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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Stimulation of normal rat splenic T cells with pertussigen (lymphocytosis-promoting factor, LPF, from Bordetella pertussis) resulted in the release of a soluble factor that enhanced the glycosylation of IgE-binding factors during their biosynthesis. The soluble factor was detected by the ability of a culture filtrate of LPF-stimulated spleen cells to switch a T cell hybridoma, 23A4, from the formation of unglycosylated IgE-binding factor to the formation of glycosylated IgE-binding factor. The glycosylation-enhancing factor (GEF) had affinity for D-galactose, and the binding of the factor to hybridoma cells via a cell surface galactose was essential for modulation of IgE-binding factors. The GEF was inactivated by irreversible inhibitors of serine proteases such as phenylmethylsulfonyl fluoride, diisopropylfluorophosphate, and p-nitrophenyl ethylpentylphosphonate but was not affected by nonphosphorylating analogues of the organophosphorus compounds. Benzamidine, a competitive and reversible inhibitor of trypsin, also inhibited the glycosylation of IgE-binding factors by GEF. The factor could be purified by absorption to p-aminobenzamidine agarose followed by elution with benzamidine. The capacity of GEF to enhance the glycosylation of IgE-binding factors was inhibited by synthetic substrates of trypsin but not by substrates of chymotrypsin, indicating that GEF is a trypsin-like enzyme. Indeed, trypsin, plasmin, and kallikrein enhanced the glycosylation of IgE-binding factors during their biosynthesis. An inhibitor of trypsin-like enzyme(s), N-alpha-p-tosyl-L-lysine chloromethylketone (TLCK), inhibited trypsin and plasmin but not kallikrein, and TLCK failed to inhibit the GEF-mediated enhancement of glycosylation. It was also found that bradykinin, the biologically active product of cleavage of kininogen by kallikrein, enhanced the glycosylation of IgE-binding factors. The results indicate that GEF is a kallikrein-like enzyme.
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PMID:Modulation of the biologic activities of IgE-binding factor. IV. Identification of glycosylation-enhancing factor as a kallikrein-like enzyme. 655 15

T lymphocytes of rats treated with Bordetella pertussis vaccine (BP) formed a soluble factor that enhanced the glycosylation of IgE-binding factors during their biosynthesis, and provided the latter factors with the biologic activity to potentiate the IgE response. The present experiments demonstrated that pertussigen (leukocytosis-promoting factor) from BP induced normal rat spleen cells to form the glycosylation-enhancing factor. The same factor was obtained by incubation of normal spleen cells with 5 micrograms/ml, but not 2 micrograms/ml, concanavalin A. When normal rat mesenteric lymph node cells were incubated with the glycosylation-enhancing factor together with IgE, IgE-binding factors formed by the cells selectively potentiated the IgE response. The IgE-binding factors formed by the same cells upon incubation with IgE alone neither enhanced nor suppressed the IgE response. The glycosylation-enhancing factor changed the nature of IgE-binding factors formed by the rat-mouse T cell hybridoma, 23A4. IgE-binding factors induced by IgE alone lacked affinity for lentil lectin, whereas those induced by IgE in the presence of the glycosylation-enhancing factor had affinity for the lectin. The cell source of the glycosylation-enhancing factor appeared to be W 3/25+ Fc gamma R+ T cells. The glycosylation-enhancing factor was protein in nature and had a m.w. of about 25,000. The factor had affinity for acid-treated Sepharose and could be recovered from the beads by elution with lactose. The factor was different from interleukin 2 with respect to both its affinity for galactose and its isoelectric point.
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PMID:Modulation of the biologic activities of IgE-binding factor. II. Physicochemical properties and cell sources of glycosylation-enhancing factor. 660 Nov 39

Continued treatment with monoclonal anti-IgD (Ig-5a) from birth in BALB/c mice causes a markedly increased responsiveness to i.v. injected dinitrophenylated ovalbumin (DNP-OVA) with Bordetella pertussis at the age of 8 weeks. The 19S plaque-forming cell (PFC)/spleen response is particularly enhanced, 6-8-fold, but all the other isotypes also show increases of 2-6-fold, including IgA and IgE. Both primary and secondary PFC responses and serum antibody titers are enhanced. After transfer of spleen cells from anti-Ig-treated mice to irradiated recipients the IgM/IgG ratio becomes similar to that of controls. In contrast, the response of anti-IgD-treated mice to i.p. immunization with either 0.2 or 100 micrograms DNP-OVA plus alum is reduced by approximately 80% for each Ig isotype except IgM and remains low upon transfer of spleen cells to recipients. It is concluded that the paucity of B cells in peripheral lymph nodes of the anti-IgD-treated mice causes the low responsiveness to i.p. immunization, but that the IgD- B cells in the spleen are quite able to respond and are, in fact, more responsive than IgD+ B cells. This increased responsiveness, together with the higher IgM/IgG ratios for all Ig isotypes and an otherwise similar order of isotype distribution (gamma 1 greater than gamma 2b greater than gamma 2a = epsilon greater than or equal to alpha) as in controls, suggests that a hyperresponsive, but less mature IgD- B cell population is selectively produced in the spleens of mice treated with anti-IgD from birth.
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PMID:Physiology of IgD. III. Effect of treatment with anti-IgD from birth on the magnitude and isotype distribution of the immune response in the spleen. 660 69

Following i.p. injection of ovalbumin (OVA) plus Bordetella pertussis vaccine into Hooded Lister rats, the time-course of sensitization of peritoneal and lung mast cells (MC) did not parallel kinetic changes in the levels of circulating OVA-specific and total IgE. OVA-induced secretion of 5-hydroxytryptamine from isolated peritoneal and lung MC and the presence of OVA-specific IgE in serum were first demonstrated at day 14 post-immunization. However, subsequent to day 14, the responsiveness of both types of MC to OVA declined, while circulating levels of OVA-specific IgE continued to rise. Peritoneal MC, but not lung MC, showed increased responsiveness to challenge with anti-IgE on day 7 post-immunization, whereas circulating levels of total IgE were not elevated until day 14, thus demonstrating that nonantigen-specific IgE was acquired by peritoneal MC before it entered the circulation. Lung MC generally showed decreased reactivity to both OVA and anti-IgE, compared with peritoneal MC; no significant correlations were demonstrated between the responses of MC from these two tissue sites.
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PMID:The kinetics of in vivo sensitization of rat peritoneal and lung mast cells: temporal dissociation from circulating levels of IgE. 666 89

Treatment of rats with Conjuvac induced no anti-pollen extract (PE) IgE and no sensitization, whereas alum-adsorbed pollen extract induced IgE antibody and marked sensitivity. Conjuvac induced anti-PE IgE in rats treated with Bordetella pertussis organisms but the antibody concentrations were less than those induced by PE with B. pertussis. There was no indication, either in rats injected with B. pertussis and Conjuvac or alginate (ALG), of sensitization to ALG. In guinea pigs, Conjuvac induced immediate hypersensitivity to PE but there was no delayed hypersensitivity. Furthermore, no immediate hypersensitivity and little or no delayed hypersensitivity to ALG was detected in guinea pigs injected with conjuvac or ALG. Histological studies at Conjuvac injection sites in rabbits revealed inflammatory reactions less intense than those produced by aluminium hydroxide.
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PMID:Grass Conjuvac. II. Pro-inflammatory activity and potential for inducing hypersensitivity. 669 79

Mice sensitized with two intraperitoneal injections of ovalbumin and challenged intranasally with the same antigen developed a non-fatal anaphylactic shock peaking in severity 30 min after challenge. Increases in haematocrit were noted which corresponded to the severity of signs of shock displayed by mice. Severity of shock also correlated with IgE and IgG levels. Sensitization by the nasal route, and use of B. pertussis vaccine as adjuvant had no qualitative effect upon the response. Cobra venom factor depletion of C3 in vivo did not alter the response of mice, which suggests anaphylaxis did not involve complement activation. Sensitivity was not transferrable to non-immune mice with serum. Passive sensitization with polyclonal and monoclonal antibodies produced inconsistent results. Possible mechanisms of anaphylaxis are discussed.
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PMID:Anaphylaxis following intranasal challenge of mice sensitized with ovalbumin. 670 76

Ammonium tetrachloroplatinate II ([NH4]2 PtCl4) was used in free and conjugated forms with ovalbumin in an attempt to elicit specific antibody directed against either the free platinum (Pt) salt or the platinum moiety of ovalbumin-Pt conjugates in the hooded Lister rat. Immunization with free Pt salt via intraperitoneal, intramuscular, intradermal, subcutaneous, intratracheal and footpad routes over a wide range of doses (1 microgram-1 mg) employing both B. pertussis and/or aluminium hydroxide gel as adjuvants failed to induce specific IgE antibody, either primary or secondary, as shown by direct skin, PCA test or RAST. Conjugation of (NH4)2 PtCl4 with ovalbumin produced conjugates, with between two and 10 haptenic Pt groups per ovalbumin molecule, capable of inducing IgE antibody directed against the Pt moiety as determined by heterologous PCA challenge, where carrier cross-reactivity was excluded, and by specific RAST, confirmed by RAST inhibition.
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PMID:Immunological responses to complex salts of platinum. I. Specific IgE antibody production in the rat. 674 66

Optimal conditions were established for induction of reaginic antibodies to Lolium perenne pollen allergens in mice by intranasal dosing of allergens with Bordetella pertussis vaccine. This antibody response could be inhibited by pretreatment of the mice by nasal administration of 100 microgram of glutaraldehyde-modified L. perenne allergens 9 times in 3 weeks before priming, whereas native allergens, in doses of 5 microgram, did not inhibit an IgE response to subsequent priming. It was not possible to suppress an ongoing reaginic antibody response by intranasal treatment with either native allergens, or glutaraldehyde-modified allergens. Relevance to immunoprophylaxis of allergic disease is discussed.
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PMID:Inhibition of murine reaginic antibody responses by nasal immunotherapy with modified allergen. 676 24

Bordetella pertussis organisms, with or without a small dose of alumhydroxide, enhance in rats the production of IgE antibodies to an unrelated antigen, even if this antigen has been administered 6 weeks beforehand. This non-specific enhancement of IgE antibodies is accompanied by a substantial rise in total serum IgE and by the production of IgE antibodies to B. pertussis. The effect of B. pertussis on IgE synthesis is dose-dependent. No effect of B. pertussis on IgE production can be observed in nude rats.
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PMID:The non-specific enhancement of allergy. I. In vivo effects of Bordetella pertussis vaccine on IgE synthesis. 686 2

An i.p. injection of Bordetella pertussis vaccine (BP) into rats induced the formation of soluble factors that had affinity for IgE (IgE-binding factors). The factor was detected in the serum of BP-treated animals 5 to 7 days after the treatment. Their circulating lymphocytes as well as spleen cells spontaneously released IgE-binding factors in the serum of BP-treated rats and those released from their circulating lymphocytes had affinity for lentil lectin, and the ability to selectively potentiate an in vitro IgE response of DNP-OA primed cells to homologous antigen. The molecular size of IgE-potentiating factor was between 10,000 and 20,000, and was comparable to that formed by lymphocytes of rats infected with Nippostrongylus brasiliensis. Evidence was obtained that IgE-potentiating factor was derived from Fc epsilon R(+) T cells, with a T cell marker identified by monoclonal antibody W 3/25. Their production of IgE-potentiating factor may be the basis of the adjuvant effect of BP on the IgE response.
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PMID:Regulatory role of IgE-binding factors from rat T lymphocytes. V. formation of IgE-potentiating factor by T lymphocytes from rats treated with Bordetella pertussis vaccine. 697 Feb 22


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