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)

A PCR-based assay for Bordetella pertussis was inhibited by using a calcium alginate fiber-tipped swab with an aluminum shaft but not by using a Dacron fiber-tipped swab with a plastic shaft. The calcium alginate fiber component inhibited the assay following storage for less than 1 min in a suspension of 10(3) CFU of B. pertussis per ml, whereas the aluminum shaft component required storage for at least 48 h in order to cause inhibition. We recommend the Dacron swab over the calcium alginate swab for collecting specimens for testing in PCR-based assays.
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PMID:Inhibition of PCR-based assay for Bordetella pertussis by using calcium alginate fiber and aluminum shaft components of a nasopharyngeal swab. 802 9

Fluoride (F-) a known stimulator of G-protein, has been reported to inhibit "P"-type ATPase activity in smooth muscles. On the other hand, vanadate, a strong "P"-type ATPase inhibitor, has been reported to stimulate G-protein in some cells. This study was designed to compare the contractile actions of fluoroaluminate (AlF4-) and vanadate and to clarify their mechanisms of actions by measuring changes in the amount of cyclic adenosine monophosphate (cAMP) and inositol phosphates. F- and vanadate induced strong contractions in canine trachealis muscle. The F(-)-induced contraction was potentiated by the addition of aluminum (Al3+, 20 microM) and inhibited by deferoxamine (200 microM), a heavy metal chelator. Ca2+ removal and 10 microM verapamil inhibited the contraction induced by AlF4- and vanadate. AlF4- and vanadate increased 45Ca influx in the absence and presence of verapamil. AlF4(-)-induced contractions were partially relaxed by isoproterenol (38.2 +/- 7.4%) in contrast with those induced by vanadate (72.1 +/- 5.3%), which could be explained by a decrease of tissue cAMP content by AlF4- in forskolin-pretreated tissues. Vanadate increased inositol phosphate accumulation as did AlF4-, although the magnitude of the increase was smaller than that produced by AlF4-. The increases of inositol phosphate content by both drugs were not affected after the pretreatment by pertussis toxin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential actions of AlF4- and vanadate on canine trachealis muscle. 807 49

Aluminium fluoride (AlF4-), a G protein activator, was used to study a possible role of G protein in the control of the pathways for Ca2+ influx through plasma membrane of human carcinoma A431 cells. Fluorimetric measurements with the Ca2+ indicator Indo-1 have shown that addition of fluoride induces an increase in concentration of cytosolic free calcium ([Ca2+]in) due to both release of Ca2+ from intracellular stores and Ca2+ influx from the extracellular medium. The cells stimulated by fluoride became unresponsive to subsequent addition of epidermal growth factor (EGF), histamine and bradykinin. The Ca2+ signal induced by fluoride as well as one induced by EGF was inhibited by the pretreatment of cells with protein kinase C activator, phorbol myristate acetate (PMA). The pretreatment of the cells with pertussis toxin produced no effect on EGF-induced calcium response. In contrast, the pretreatment with cholera toxin (CTX) increased the basal level of [Ca2+]in and abolished the effect of EGF. The effects of CTX could not be reproduced by treating the cells with forskolin or IBMX, agents known to elevate cAMP content in the cell. Patch clamp experiments have shown that fluoride increases the activity of Ca(2+)-permeable channels identical to those activated by EGF from the extracellular side of the membrane [Mozhayeva et al. (1991) J. Membr. Biol. 124, 113-126]. The results obtained suggest the involvement of GTP-binding protein in signal transduction from the EGF receptor to Ca(2+)-permeable channel of plasma membrane in A431 cells.
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PMID:Evidence for involvement of a GTP-binding protein in activation of Ca2+ influx by epidermal growth factor in A431 cells: effects of fluoride and bacterial toxins. 831 33

The activity of a hormone- and growth-factor-stimulated NADH oxidase of the rat liver plasma membrane responds to guanine nucleotides, but in a manner that differs from that of the classic trimeric and low-molecular-mass monomeric G-proteins. In the absence of added bivalent ions, both GTP and GDP as well as guanosine 5'-[gamma-thio]triphosphate (GTP[gamma-S]) but not guanosine 5'[beta-thio]diphosphate (GDP[beta-S]) stimulate the activity over the range 1 microM to 100 microM. Other di- and tri-nucleotides also stimulate, but only at concentrations of 100 microM or higher. Added bivalent ions are not required either for NADH oxidation or guanine nucleotide stimulation. Bivalent ions (Mg2+ > Mn2+ > or = Ca2+) alone stimulate only slightly at low concentrations and then inhibit at high concentrations. The inhibitions are augmented by GDP or GTP [gamma-S] but not by GTP. Although the activity is the same, or less, in the presence of 0.5 mM MgCl2, GTP at 1-100 nM and other nucleotides at 0.1 mM or 1 mM still stimulate in its presence. The NADH oxidase is activated by mastoparan but aluminum fluoride is weakly inhibitory. Cholera and pertussis toxins elicit only marginal responses. Both the Mg2+ and the GDP and GTP[gamma-S] inhibitions (but not the GTP stimulations) shift to higher concentrations when the membrane preparations are first solubilized with Triton X-100. The results suggest a role for guanine nucleotides in the regulation of plasma membrane NADH oxidase, but with properties that differ from those of either trimeric or the low-molecular-mass G proteins thus far described.
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PMID:NADH oxidase activity of rat liver plasma membrane activated by guanine nucleotides. 831 95

Four patients each had a single subcutaneous nodule at the site of a previous vaccine injection; three after injection of diphtheria, tetanus, and pertussis vaccination and one after tetanus toxoid vaccination. Presentation was with a mass 4-22 months after vaccination at the site of injection. Histologically, three patients had a necrotizing granulomatous reaction with a surrounding infiltrate of lymphocytes, plasma cells, histiocytes, and associated fibrosis. The fourth patient demonstrated a lymphohistiocytic reaction with a predominance of histiocytic cells as well as associated plasma cells, fibroblasts, and fibrosis. The lymphoid infiltration in these reactions showed a predominance of T-lymphocytes over B-lymphocytes. Aluminum was demonstrated in necrotic foci, inflammatory stroma, and the granular cytoplasm of histiocytes with the aid of solochrome azurine and solochrome cyanine stains as well as by energy-dispersive x-ray microanalysis. The reactions are thought to be immunologic (hypersensitivity) reactions associated with the aluminum contents of the preparation.
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PMID:Postimmunization (vaccination) injection-site reactions. A report of four cases and review of the literature. 781 82

Extracellular cations have paradoxical trophic and toxic effects on osteoblast function. In an effort to explain these divergent actions, we investigated in MC3T3-E1 osteoblasts if polyvalent cations differentially modulate the agonist-stimulated cyclic adenosine monophosphate (cAMP) pathway, an important regulator of osteoblastic function. We found that a panel of cations, including gadolinium, aluminum, calcium, and neomycin, inhibited prostaglandin E1 (PGE)-stimulated cAMP accumulation but paradoxically potentiated parathyroid hormone (PTH)-stimulated cAMP production. In contrast, these cations had no effect on forskolin- or cholera toxin-induced increases in cAMP, suggesting actions proximal to adenylate cyclase and possible modulation of receptor interactions with G proteins. Phorbol 12-myristate 13-acetated (PMA) mimicked the effects of cations on PGE1- and PTH-stimulated cAMP accumulation in MC3T3-E1 cells, respectively, diminishing and augmenting the responses. Moreover, down-regulation of protein kinase C (PKC) by overnight treatment with PMA prevented gadolinium (Gd3+) from attenuating PGE1- and enhancing PTH-stimulated cAMP production, indicating involvement of PKC-dependent pathways. Cations, however, activated signal transduction pathways not coupled to phosphatidylinositol-specific phospholipase C (PI-PLC), since there was no corresponding increase in inositol phosphate formation or intracellular calcium concentrations. In addition, pertussis toxin treatment failed to prevent Gd(3+)-mediated suppression of PGE1-stimulated cAMP, suggesting actions independent of Gm. Thus, polyvalent cations may either stimulate or inhibit hormone-mediated cAMP accumulation in osteoblasts. These differential actions provide a potential explanation for the paradoxical trophic and toxic effects of cations on osteoblast function that occur in vivo under different hormonal conditions.
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PMID:Differential regulation of receptor-stimulated cyclic adenosine monophosphate production by polyvalent cations in MC3T3-E1 osteoblasts. 872 76

We assessed the sensitivity of phospholipase D (PLD) activity in vascular smooth muscle to cytosolic Ca2+ by increasing cytosolic Ca2+ levels independently of agonist stimulation. When rat tail artery was preloaded with the Ca2+ indicator fluo 3 pentaacetoxymethyl ester, the addition of high extracellular K+, caffeine, or norepinephrine rapidly enhanced cytosolic Ca2+ levels. Neither increased extracellular K+ nor caffeine addition increased phosphatidylethanol production, indicating that cytosolic Ca2+ elevation alone did not stimulate PLD. In contrast, norepinephrine stimulated phosphatidylethanol production in this tissue. In strips of tail artery permeabilized with alpha-toxin and incubated in solutions containing free Ca2+ concentrations observed during physiological stimulation (pCa 6.4), PLD was not stimulated, whereas incubation with guanosine 5'-O-(3-thiotriphosphate) at pCa 7.0 activated this enzyme. Aluminum fluoride (AlF4-) stimulated PLD, and this activity was insensitive to pertussis toxin after stimulation by either norepinephrine or AlF4-. These results indicate that PLD in vascular smooth muscle is activated by norepinephrine via stimulation of a pertussis toxin-insensitive G protein and not via an increase in intracellular Ca2+ levels.
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PMID:Phospholipase D is activated by G protein and not by calcium ions in vascular smooth muscle. 878 Feb

Recent studies have provided evidence that apoptosis of pancreatic beta-cells is important in the early etiology of both type I and type II diabetes mellitus. The mechanisms responsible for induction of apoptosis are unknown, but we present evidence that the signal transduction pathway controlling the process in pancreatic beta-cells is regulated by G-proteins. We have employed the global G-protein activator fluoride and show that this agent induces apoptosis in clonal RINm5F pancreatic beta-cells and also in the cells of normal rat islets of Langerhans. The process is time and concentration dependent and may reflect the formation of AIF4- since it was inhibited by the aluminum chelator deferoxamine. Induction of apoptosis by fluoride was confirmed by acridine orange staining of cell nuclei, by electron-microscopic examination of chromatin condensation, and by oligonucleosomal degradation of DNA. The involvement of G-proteins was confirmed by culture of beta-cells in the presence of pertussis toxin (PTX) prior to exposure to fluoride. PTX did not affect the extent of cell death under control conditions but it consistently, and markedly, enhanced the response to fluoride. The results demonstrate that apoptosis can be induced in pancreatic beta-cells by sustained activation of a G-protein-dependent signaling pathway(s) and they further suggest that a pertussis toxin-sensitive G-protein is involved in attenuation of the response. Treatment of RINm5F pancreatic beta-cells with dibutyrylcAMP resulted in a dose-dependent, saturable increase in cell death, suggesting that a sustained rise in intracellular cAMP may form part of the effector system controlling apoptosis.
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PMID:Heterotrimeric G-proteins are implicated in the regulation of apoptosis in pancreatic beta-cells. 894 Feb 50

Upper respiratory tract viral infections have been reported in clinical studies to serve as risk factors for allergic sensitization. In order to study the relationship linking influenza virus illnesses to development of allergy, murine models of allergen sensitization were previously employed. These models showed that lethal influenza viruses were able to trigger allergen-specific immunoglobulin E (IgE) production and to inhibit tolerance to repeated exposure to aerosolized allergen in the mouse. The disadvantage of these murine models consists in the utilization of virulant and lethal strains of influenza virus. A nonlethal rat-adapted influenza virus (RAIV) host resistance model has been developed in our laboratory. It was used to evaluate the effect of influenza virus infection on IgE responses to inhaled ovalbumin (OA) in the rat. The high IgE-responder Brown-Norway (BN) rat was chosen for further study after comparing the IgE response to OA in Fischer 344 (F344) and BN rats. On d 1, BN rats were sensitized by administration of 1 mg OA subcutaneously alone or together with aluminum hydroxide (200 mg) and Bordetella pertussis (15 x 10(9) killed bacilli per rat in 1 ml), or only received saline. Rats were either infected with RAIV or sham-infected on d 0 (24 h prior to sensitization) or on d 15, 17, or 57. Rats were exposed for 3 min to aerosolized OA (OA 3% in phosphate-buffered saline) every week, starting on d 18. Serum OA-specific IgE was evaluated by reverse enzyme-linked immunosorbent assay (ELISA) 3 d after each OA challenge. BN rats elicited a detectable OA-specific IgE response that decreased after repeated aerosol exposures. Influenza virus infection transiently increased the OA-specific IgE response when rats were immunized with OA alone and were infected 1 d prior to the first challenge and also when rats received only saline on d 1, were exposed each week to aerosolized OA, and were infected prior to the seventh challenge. These results, with data previously reported in mice, emphasize the importance of upper respiratory tract viral infection in increasing IgE responses to allergens and may be of importance in human disease.
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PMID:Effect of influenza virus infection on ovalbumin-specific IgE responses to inhaled antigen in the rat. 897 28

Fluoride is an acknowledged bone-forming agent that may act through stimulation of osteoblast proliferation. Fluoride's action on osteoblasts and bone is potentiated by aluminum, which can form a complex with fluoride (fluoroaluminate) and activate heterotrimeric G proteins. Here we examined signaling pathways activated by fluoroaluminate in MC3T3-E1 osteoblastic and in NIH3T3 fibroblastic cells. In MC3T3-E1 cells, fluoroaluminate induced a decrease in cAMP levels and an increase in MAP and p70 S6 kinase phosphorylations. These responses were partially or completely prevented by pertussis toxin, an inhibitor of G alpha i proteins. In NIH3T3 cells, fluoroaluminate induced weaker tyrosine and MAP kinase phosphorylations. Fluoroaluminate, but not PDGF, induced a long-lasting tyrosine phosphorylation of a 130 kDa protein only in MC3T3-E1 cells. The expression of G alpha i2, but not of G alpha s and G alpha q/11 proteins was about 10-fold higher in MC3T3-E1 cells. Thus, different signaling in osteoblastic and fibroblastic cells may be due to differential expression of G alpha i proteins and tyrosine kinase substrates and could underlie fluoride's pharmacological action in bone.
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PMID:Fluoroaluminate induces pertussis toxin-sensitive protein phosphorylation: differences in MC3T3-E1 osteoblastic and NIH3T3 fibroblastic cells. 920 19


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