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)

The nature of the leukotriene-D4 (LTD4) induced cell shrinkage in Ehrlich ascites tumor cells has been investigated. LTD4 treatment of Ehrlich cells induces net loss of cellular KCl and cell shrinkage independent of the initial cell volume. LTD4 also produces water loss and reduction in cell volume when all extracellular and all intracellular Cl has been replaced by NO3. On the other hand, LTD4 fails to produce any significant changes in cell volume in the presence of the K-channel blocker quinine, suggesting that LTD4 in Ehrlich cells induces Cl-independent K loss through the Ca2+-dependent K channels. However, the effect of physiological doses of LTD4 on cell volume seems not to be as potent in Cl-free, NO3 cells when compared to Cl-containing cells, indicating that LTD4 in Ehrlich cells also provokes Cl-dependent K loss. LTD4 seems not to produce K loss through an electroneutral K+/H+ exchange system. LTD4 still produces Cl-independent K loss and cell shrinkage in the presence of the anti-calmodulin drug pimozide but not in the presence of the LTD4 receptor antagonist L-649,923 or the 5-lipoxygenase inhibitor NDGA. Pretreatment of the cells with pertussis toxin, which inactivates inhibitory guanine nucleotide binding proteins (G-proteins), leads to partial inhibition of the LTD4-induced shrinkage. It is suggested that the LTD4-induced activation of K and Cl transporting systems in Ehrlich ascites tumor cells is mediated via a G-protein coupled receptor and that LTD4 might exert its effect through another lipoxygenase product. The Ca2+-calmodulin complex is not involved in the LTD4-induced activation of K and Cl transporting systems.
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PMID:Leukotriene-D4 induced cell shrinkage in Ehrlich ascites tumor cells. 247 62

Endothelins (ET) produce endothelium-dependent vasodilation through nitric oxide (NO) synthesis. The present study was designed to elucidate the cellular mechanism by which ET induces synthesis and release of endothelium-derived NO by cultured bovine endothelial cells (EC). Binding studies revealed that bovine EC membrane had the binding sites of a novel agonist (BQ3020) for non-isopeptide-selective receptor subtype (ETB). Affinity labeling studies showed a major labeled band with the apparent molecular mass of 50 kD. Northern blot analysis demonstrated the expression of mRNA for ETB receptor. BQ3020 rapidly and dose dependently induced formation of inositol-1,4,5-triphosphate and increased intracellular Ca2+ concentrations in fura-2-loaded cells. Concomitantly, BQ3020 dose dependently stimulated production of both nitrate/nitrite (NOx) and cyclic GMP; a highly significant correlation existed between NOx and cGMP production. The stimulatory effect on NOx and cGMP production by ETB agonist was inhibited by NO synthase inhibitor monomethyl-L-arginine; this effect was reversed by coaddition of L-arginine, but not D-arginine. NOx and cGMP production stimulated by BQ3020 was inhibited by pretreatment with pertussis toxin. ETB agonist-induced NOx production was blocked by a calmodulin inhibitor and an intracellular Ca2+ chelator, but not by an extracellular Ca2+ chelator or a Ca2+ channel blocker. These data suggest that endothelins stimulate ETB receptor-mediated phosphoinositide breakdown via pertussis toxin-sensitive G-protein(s), which triggers release of intracellular Ca2+, thereby activating Ca2+/calmodulin-dependent NO synthase in EC.
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PMID:Endothelin receptor subtype B mediates synthesis of nitric oxide by cultured bovine endothelial cells. 768 70

Exposure of cultured endothelial cells to shear stress resulting from well-defined fluid flow stimulates the production of nitric oxide (NO). We have established that an initial burst in production is followed by sustained steady-state NO production. The signal transduction events leading to this stimulation are not well understood. In the present study, we examined the role of regulatory guanine nucleotide binding proteins (G proteins) in shear stress-mediated NO production. In endothelial cells not exposed to shear stress, AIF4-, a general activator of G proteins, markedly elevated the production of guanosine 3',5'-cyclic monophosphate (cGMP). Pretreatment with NO synthase inhibitor N omega-nitro-L-arginine completely blocked this stimulation. Incubation with guanosine 5'-O-(2-thiodiphosphate) (GDP beta S), a general G protein inhibitor, blocked the flow-mediated burst in cGMP production in a dose-dependent manner. Likewise, GDP beta S inhibited NOx (NO2 + NO3) production for the 1st h. However, inhibition was not detectable between 1 and 3 h. Pertussis toxin (PTx) had no effect on the shear response at any time point. The burst in NO production caused by a change in shear stress appears to be dependent on a PTx-refractory G protein. Sustained shear-mediated production is independent of G protein activation.
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PMID:Role of G proteins in shear stress-mediated nitric oxide production by endothelial cells. 794 4

1. We have previously reported that the Na+ conductance in mouse intralobular salivary duct cells is controlled by cytosolic anions, being inhibited by high cytosolic concentrations of Cl- and NO3- but not of glutamate. In the present paper, we use whole-cell patch-clamp methods to investigate whether this anion effect is mediated by a G protein. 2. Inclusion of 100 mumol l-1 GTP-gamma-S, a non-hydrolysable GTP analogue, in the glutamate-containing pipette solution, i.e. when the Na+ conductance is active, reduced the size of the Na+ conductance whereas inclusion of 100 mumol l-1 GDP-beta-S, a non-hydrolysable GDP analogue, had no effect. 3. Inclusion of 100 mumol l-1 GDP-beta-S in the NO3(-)-containing pipette solution, i.e. when the Na+ conductance is inhibited, reactivated the conductance. Inclusion of 500 ng ml-1 activated pertussis toxin in the NO3(-)-containing pipette solution had a similar effect on the Na+ conductance. 4. We conclude that the inhibitory effect of intracellular anions such as NO3- and Cl- on the amiloride-sensitive Na+ conductance in mouse mandibular intralobular duct cells is mediated by a G protein sensitive to pertussis toxin.
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PMID:Control of the amiloride-sensitive Na+ current in mouse salivary ducts by intracellular anions is mediated by a G protein. 854 20

During the pertussis clinical trials, the best conditions for isolating B. pertussis were determined. Isolation is higher if two nasopharyngeal aspirates are collected, transport is carried out at ambient temperature and takes no longer than 48 hours, Reagan Lowe or Bordet Gengou selective and non-selective plates are used and incubated at 36 degrees C for seven days. Identification must include Gram stain and urease, oxidase and nitrate reactions. Confirmation is obtained with specific anti-B. pertussis antiserum. Characterization of the isolates can be performed by using the polymerase chain reaction, serotyping and pulsed-field gel electrophoresis.
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PMID:Isolation, identification and characterization of Bordetella pertussis. 927 55

To investigate effect of MMLA, an inhibitor of nitric oxide (NO) production, on regulation of inflammatory responses to Bordetella pertussis infection, mice were infected intranasally, and treated with various concentrations of MMLA. Ten days after infection, mice treated with MMLA at dosage of 100 mg/kg, given intraperitoneally in a single dose or for 5 consecutive days, showed at histopathologic examination, a significant decrease of intensity of inflammation (scores, 0.6 +/- 0.2 and 0.9 +/- 0.5 respectively). A decrease of cellular accumulation of neutrophils and lymphocytes in the bronchoalveolar lavage (BAL) fluid was observed in infected mice treated with MMLA, especially at dosage of 10 mg/kg, given in a single dose intraperitoneally. In addition, BP-infected mice treated with MMLA (100 mg/kg, intraperitoneally) for 5 consecutive days showed higher mortality rate than untreated mice infected with B. pertussis, and the number of B. pertussis in lungs of mice treated with MMLA was significantly increased. However, MMLA treatment of infected mice had some effect on levels of IFN-gamma and nitrite/nitrate (end-stable products of NO) in the BAL fluid. This study indicates that NO may play a role either as microbiocidal agent or as a modulator of immune regulation, inasmuch as it may upregulate tissue inflammatory response to B. pertussis.
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PMID:Regulation of inflammatory responses to Bordetella pertussis by N(G)-monomethyl-L-arginine in mice intranasally infected. 1070 86

We hypothesized that an impairment of endothelial dysfunction and an increased response to alpha-adrenoceptor agonists may occur in fructose-fed, insulin-resistant mice. The aim of the present study was to assess the relationship between endothelial dysfunction and agonist-induced contractile responses in such mice. The acetylcholine-induced relaxation was significantly attenuated in streptozotocin-diabetic and fructose-fed mice. The contractile response to noradrenaline was significantly weaker than the control in fructose-fed but not in streptozotocin-diabetic mice; treatment with N(G)-nitro-L-arginine effectively restored this response. Incubating aortic rings with noradrenaline increased the NO(x) [nitrite (NO(2)(-)) and nitrate (NO(3)(-))] level and this level was significantly higher in fructose-fed mice than in control mice. Clonidine induced a dose-dependent relaxation in aortic rings pre-contracted with prostaglandin F(2alpha) that was completely abolished by N(G)-nitro-L-arginine; this relaxation was markedly enhanced in fructose-fed mice. In both control and fructose-fed mice, the clonidine-induced relaxation was significantly attenuated and the noradrenaline-induced contraction augmented by pertussis toxin. These results suggest that endothelial function is attenuated in both fructose-fed and streptozotocin-diabetic mice. It is suggested that the decreased noradrenaline contractile response in fructose-fed mice (compared to both controls and streptozotocin-diabetic mice) may be due to an increase in nitric oxide formation mediated by endothelial GTP-binding-coupled alpha(2)-adrenoceptors.
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PMID:Mechanisms underlying attenuated contractile response of aortic rings to noradrenaline in fructose-fed mice. 1167 42

In the present study, the involvement of GABA(B) binding parameters were analyzed in partial hepatectomized (PH), lead nitrate (LN) induced hyperplastic and N-nitrosodiethylamine (NDEA) treated neoplastic rat livers at the peak DNA synthesis. The receptor up-regulated significantly in NDEA treated group compared with respective control. The affinity of the receptor decreased in PH while it increased in LN treated rats. In the other groups, the binding parameters remained unaltered. The displacement analysis using GABA(B) receptor agonist, [3H]baclofen, against baclofen showed a shift in affinity of the receptor towards high-affinity in PH rats and towards low-affinity in LN treated rats. Baclofen dose-dependently induced EGF mediated DNA synthesis in primary hepatocyte cultures. Also, it significantly reduced the TGFbeta1 suppression of EGF induced DNA synthesis. The effect of baclofen on hepatocyte DNA synthesis was abolished by the addition of G(i)-protein inhibitor, pertussis toxin, suggesting the involvement of GABA(B) receptor mechanisms in hepatocyte DNA synthesis. Baclofen alone could not elicit any significant change in DNA synthesis. Thus, our results show that GABA(B) receptor enhancement induce hepatic neoplasia. Also, baclofen is seen to act as a potent co-mitogen, triggering DNA synthesis in primary cultures of rat hepatocytes, mediated through the G(i) protein coupled GABA(B) receptors.
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PMID:Enhanced GABA(B) receptor in neoplastic rat liver: induction of DNA synthesis by baclofen in hepatocyte cultures. 1218 56

Thirty-five strains of Bordetella bronchiseptica, recovered primarily from pigs, rabbits, dogs, cats and humans, were characterized by phenotypic and genotypic markers. Biochemical typing only showed variation in the ability to reduce nitrate to nitrite. OMP profiles from virulent strains showed variations in the region of 85-95kDa, which lead us to describe five OMP-types alpha, beta, gamma, delta and epsilon. Genotypic markers included the presence of IS1001, and polymorphisms in the flagellin gene (flaA) and pertussis toxin (PT) promoter region. The IS1001 was detected in 16 isolates (2 from humans and 10 from pigs) but was absent in rabbit isolates. The restriction profiles of the flaA gene allowed us to differentiate the strains into types A-C. The PT types were characterized by an RFLP assay and could be typed through patterns III-V. There was no apparent association between the flaA or PT types and the origin of the isolates. Eleven groups of isolates were identified on the basis of specific combinations of the analyzed markers. The combination of phenotypic and genotypic tests used could be useful in characterizing isolates and differentiating between certain clonal types of B. bronchiseptica.
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PMID:Characterization of Bordetella bronchiseptica strains using phenotypic and genotypic markers. 1683 14