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)

Injection of chickens with FCA or FIA supplemented with either Bordetella pertussis or Nocardia rubra induced greatly increased serum levels of 7S Ig and proteins with alpha-, beta-, and gamma-mobility in electrophoresis. The serum protein changes were correlated with the development of DHS and the formation of a large allergic granuloma. The 7S Ig was considered "nonspecific" since it was not adsorbed with the bacterial cells. The alpha-, beta-, and gamma-mobility proteins were identified as acute phase proteins as they also were induced by injection of chickens with turpentine-oil; however, increased serum levels of 7S Ig were not similarly increased.
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PMID:Elevated 7S immunoglobulin and acute phase proteins in adjuvant-injected chickens. 81 35

A comparison was made of seven recognized adjuvants, Freund's incomplete and complete, alhydrogel, Corynebacterium parvum, Bordetella pertussis, muramyl dipeptide and saponin, administered with BSA or SRBC by the S.C. route of immunization. Strong selectivity as well as differences in potency were revealed in relation to these two antigens. Only FIA, FCA, alhydrogel and MDP promoted the primary response to 50 microgram of BSA, and FIA was significantly superior to FCA. Immunological memory to a low dose (0.5 microgram) of BSA, which did not evoke a primary response with any adjuvant, was potentiated by alhydrogel and by MDP and, relatively poorly, by FIA. Radioimmunoelectrophoresis showed that potentiation of the response with MDP was confined to IgG1, whereas alhydrogel, FIA and FCA stimulated both IgG1 and IgG2. Saponin was outstandingly the best adjuvant for both primary and secondary haemagglutinin responses to SRBC. Of the others, alhydrogel for the primary, and alhydrogel and B. pertussis for the secondary were active to a lesser degree. The results show that the relative potency of adjuvants differs markedly according to the antigen used, and suggest that saponin may be a particularly effective adjuvant for antigens in cell membranes.
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PMID:The comparative selectivity of adjuvants for humoral and cell-mediated immunity. I. Effect on the antibody response to bovine serum albumin and sheep red blood cells of Freund's incomplete and complete adjuvants, alhydrogel, Corynebacterium parvum, Bordetella pertussis, muramyl dipeptide and saponin. 624 82

Humoral responses to ovalbumin (OA) administered i.p. with Al(OH)3 were depressed in C57BL mice immunized 5-13 days after infection with N. dubius, but not N. brasiliensis or T. muris. These two parasites induced elevated IgM responses, possibly as a result of systemic contact with parasite larvae or debris since i.v. administered N. dubius also increased IgM titres to OA. Depression of anti-OA IgG titres by N. dubius was also observed in infected BALB/c and CBA mice given OA-Al(OH)3 (i.p.), but not in C57BL mice given OA-Al(OH)3 (s.c.), OA-FCA (i.p. or s.c.), or OA-B, pertussis (i.p.). These findings suggest that local effects of N. dubius within the peritoneum reduce the adjuvanticity of Al(OH)3, resulting in depressed responses to OA-Al(OH)3.
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PMID:Immunological consequences of intestinal helminth infections. Humoral responses to ovalbumin. 652 95

The B-cell population responsible for in vitro antigen-mediated proliferation and expansion of the memory B-cell population is a large activated blast. Such cells predominate early after antigen priming and can be regenerated by adjuvant (Bordetella pertussis) stimulation in vivo. Although these cells are proliferating in vivo, additional stimuli are needed for expansion of the memory population in vitro. These triggering requirements include specific antigen (DNP-OVA) and the assistance of adherent accessory cells. Although T cells are present in the culture, their role in the propagation of memory is not completely clear. Using the unrelated antigen, sheep erythrocytes, we have shown that "bystander" T-cell help can mediate differentiation of these memory B-cell blasts to AFC, but it cannot induce expansion of the memory-cell population. However, the fact that the TI-2 antigen DNP-Ficoll is a relatively ineffective inducer of memory-cell propagation (inducing an expanded response which is less than 10% of that induced by the T-cell-dependent antigen, DNP-OVA) suggests that T cells may be involved, possibly via production of B-cell growth factor. Thus, the minimal requirements for triggering the propagation of B-cell memory include (i) a blastogenic signal which can be mediated by adjuvant, (ii) specific antigen, and (iii) adherent accessory-cell help.
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PMID:The correlation between the activation state of B cells and their capacity for in vitro propagation of immunologic memory. 660 15

The protective immunity conferred by subcutaneous injection of outbred CD-1 mice with a killed Plasmodium yoelii (YM strain) vaccine was strongly potentiated by saponin. By adjusting the dose of antigen, the number of immunizations and the number of living parasites in the challenge infection, conditions were defined where antigen alone was non-protective but 100% protection was obtained by the addition of saponin. Inbred BALB/c, CBA/CA and C57 B1 mice were much less responsive than the CD-1 mice. The following adjuvants were compared with saponin: mineral oil emulsions (Freund's incomplete and complete adjuvants); A1(OH)3(Alhydrogel); bacteria and synthetic bacterial derivatives (Bordetella pertussis, Corynebacterium parvum and muramyl dipeptide); surface active materials (digitonin, vitamin A, Arquad 18, dimethyldioctadecyl ammonium bromide, and the polyene antibiotics, Nystatin and Amphotericin B). None of these adjuvants were as effective as saponin, although FCA, A1(OH)3 and C. parvum augmented immunity considerably. The possible reasons for the efficacy of saponin as an adjuvant for protozoal vaccines are discussed. The P. yoelli/mouse system provides a sensitive and rapid screening assay for comparison of potential adjuvants suitable for use with a malaria vaccine.
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PMID:A comparison of saponin with other adjuvants for the potentiation of protective immunity by a killed Plasmodium yoelii vaccine in the mouse. 714 65

In order to gain insight into the earliest pathological changes underlying the development of autoimmune aspermatogenic orchitis (AIAO) the blood-testis barrier was studied by light and electron microscopy, freeze-etching, and cytochemical techniques early (from 1 to 8 days after adjuvant treatment of isoimmunization). At later times (16 to 21 days) the study was carried out by light microscopy only. Adult male guinea pigs were used either as controls or immunized with Freund's complete adjuvant alone or together with pertussis vaccine. An additional group comprised animals immunized with a suspension of isologous spermatozoa emulsified in Freund's complete adjuvant and with pertussis vaccine. Ultrastructural studies of the testes of experimental animals showed, at earlier periods, apparently normal Sertoli junctions. However, in the adluminal compartment, distended gaps were seen between the facing membranes of adjacent Sertoli cells. At later periods, a massive destruction of the germinal cells were observed. In freeze-fracture replicas, the Sertoli junctions of testes belonging to all the experimental groups were characterized by an irregular network of occasionally interrupted strands of particles associated with the P face (PF). Large concavities determined distensions between interconnecting ridges. The gap junctions were increased in number and in surface. Tracer studies using horseradish peroxidase showed that the marker permeated the myoid cells of a greater proportion of tubules than in control animals. Within the seminiferous epithelium there was only a limited passage of the marker towards the lumina of the tubules. Yet the tracer was always excluded from the adluminal compartment by the Sertoli tight junctions. Our observations suggest the possibility that the FCA causes a loosening of the Sertoli junctions. This condition could enhance exchanges between two antigenically different cellular compartments and, thus, favor occurrence of an autoimmune reaction when cytotoxic factors are experimentally induced, as in iso- or autoimmunization.
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PMID:Effects of immunization with Freund's complete adjuvant and isologous spermatozoa on the seminiferous epithelium and blood-testis barrier in guinea pigs. 721 20

We have previously shown that the S-prenylated cysteine analogue N-acetyl-S-trans,trans-farnesyl-L-cysteine (L-AFC) inhibits basal and formyl peptide receptor-stimulated binding of guanosine 5'-O-(3-thiotriphosphate) (GTP[S]) to and hydrolysis of GTP by membranes of HL-60 granulocytes and have presented evidence suggesting that this inhibition was not caused by reduced protein carboxyl methylation [Scheer, A., & Gierschik, P. (1993) FEBS Lett. 319, 110-114]. We now report a detailed analysis of the structural properties of S-prenylated cysteine analogues required for this inhibition and demonstrate that S-prenylcysteines also suppress basal and receptor-stimulated GTP[S] binding to human peripheral neutrophil and HL-60 granulocyte membranes when stimulated by formyl peptide and complement C5a, respectively. S-Prenylcysteines did not affect pertussis toxin-mediated [32P]ADP-ribosylation of Gi proteins. The inhibitory effect of L-AFC was reversible and was not mimicked by farnesylic acid. L-AFC also interfered with GTP[S] binding to retinal transducin when stimulated by light-activated rhodopsin in a reconstituted system. This inhibitory effect was fully reversed upon increasing the concentration of either the G protein beta gamma dimer or the activated receptor. On the basis of these results, we suggest that S-prenylated cysteine analogues like L-AFC inhibit receptor-mediated G protein activation by specifically and reversibly interfering with the interaction of activated receptors with G proteins, most likely with their beta gamma dimers, rather than by inhibiting alpha.beta gamma heterotrimer formation.
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PMID:S-prenylated cysteine analogues inhibit receptor-mediated G protein activation in native human granulocyte and reconstituted bovine retinal rod outer segment membranes. 771 Oct 17

Antigen induced arthritis is a unilateral T-cell driven model caused by direct injection of an antigen into the knee joint of a FCA preimmunized animal. The chronicity is determined by antigen retention in avascular structures of the joint through charge mediated binding or antibody mediated trapping. Cationicity of the antigen is a prerequisite in this model in the mouse and commercial mBSA is a suitable antigen. Cartilage erosive character is strongly enhanced in the presence of marked antibody titer. Concomitant boosting of the immune response with Bordetella pertussis adds to this. T-cell mediated flares can be induced by local or systemic rechallenge with low dose antigen, and display a strong erosive phenotype.
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PMID:Murine antigen-induced arthritis. 1798 53