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)

Sprague Dawley rats were sensitized with 20 microgram or 100 mg egg albumin (using pertussis vaccine as adjuvant). Mast cells isolated from the former group of animals showed a higher degree of histamine release upon challenge in vitro with egg albumin than those from the latter group. Using the lower amount of antigen for immunization mast cells from Hooded Lister rats showed an even higher degree of histamine release induced by antigen. An increased antigen-induced histamine release was associated with an increased spontaneous and phosphatidylserine-induced histamine release. Histamine release induced by phosphatidylserine was found to be specific in so far as it was calcium dependent and theophylline-inhibited. The basal level of cyclic AMP in mast cells was significantly depressed by sensitization. There was a relationship between the cyclic AMP/cyclic GMP ratio and the degree of spontaneous, phosphatidylserine-induced and anaphylactic histamine release. The results suggest that sensitization induces an increased release of histamine not only to the specific antigenic stimulus but also to more unspecific stimuli. Concomitantly there is a fall in the cyclic AMP/cyclic GMP ratio. The relationship between these two phenomena is discussed.
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PMID:Effect of sensitization on spontaneous and phosphatidylserine-induced histamine release and on cyclic AMP and GMP levels in isolated rat mast cells. 9 6

The effects of exogenous nucleotides on the histamine hypersensitivity of pharmacologically beta-blocked mice were investigated. Female HLA-SW (ICR) mice, 27-29 gm, were injected intraperitoneally with 20 to 100 mug of propranolol 45 min before intraperitoneal challenge with 1 mg histamine. These animals had a mortality which averaged approximately 80%. At various time intervals before histamine, doses of from 0.5 to 12 mumoles of nucleotides were administered intravenously. Noncyclic nucleotides, adenosine, adenosine 5'-monophosphate (AMP), and guanosine 5'-monophosphate (GMP) showed clear, dose-response protection against histamine death of propranolol-treated mice when they were given 45 to 90 min before histamine. Cyclic AMP showed significant protection only when it was given at a dose of 8 mumoles 45 to 90 min before histamine, and lower or higher doses gave equivocal or no protection. Cyclic GMP WAS Not protective at any dose tested. Propranolol treatment also produced enhanced sensitivity to passive systemic anaphylaxis. Mice were passively sensitized by intraperitoneal injection of mouse anti-egg albumin antibody 6 hr before intravenous challenge with 0.5 mg egg albumin. The mortality from anaphylaxis in the group treated with 20 mug propranolol 45 min before antigen challenge increased to 83%, while that of the group not given propranolol was only 10%. Nucleotides were given intravenously 45 min before antigen challenge. The nucleotides that protected mice from death due to histamine challenge also protected them from death due to systemic anaphylaxis. These protective nucleotides were the same nucleotides that had been reported previously to be protective against Bordetella pertussis-induced hypersensitivity to histamine and anaphylaxis.
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PMID:Hypersensitivity to histamine and systemic anaphylaxis in mice with pharmacologic beta adrenergic blockade: protection by nucleotides. 18 34

Pulmonary levels of cGMP and cAMP in mice sensitized to methacholine and histamine with B. pertussis were examined to determine whether sensitization could be the result of an alteration in the metabolism of these cyclic nucleotides. The results presented show that in sensitized mice, methacholine raised cGMP to levels that were about double those produced without sensitization. In analogous experiments, histamine raised cGMP by approximately 100% in sensitized mice without producing significant increases in nonsensitized groups. Atropine completely blocked the cGMP rises produced by methacholine but did not eliminate those produced by histamine, thus indicating that cholinergic, but not the histaminergic elevation of cGMP involves activation of muscarinic receptors. The influence of pertussis on cAMP appeared to be opposite in direction from cGMP, i.e., a small but significant drop in cAMP levels was found following methacholine administration to sensitized, but not to nonsensitized mice. It was concluded that pertussis sensitization increases the responsiveness of the pulmonary guanylate cyclase-cGMP system to methacholine and histamine, and that the altered patterns of cGMP accumulation may contribute to the biochemical mechanism of sensitization.
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PMID:Effects of methacholine, histamine and atropine on pulmonary guanosine-3', 5'-monophosphate levels in hypersensitive mice. 18 63

Prostaglandin synthesis inhibitors (indomethacin and acetylsalicylic acid) were studied in mice under control conditions and during a period of B. pertussis-induced increased sensitivity to histamine. These compounds were employed to inhibit the generation of prostaglandins and thus allow for analysis of prostaglandin participation in the heightened accumulation of pulmonary cyclic nucleotides in pertussis-sensitized mice. The results show that the two non-steroid antiinflammatory agents studied caused a reduction in basal cyclic GMP levels in pulmonary tissue of mice. Cyclic AMP levels were unaltered. Histamine raised cyclic GMP levels in sensitized mice even in the presence of cyclo-oxygenase inhibition, but these rises never exceeded basal levels in mice that had not received cyclo-oxygenase inhibitors. It can be concluded that prostaglandin synthesis inhibitors suppress the cyclic GMP system.
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PMID:Divergent effects of prostaglandin synthesis inhibitors on pulmonary cyclic 3', 5'-adenosine monophosphate and cyclic 3', 5'-guanosine monophosphate levels in untreated and histamine sensitized mice. 23 Jul 93

5-hydroxytryptamine (5-HT) is a mitogen for fibroblasts, vascular smooth muscle cells, renal mesangial cells, and jejunal crypt cells. The human carcinoid cell line (termed BON) that we established in our laboratory from a pancreatic carcinoid tumor produces and secretes 5-HT. In this study, therefore, we examined the effect of 5-HT on growth of BON cells. Furthermore, by use of selective 5-HT receptor antagonists, we examined receptor and post-receptor mechanisms by which 5-HT-induced responses were produced. 5-HT stimulated growth of BON cells. 5-HT stimulated phosphatidylinositol (PI) hydrolysis in a dose-dependent fashion and inhibited cyclic AMP production in a dose-dependent fashion. The 5-HT1A/1B receptor antagonist, SDZ 21-009, prevented the reduction of cyclic AMP production evoked by 5-HT and inhibited the mitogenic action of 5-HT. The 5-HT1C/2 receptor antagonist, mesulergine, competitively inhibited PI hydrolysis, but did not affect the mitogenic action of 5-HT. The mitogenic action of 5-HT and the reduction of cyclic AMP production evoked by 5-HT were also inhibited by pertussis toxin. These results suggest that 5-HT is an autocrine growth factor for BON cells and that mitogenic mechanism of 5-HT involves receptor-mediated inhibition of the production of cyclic AMP which may be linked to pertussis toxin-sensitive GTP binding protein. 8-bromo-cyclic AMP inhibited growth of BON cells whereas 8-bromo-cyclic GMP had no effect on cell growth. Involvement of protein kinase A in BON cell growth regulation was confirmed by the observation that a cAMP-dependent protein kinase antagonist (Rp-cAMPS) could stimulate BON cell growth.
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PMID:Receptor-mediated autocrine growth-stimulatory effect of 5-hydroxytryptamine on cultured human pancreatic carcinoid cells. 130 21

To understand the signals transmitted by interleukin-2 (IL-2) during T-cell proliferation, the effect of this cytokine was compared to the bacterial product pertussis toxin (PT). Both IL-2 and PT induced the incorporation of [3H]thymidine into T cells. Cholera toxin (CT) inhibited IL-2-induced, but enhanced PT-induced T-cell proliferation. The effect of CT is mimicked by the cyclic AMP (cAMP) analogue 2'-O-dibutyryladenosine 3':5'-cyclic monophosphate (dicAMP) or by the phosphodiesterase inhibitors isobutylmethylxanthine and aminophylline. Measurement of the intracellular level of cAMP showed that CT enhanced this level during both IL-2 or PT incubation with T cells. To delineate the differential effects of cAMP on IL-2 versus PT activity, it was observed that the blocker of intracellular calcium (TMB8), or the guanosine triphosphate (GTP) analogue (GTP gamma S) inhibited both PT and IL-2 activities, whereas the protein kinase C (PKC) inhibitor (H7) was without effect for both stimuli. Further experiments showed that both IL-2 and PT stimulate the endogenous level of cGMP and that CT enhanced this level following PT activation, but reduced it following IL-2 activation of T cells. Hence, there is a major difference between IL-2 and PT activation of T cells in as far as their susceptibility to treatment with cholera toxin is concerned. Furthermore, an increase of cGMP level resulted in the enhancement of proliferation, whereas a decrease in cGMP level resulted in the inhibition of proliferation.
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PMID:Cholera toxin inhibits interleukin-2-induced, but enhances pertussis toxin-induced T-cell proliferation: regulation by cyclic nucleotides. 131 Dec 82

N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) causes a concentration-dependent increase of the cGMP level in rabbit peritoneal neutrophils. MNNG has a strong chemokinetic effect on neutrophils. In addition the compound also possesses a moderate chemotactic effect. The potentiating effect of MNNG on neutrophil migration is completely inhibited by pertussis toxin. The results support the view that in neutrophils cGMP is involved in chemokinesis and chemotaxis and that the cGMP-mediated potentiation of migration is controlled by a pertussis toxin-sensitive G-protein.
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PMID:N-methyl-N'-nitro-N-nitrosoguanidine: the effect on migration and cGMP level of neutrophils. 131 69

Studies were performed to examine the regulation of atrial natriuretic peptide- (ANP) stimulated guanylate cyclase in the the inner medulla. Primary cultures of rat inner medullary collecting tubular cells exposed to 10(-7) M ANP increased cGMP formation to 31.2 +/- 1.8 compared to the basal production of 2.1 +/- 0.6 fm/micrograms protein. This response did not appear to be transduced via a Gi protein, as preincubation with pertussis toxin did not alter the response to 10(-7) M ANP, and saponized cells exposed to 10 microM GTP gamma S did not enhance the response to ANP (77.3 +/- 5.9 vs. 86.7 +/- 6.3 g/micrograms). Likewise, changes in extracellular Ca2+ from 0.5 to 3.0 mM, decrements in intracellular Ca2+ with EGTA or increments in intracellular Ca2+ with ionomycin (5 microM) did not significantly alter the response to ANP. Neither activation of protein kinase A with forskolin (36.5 +/- 5.1) nor of protein kinase C with s,n-1,2-dioctanoylglycerol (33.2 +/- 2.5) altered the response to 10(-7) M ANP (32.2 +/- 3.3, NS). As the inner medullary environment was hypertonic, the effect of altering tonicity was studied. Cells grown for 48 hours in hypertonic media (600 mOsm/kg H2O) displayed enhanced response to 10(-8) and 10(-7) M ANP when osmolality was raised by either Na+ alone or in combination with urea, but not by urea alone. Our studies demonstrate that ANP-stimulated guanylate cyclase is insensitive to alterations in either intra- or extracellular Ca2+, is not subject to inhibition by protein kinase, and does not involve a pertussis-sensitive G protein.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regulation of atrial natriuretic peptide-stimulated cGMP production in the inner medulla. 131 78

A protein that binds kainate with high affinity has been purified and cloned from frog brain (Rana pipiens) and has approximately 35% sequence homology with mammalian non-N-methyl-D-aspartate glutamate receptors, some of which have been shown to be ligand-gated ion channels. Frog brain membranes and membranes from Chinese hamster ovary (CHO) cells transfected with the cDNA coding for the frog kainate-binding protein (CHO-4 cells) bound kainate with essentially identical affinity (KD values of 1.9 and 2.1 nM, respectively). In both tissues, the affinity for kainate decreased 9-fold in the presence of 100 microM GTP gamma S (guanosine 5'-O-(3-thio)triphosphate). No specific kainate binding to nontransfected CHO cell membranes was observed. GTP gamma S and GDP were effective inhibitors of kainate binding, while cGMP and adenosine 5'-O-(3-thio)triphosphate had no effect in either frog brain membranes or CHO-4 membranes. Pretreatment of CHO-4 cell membranes with pertussis toxin led to a 34% decrease in kainate binding. Kainate increased the binding of [3H]5'-guanylyl imidodiphosphate by 61%, and the rate of GTP hydrolysis by up to 5-fold. These results indicate that the kainate receptor cloned from frog brain can interact functionally with a G protein present in CHO-4 cell membranes.
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PMID:Interaction of the frog brain kainate receptor expressed in Chinese hamster ovary cells with a GTP-binding protein. 132 45

Transducin (T alpha beta gamma), the heterotrimeric GTP-binding protein that interacts with photoexcited rhodopsin (Rh*) and the cGMP-phosphodiesterase (PDE) in retinal rod cells, is sensitive to cholera (CTx) and pertussis toxins (PTx), which catalyze the binding of an ADP-ribose to the alpha subunit at Arg174 and Cys347, respectively. These two types of ADP-ribosylations are investigated with transducin in vitro or with reconstituted retinal rod outer-segment membranes. Several functional perturbations inflicted on T alpha by the resulting covalent modifications are studied such as: the binding of T alpha to T beta gamma to the membrane and to Rh*; the spontaneous or Rh*-catalysed exchange of GDP for GTP or guanosine 5-[gamma-thio]triphosphate (GTP[gamma S]), the conformational switch and activation undergone by transducin upon this exchange, the activation of T alpha GDP by fluoride complexes and the activation of the PDE by T alpha GTP. ADP-ribosylation of transducin by CTx requires the GTP-dependent activation of ADP-ribosylation factors (ARF), takes place only on the high-affinity, nucleotide-free complex, Rh*-T alpha empty-T beta gamma and does not activate T alpha. Subsequent to CTx-catalyzed ADP-ribosylation the following occurs: (a) addition of GDP induces the release from Rh* of inactive CTxT alpha GDP (CTxT alpha, ADP-ribosylated alpha subunit of transducin) which remains associated to T beta gamma; (b) CTxT alpha GDP-T beta gamma exhibits the usual slow kinetics of spontaneous exchange of GDP for GTP[gamma S] in the absence of Rh*, but the association and dissociation of fluoride complexes, which act as gamma-phosphate analogs, are kinetically modified, suggesting that the ADP-ribose on Arg174 specifically perturbs binding of the gamma-phosphate in the nucleotide site; (c) CTxT alpha GDP-T beta gamma can still couple to Rh* and undergo fast nucleotide exchange; (d) CTxT alpha GTP[gamma S] and CTxT alpha GDP-AlFx (AlFx, Aluminofluoride complex) activate retinal cGMP-phosphodiesterase (PDE) with the same efficiency as their unmodified counterparts, but the kinetics and affinities of fluoride activation are changed; (e) CTxT alpha GTP hydrolyses GTP more slowly than unmodified T alpha GTP, which entirely accounts for the prolonged action of CTxT alpha GTP on the PDE; (f) after GTP hydrolysis, CTxT alpha GDP reassociates to T beta gamma and becomes inactive. Thus, CTx catalyzed ADP-ribosylation only perturbs in T alpha the GTP-binding domain, but not the conformational switch nor the domains of contact with the T beta gamma subunit, with Rh* and with the PDE.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Functional modifications of transducin induced by cholera or pertussis-toxin-catalyzed ADP-ribosylation. 133 64


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