections.
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PMID:Immunological aspects of aortitis syndrome. 112 Oct 58

Infection with group B streptococci (GBS) is associated with a poor acute inflammatory response in which neutrophils fail to localize at the site of invasion. In the present studies, we have examined the effects of group B streptococci on C-derived chemotactic activity in human serum. Fresh human serum was activated to form C5a and C5adesarg by incubation with zymosan. The activated serum was then incubated with group B organisms, centrifuged, and the supernatants tested for chemotactic activity for human polymorphonuclear leukocytes. Group B organisms caused a dose-dependent decrease in C-dependent chemotactic activity. The degree of inhibition was profound with 1 X 10(9) bacteria/ml (10% of control). Experiments indicated that significant chemotactic factor inactivation occurred within 2 min of exposure to GBS organisms, while maximal inhibition occurred after 30 min incubation. A number of different strains of GBS of types I, II, and III possessed inhibitory activity. In contrast, group D streptococci, Staphylococcus aureus, Escherichia coli and Klebsiella pneumoniae failed to inhibit the C-derived chemotactic activity in human serum. Group A streptococci that were M protein positive also inactivated C-dependent chemotactic activity in serum, as previously reported. The inhibitory activity of the GBS strains could be abolished by heat or trypsin treatment but not by neuraminidase, pronase, or pepsin. C5a levels in zymosan-activated serum as measured by RIA were not decreased after incubation with an inhibitory strain suggesting that absorption was not involved. SDS-PAGE analysis revealed that group B streptococci degrade the C5a molecule, increasing its electrophoretic mobility by removing a fragment with a m.w. of approximately 650 Da. Thus, one of the reasons for the poor inflammatory response at the site of GBS infection may reside in the ability of these pathogens to inactivate C-derived inflammatory mediators. The GBS C5a-ase activity probably serves as an additional virulence factor for these organisms contributing to the poor inflammatory response characteristic of group B streptococcal infection.
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PMID:Group B streptococci inhibit the chemotactic activity of the fifth component of complement. 305

Streptococcal mitogen (SM) is an extracellular product of group A streptococci, which is nonspecifically mitogenic for both B and T lymphocytes. The mitogenic activity of SM is resistant to digestion with trypsin, to heating at 100 degrees C for 5 min and to treatment with dithiothreitol. The proliferative response of lymphocytes from patients with a history of rheumatic fever is similar to that of lymphocytes from healthy donors when stimulated with optimal concentrations of SM, but is significantly reduced when low doses of SM are used. T lymphocytes stimulated with SM acquire la antigens and the ability to stimulate allogeneic and autologous lymphocytes in mixed lymphocyte reactions. An involvement of la antigens in these reactions is indicated by the specific block by monoclonal antibodies. T lymphocytes may acquire la antigens following exposure to an appropriate antigen. If this occurs following a streptococcal infection, these in vitro findings suggest that la bearing T cells may play a role in the immunopathological events which can follow a streptococcal infection. The system described may be a useful in vitro model to analyse the immunopathological events which can follow a streptococcal infection and to develop therapeutic approaches to autoimmune conditions.
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PMID:Appearance of Ia antigens on T lymphocytes stimulated by streptococcal mitogen as an in vitro model of autoimmunity. 387 85

Streptococcal mitogen (SM) is an extracellular product of group A streptococci, nonspecifically mitogenic for both B and T lymphocytes. The mitogenic activity of SM is resistant to digestion with trypsin, to heating at 100 degrees C for 5 min and to treatment with dithiothrietol. The proliferative response of lymphocytes from patients with a history of rheumatic fever is similar to that of lymphocytes from healthy donors when stimulated with optimal concentrations of SM, but is significantly reduced when low doses of SM are used. Rats were treated with s.c. injections of SM for 21 days at various times from the injection with adjuvant: both primary and secondary reactions in the joints were depressed, more so with pretreatment and early treatment. A similar pattern of response was observed in the survival of A tail skin grafts on the flank of CBA mice: a strain combination with strong H-2 incompatibility. Human T lymphocytes stimulated with SM acquired Ia antigens and the ability to stimulate allogeneic and autologous lymphocytes in mixed lymphocyte reactions. An involvement of Ia antigens in these reactions was indicated by the specific block by monoclonal antibodies to human Ia antigens. T lymphocytes may acquire Ia antigens following exposure to an appropriate antigen. If this occurs following a streptococcal infection, our in vitro findings suggest that Ia bearing T cells may play a role in the immunopathological events which can follow a streptococcal infection. This in vitro system may be a useful model to analyse these immunopathological events and to develop therapeutic approaches in autoimmune conditions. The in vitro findings, together with the observed suppressive effects on the in vivo models described, indicate that SM is a valuable means for study and manipulation of a variety of immune responses.
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PMID:In vivo and in vitro immunomodulatory ability of streptococcal mitogen: effects on adjuvant disease in the rat; on homograft rejection in the mouse; and on the appearance of Ia antigens on human T lymphocytes. 391 83

Sera from patients with recent streptococcal infection or non-suppurative sequelae exhibit with variable frequency a precipitin reaction in agar gel with a partially purified streptococcal antigen which has been shown previously to be immunologically related to human heart tissue. This precipitin could be absorbed from sera with normal human heart tissue homogenates but not with homogenates of other organs. Demonstration of this cross-reaction by heart absorption was found dependent both upon the serologic properties of individual sera and the nature or state of purification of the streptococcal product employed as test antigen. Evidence was obtained of a close association of heart-related and non-heart-related antigenic determinants in partially purified preparations of the streptococcal antigen by both gel diffusion and immunoelectrophoresis. On immunoelectrophoretic analysis, cross-reactive antigen exhibited a more rapid mobility toward the anode than M protein. It was destroyed by digestion with trypsin, pepsin, and chymotrypsin. Based on specific absorption tests with a Type 5 and Type 19 strain, the antigen was localized to cell walls and to a lesser extent to cell membranes of these strains. Precipitating activity related to cross-reactive antibody was localized to the immunoglobulin zone in immunoelectrophoresis. Reactive sera showed diminution or loss of serological activity following heat inactivation at 56 degrees C or after prolonged storage at 4 degrees C. Sera containing cross-reactive precipitating antibody exhibited an immunofluorescent reaction with sarcolemma of cardiac myofibers, which was inhibited by streptococcal cross-reactive antigen. By this inhibition test, the immunofluorescent reaction related to cross-reactive antibody could be distinguished from that due to other heart-reactive factors. Antibody to streptococcal cross-reactive antigen defined by precipitation-absorption tests was observed in 24 per cent of patients with recent history of uncomplicated streptococcal infection and in the majority of patients with acute rheumatic fever, rheumatic heart disease, or acute glomerulonephritis. It was observed rarely in patients with non-streptococcal related disease. These data provide evidence that induction of cross-reactive autoantibody to heart in certain individuals is associated with streptococcal infection.
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PMID:IMMUNOLOGIC RELATION OF STREPTOCOCCAL AND TISSUE ANTIGENS. III. PRESENCE IN HUMAN SERA OF STREPTOCOCCAL ANTIBODY CROSS-REACTIVE WITH HEART TISSUE. ASSOCIATION WITH STREPTOCOCCAL INFECTION, RHEUMATIC FEVER, AND GLOMERULONEPHRITIS. 1415 Nov 5

Streptococcal pyrogenic exotoxin B (SPE B) is a virulent factor in group A streptococcal infection. We previously showed that SPE B reduced phagocytosis in human monocytic U937 cells. Here we show that the mycelium extract of Cordyceps sinensis (CS), a Chinese immunomodulatory herbal medicine, increased phagocytosis in U937 cells. Neither heat nor trypsin pretreatment prevented CS extract from causing this increase. Further studies indicated that SPE B-mediated suppression of U937 cell phagocytic activity was abrogated by CS extract. Factors in the conditioned medium from CS-extract-treated U937 cells were responsible for blocking the SPE B-mediated suppression of phagocytosis. Heating the conditioned medium eliminated the increase, which suggested that the U937-cell protein products augmented phagocytosis. Analyzing cytokine mRNA expression of U937 cells revealed increases in interferon-gamma (IFN-gamma), interleukin (IL)-12 p35 and p40, and tumor necrosis factor-alpha (TNF-alpha), but not in IL-1beta, IL-6, or IL-8. Treating U937 cells with anti-IFN-gamma, IL-12, and TNF-alpha antibodies also eliminated the conditioned medium-induced increase in phagocytosis. Taken together, SPE B inhibited phagocytosis, but CS mycelium extract abrogated this inhibition by causing cytokine production.
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PMID:Abrogation of streptococcal pyrogenic exotoxin B-mediated suppression of phagocytosis in U937 cells by Cordyceps sinensis mycelium via production of cytokines. 1702 26