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

Thymus of (C57Bl/6 x DBA/2) F1 mice was examined histologically, histochemically and ultrastructurally, seven days after intravenous injection of BCG, pertussis vaccine, lipopolysaccharide or human gamma globulin, or intraperitoneal injection of complete or incomplete Freund's adjuvants or of phytohemagglutinin. Only BCG induced a marked increase of the secretory activity of the thymic epithelium at all histological sites (cortex, corticomedullary junction and medullar). Only with this adjuvant was the epithelial hyperplasia associated with marked mitotic activity and high percentage of cells with cytoplasmic pyroninophilia among cortical lymphoid cells. The other substances tested produced different changes in the thymic epithelial cells according to the histologic zones. These results suggest that the epithelial cells of the cortex, the corticomedullary junction and the medulla respond differently to the agents tested and that the action of these substances upon thymus-dependent lymphoid cells may be indirect perhaps involving factors secreted by the epithelial cells.
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PMID:The effects of certain immunity systemic advuvants, PHA, and human gamma globulin on the thymic cortex of mice: a light and electron microscope study. 6 71

(Responder [R] X nonresponder [NR])F1 mice give indistinguishable primary in vitro plaque-forming cell (PFC) responses to either R or NR parental macrophages (Mphi) pulsed with the Ir-gene controlled antigen L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT). However, such (R X NR)F1 mice, if primed to GAT, retained in vitro responsiveness to GAT-R-Mphi, but no longer responded to GAT-NR-Mphi. This suggested (a) a possible Mphi-related locus for Ir gene activity in this model, and (b) the occurrence of active suppression after priming with GAT leading to a selective loss of the usual primary responsiveness of (R X NR)F1 mice to GAT-NR-Mphi. This latter interpretation was tested in the current study. [Responder C57BL/6 (H-2b) X nonresponder DBA/1 (H-2q)]F1 mice were primed with 100 microgram GAT in pertussis adjuvant. 4-8 wk later, spleen cells from such mice were tested alone or mixed with normal unprimed F1 spleen cells for PFC responses to GAT-R-Mphi and GAT-NR-Mphi. The primed cells failed to respond to GAT-NR-Mphi, and moreover, actively suppressed the normal response of unprimed F1 cells to GAT-NR-Mphi. If the primed spleen cell donor had been treated with 5 mg/kg cyclophosphamide 3 days before priming or with 5-10 microliter/day of an antiserum to the I-Jb subregion [B10.A(5R) anti B10.A(3R)] during the first 4 days postpriming (both procedures known to inhibit suppressor T-cell activity), cells from such mice responded in secondary culture to both GAT-R-Mphi and also GAT-NR-MPhi. In addition, such spleen cells no longer were capable of suppressing normal F1 cells in response to GAT-NR-Mphi. Similar data were obtained using [CBA (H-2k) X DBA/1 (H-2q)]F1. Further, it was shown that (a) primary responsiveness to GAT-NR-Mphi was not an artifact of in vitro Mphi pulsing, because in vivo GAT-pulsed Mphi showed the same activity and (b) the secondary restriction for Mphi-antigen presentation was controlled by H-2 linked genes. These data suggest an important role for suppressor T cells in H-2 restricted secondary PFC responses, and also provide additional support for the hypothesis that Ir-gene controlled differences in Mphi antigen presentation are related to both suppressor cell generation and overall responsiveness in the GAT model.
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PMID:The involvement of suppressor T cells in Ir gene regulation of secondary antibody responses of primed (responder X nonresponder)F1 mice to macrophage-bound L-glutamic acid60-L-alanine30-L-tyrosine. 10 25

Inheritance of responsiveness to histamine-sensitizing factor of pertussis bacilli (HSF) was investigated in (C3H/HeJ times C57BL/6J)F1 hybrids, backcross progeny of this hybrid to C57BJ/6J parent (C3H/HeJ times DBA/2J)F1 hybrids, and in backcross progeny of this hybrid to DBA/2J parent. It was found that transmission is not by virtue of a single autosomal dominant gene, as has been postulated. Rather, inheritance of responsiveness to HSF is far more complex, probably involving polygenic transmission.
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PMID:Further studies on the inheritance of responsiveness to pertussis HSF in mice. 16 3

The age dependence of the susceptibility to passive anaphylactic shock was studied in the mouse. Anti-BPO IgE monoclonal antibody produced potent systemic sensitization sufficient for provocation of lethal shock in most aged (6 to 10 months) CTS, DS and C57BL/6J mice but only in a very few young (1.5 to 2.5 months) mice. A similar trend was found in the NOD strain, though it was not as definite as in the above three strains. Age-dependent potentiation of the IgE antibody-mediated anaphylactic shock was not found in both sexes of five other strains, C3H/He, DBA/2, NON, BALB/c and B6D2F1. However, the potentiation became obvious even in these strains, when they were treated with Bordetella pertussis before the antigen challenge. Age-dependent potentiation was also clear with IgG1 antibody-mediated anaphylactic shock in DS females and NON males. In contrast, no age-dependent difference was seen for the shock induced by PAF which is estimated to be the main mediator for anaphylactic shock in the mouse. This suggests that the age-dependent potentiation of anaphylactic shock does not seem to be due to elevated susceptibility to the mediator but to its increased release. The sex-dependent differences was also studied and found to be particularly clear in the case of IgG1 antibody-mediated anaphylactic shock in young DS and aged NON mice.
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PMID:Age-dependent difference in susceptibility to IgE antibody- and IgG1 antibody-mediated passive anaphylactic shock in the mouse. 179 Oct 39

The susceptibility of cataract Shionogi (CTS) mice as young as 8 to 10 weeks of age to passive anaphylactic shock mediated by anti-benzylpenicilloyl IgE and IgG1 monoclonal antibodies was compared with those of other strains of the same age including sister strains such as nonobese-diabetic (NOD) and nonobese-nondiabetic (NON). When the animals had been treated with killed Bordetella pertussis organisms, potent sensitization, enough to cause lethal shock, was produced by either monoclonal antibody preparation in CTS, NOD, C57BL/6J and DS/Shi strains, but not at all in C3H/He, DBA/2 and BALB/c strains. In the NON strain, lethal shock was elicited in the animals sensitized with the IgG1 antibody but not in those sensitized with the IgE antibody. Without the pertussis pretreatment, sensitization sufficient to cause lethal shock was produced at a high frequency by the IgG1 antibody in CTS and NOD mice but not in the other strains. When the IgE antibody was used, lethal shock was not observed in any of the mouse strains tested except for one CTS mouse. These results indicate that CTS as well as NOD are highly susceptible strains, and that IgG1 antibody is more effective than IgE antibody for producing systemic sensitization for anaphylactic shock. In addition to these findings, the results revealed an age-dependent potentiation of anaphylactic shock in CTS mice. The IgE antibody-mediated lethal shock was produced in all the aged animals of this mouse strain tested without the Bp treatment, but not in aged NOD and NON mice.
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PMID:High susceptibility of cataract Shionogi (CTS) mice to passive anaphylactic shock mediated by allogeneic IgE and IgG1 monoclonal antibodies. 187 60

Experimental autoimmune orchitis (EAO) was produced in C3H/He mice with as high as 100% incidence by two or three s.c. injections of 1 x 10(7) viable syngeneic testicular germ cells (TC) without resorting to adjuvants, Bordetella pertussis vaccine, or other immunological manipulations. On day 40 after the first injection of TC, the lesions induced were characterized by interstitial infiltration of inflammatory cells and severe hypospermatogenesis in the testis with resulting whole organ atrophy and, in contrast, by a complete lack of epididymitis. Immunological studies revealed that this form of immunization caused both delayed-type hypersensitivity and humoral antibody responses to syngeneic TC. We compared the susceptibilities to the induction of this type of EAO among six different strains of inbred mice comprising A/J, AKR, BALB/c, C3H/He, C57BL/6 and DBA/2 mice. All strains except for DBA/2 mice developed lesions of EAO to a greater or lesser extent, and severe disease was induced with high frequency in two strains, C3H/He and A/J. As this murine model of EAO can be induced without the use of Freund's complete adjuvant and B. pertussis vaccine, it is simply 'autoimmune' in nature and may provide new ways for further investigation into the immunological mechanisms which regulate deleterious autoimmune reactions to germ cell antigens leading to the male infertility.
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PMID:A new murine model of autoimmune orchitis induced by immunization with viable syngeneic testicular germ cells alone. I. Immunological and histological studies. 198 20

Earlier experiments from our laboratory revealed that the medication most commonly used for depigmenting patients with vitiligo, monobenzyl ether of hydroquinone (MBEH), when applied to the skin of DBA/2 mice caused an increase in the population density (cells/mm2) of identifiable Ia+ and ATPase+ Langerhans cells. Further, this increase in Langerhans cell density could be correlated with an increase of contact hypersensitivity (CHS) reactivity to dinitrofluorobenzene (DNFB). The current experiments demonstrated that other compounds chemically similar to MBEH, such as butylated hydroxytoluene (BHT) and butylated hydroxyanisole (BHA), which are used as preservatives/antioxidants in many topical medications, cosmetics, food, and rubber products, can in five days significantly increase the population density of Thy-1+ dendritic epidermal cells. These compounds had no effects on Ia+ cells. This observation suggests that the Thy-1+ DEC cells may be more mobile and/or their surface markers may be readily expressed and are not a slowly mobile (trafficking) population of cells as suggested by the results of previous work. In addition, these parasubstituted phenolic compounds behaved like pertussis toxin and induced Thy-1 and Ia expression on keratinocytes. These changes in Thy-1 immune markers were not accompanied by functional alterations in the immune response to contact allergens as measured by the ear swelling technique.
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PMID:Rapid induction of Thy-1 antigenic markers on keratinocytes and epidermal immune cells in the skin of mice following topical treatment with common preservatives used in topical medications and in foods. 288 82

Sensitization of mice with 1 mg of bovine serum albumin (BSA) or chicken egg albumin (EA) given intraperitoneally and 300 to 400 ng of pertussigen (pertussis toxin [Ptx]) given intravenously (i.v.) induced a high degree of anaphylactic sensitivity when the mice were challenged i.v. with 1 mg of antigen 14 days later. Regardless of H-2 haplotype, all of the strains tested (CFW, BALB/cJ, DBA/2J, and C3H.SW/SnJ) were susceptible to anaphylaxis. Sensitization of mice by a multiple-dose procedure that has been reported to induce fatal encephalopathy in mice (L. Steinman, A. Weiss, N. Adelman, M. Lim, R. Zuniga, J. Oehlert, E. Hewlett, and S. Falkow, Proc. Natl. Acad. Sci. USA 82, 8733-8736, 1982) (1 mg of BSA on day -1, 100 to 400 ng of Ptx on day zero 1 mg of BSA on day +1, 100 to 400 ng of Ptx on day +2, and 1 mg of BSA on day +6) induced shock in BALB/cJ, DBA/2J, and C3H.SW/SnJ mice, but not in CFW mice. When EA was used instead of BSA, CFW, BALB/cJ, and C3H.SW/SnJ mice did not develop fatal shock, whereas DBA/2J mice did. When dose 3 of antigen (BSA or EA) was postponed to day +21, all mouse strains sensitized by the multiple-dose procedure were found to be susceptible to shock. The fatal shock induced by this procedure, as well as that induced by giving a single sensitizing dose of antigen and Ptx, could be prevented by one to three 1-ml doses of saline given i.v. at the time signs of severe shock appeared. Although only one dose of saline was often sufficient to save the mice, two or three doses were usually needed. Microscopic changes were not found in midsagittal sections of the brains of mice sensitized by either procedure. This was true of mice that died from shock or were saved from shock by injections of saline. From these results, we concluded that the proposed model for encephalopathy induced in mice by Ptx and BSA demonstrates only the well-known anaphylactogenic effect of Ptx or pertussis vaccine. Since there are many other more sensitive methods to detect Ptx, induction of anaphylaxis is not of much value for detection or quantitation of Ptx in pertussis vaccine.
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PMID:Anaphylaxis or so-called encephalopathy in mice sensitized to an antigen with the aid of pertussigen (pertussis toxin). 355 17

Inbred strains of mice were studied for their susceptibility to the induction of experimental allergic orchitis after sensitization with mouse testicular homogenate in complete Freund's adjuvant accompanied by injections of extract from Bordetella pertussis. Susceptibility to autoimmune orchitis was found to be linked to the major histocompatibility complex in BALB/c and C57BL/10 mice and mapped to genes encoded within the H-2Dd region. In five of six groups of bidirectional (susceptible X resistant)F1 hybrids, H-2Dd-linked susceptibility was inherited as a dominant autosomal trait. However, in (BALB/cByJ X DBA/2J)F1 and (DBA/2J X BALB/cByJ)F1 hybrids, dominant autosomal resistance to the induction of autoimmune orchitis was observed. Backcross analysis between the resistant F1 hybrid and the susceptible BALB/cByJ parent suggests that a single independently segregating DBA/2J locus is capable of negating H-2Dd-linked susceptibility, and controls resistance to the induction of autoimmune orchitis.
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PMID:Experimental allergic orchitis in mice. I. Genetic control of susceptibility and resistance to induction of autoimmune orchitis. 393 96

Strains of mice (BALB/c An Bradley/Wehi, C57B1/10J, CBA/ca H Wehi, DBA/2 Wf, A/J Wehi), thought to be genetically resistant to experimental allergic encephalomyelitis (EAE) and known to be resistant to becoming hypersensitive to histamine after administration of pertussis vaccine were tested for their ability to develop EAE when purified pertussigen was included in the immunization. It was found that C57B1/10J, CBA/ca H Wehi, BALB/c An Bradley/Wehi and DBA/2 Wf developed typical signs and histologic evidence of EAE. The A/J Wehi and the B10D2/n Sn (not previously tested) strains developed only mild signs of EAE, while the known susceptible (SJL/J X BALB/c An Bradley/Wehi) F1 hybrids developed severe EAE. Histologic evidence of EAE was lacking in A/J Wehi mice and was minimal in B10D2/n Sn mice. These results suggest that neither the H-2 complex nor the gene controlling susceptibility to sensitization to histamine by administration of pertussigen are wholly responsible for susceptibility to EAE.
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PMID:Production of experimental allergic encephalomyelitis with the aid of pertussigen in mouse strains considered genetically resistant. 654 69


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