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

The fatty acid composition of the total extractable cellular lipids of Bordetella pertussis was very characteristic and was mostly hexadecenoic and hexadecanoic acids (90%) in a ratio of about 1:1. The fatty acid composition of Bordetella parapertussis and Bordetella bronchiseptica differed from that of B. pertussis. The two species were distinguished by the fatty acid composition of cell-bound lipids. The ornithine-containing lipid was characteristic of the genus Bordetella and its main structure was 3-hydroxyhexadecanoic acid amide-linked to ornithine and esterified to the second hexadecanoic acid. The lipid agglutinated human and some animal erythrocytes. The lipid is a new type of hemagglutinin and we proposed that hemagglutination occurred mainly by the hydrophobic interaction between the lipid moiety of the ornithine-containing lipid and phosphatidylcholine in the cell membrane of the erythrocytes. A relatively high content of ornithine-containing lipid was also found in opportunistic pathogens such as Flavobacterium meningosepticum which causes meningitis in babies and children. As the pathogenicity of the opportunistic pathogens is unclear, the ornithine-containing lipid may have an important role in pathogenicity.
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PMID:Characteristic cellular fatty acid composition and an ornithine-containing lipid as a new type of hemagglutinin in Bordetella pertussis. 287 10

The lipids and fatty acids of Bordetella pertussis (phases I to IV) were analyzed by thin-layer chromatography, gas-liquid chromatography, and mass spectrometry and compared with those of B. parapertussis and B. bronchiseptica. The major lipid components of the three species were phosphatidylethanolamine, cardiolipin, phosphatidylglycerol, lysophosphatidylethanolamine, and an ornithine-containing lipid. The ornithine-containing lipid was characteristic of the genus Bordetella. The fatty acid composition of the total extractable cellular lipids of B. pertussis was mostly hexadecanoic and hexadecenoic acids (90%) in a ratio of about 1:1. The hexadecenoic acid of B. pertussis was in the cis-9 form. The fatty acid composition of the residual bound lipids was distinctly different from that of the extractable lipids, and residual bound lipids being mainly 3-hydroxytetradecanoic, tetradecanoic, and 3-hydroxydecanoic acids, with 3-hydroxydodecanoic acid occurring in some strains. It was determined that the 3-hydroxy fatty acids were derived from lipid A. The fatty acid composition of the total extractable cellular lipids of B. parapertussis and B. bronchiseptica, mainly composed of hexadecanoic and heptadecacyclopropanoic acid, differed from that of B. pertussis. Although the fatty acid composition of the residual bound lipids of B. parapertussis was similar to that of the residual bound lipids of B. pertussis, 2-hydroxydodecanoic acid was detected only in the bound lipids of B. bronchiseptica.
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PMID:Characteristic lipids of Bordetella pertussis: simple fatty acid composition, hydroxy fatty acids, and an ornithine-containing lipid. 628 19

The proposed structure of the ornithine-containing lipid of Bordetella pertussis is 3-hydroxyhexadecanoic acid amide-linked to ornithine and esterified to the second hexadecanoic acid. The aminolipid strongly agglutinates type A and B human erythrocytes.
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PMID:Ornithine-containing lipid of Bordetella pertussis that carries hemagglutinating activity. 629 Apr 56

The ornithine-containing lipids of six strains (phases I-IV) of Bordetella pertussis were prepared from the total extractable cellular lipids by thin-layer chromatography and treatment with phospholipase A. They were compared with those prepared from two strains each of Bordetella parapertussis and Bordetella bronchiseptica. The structures of the ornithine-containing lipid of B. pertussis and the other two species were resolved by acid and alkaline hydrolysis, gas-liquid chromatography, infrared absorption spectroscopy, amino acid analysis and combined gas-liquid chromatography/mass spectrometry. The main structure of the aminolipid of the three species of Bordetella was 3-hydroxyhexadecanoic acid, amide-linked to ornithine and esterified to the second hexadecanoic acid. The aminolipid of B. pertussis Sakurayashiki (phase III) exhibited high hemagglutinating activity for human and rabbit erythrocytes, having a minimum hemagglutinating concentration of 1 microgram/ml against 8-16 micrograms/ml for the other strains of Bordetella. All of these aminolipids showed some degree of microheterogeneity. Because the 3-hydroxyhexadecanoic acid content was especially high in strain Sakurayashiki, it was presumed that the intensity of hemagglutinating activity of the aminolipid was affected by the chain length of the central 3-hydroxy fatty acid, that is the aminolipid containing 3-hydroxyhexadecanoic acid had high hemagglutinating activity. The hemagglutination was inhibited by phosphatidylcholine at concentrations of more than 20 micrograms/ml. Other inhibitory substances were cysteine, sphingomyelin, acidic amino acids, histidine, unsaturated fatty acid and basic amino acids. Furthermore, the divalent cations Ca2+ and Mg2+ inhibited this hemagglutination at a concentration of 1 mM. The O-deacylated ornithine-containing lipid that had lost hexadecanoic acid did not have any hemagglutinating activity but did have hemolytic activity. Observation by electron microscopy indicated that erythrocytes were combined by the liposomes of the ornithine-containing lipids. On the basis of these results, the proposed mechanism of hemagglutination by the aminolipids is that the liposomes of the aminolipids combine erythrocytes by hydrophobic interaction between the fatty acid moieties of the aminolipid and the lipids of the surface of erythrocytes, and by ionic interaction between the ornithine of the aminolipid and the protein of the surface of the erythrocytes. In addition, the hemagglutinating activity of phosphatidylserine was found to be due to its similar structure to that of the ornithine-containing lipid and the mechanism was also presumed to be similar. The mechanism of hemagglutination by these aminolipids was distinct from that of lectins.
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PMID:Ornithine-containing lipid of Bordetella pertussis, a new type of hemagglutinin. 631 33

Activation of endothelial nitric oxide synthase (eNOS) results in the production of nitric oxide (NO) that mediates the vasorelaxing properties of endothelial cells. The goal of this project was to address the possibility that 5-hydroxytryptamine (5-HT) stimulates eNOS activity in bovine aortic endothelial cell (BAEC) cultures. Here, we tested the hypothesis that 5-HT receptors mediate eNOS activation by measuring agonist-stimulated [3H]L-citrulline ([3H]L-Cit) formation in BAEC cultures. We found that 5-HT stimulated the conversion of [3H]L-arginine ([3H]L-Arg) to [3H]L-Cit, indicating eNOS activation. The high affinity 5-HT1B receptor agonist, 5-nonyloxytryptamine (5-NOT)-stimulated [3H]L-Cit turnover responses were concentration-(0.01 nM to 100 microM) and time-dependent. Maximal responses were observed within 10 min following agonist exposures. These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the eNOS selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and L-N omega-iminoethyl-L-ornithine (L-NIO). Pretreatment of BAEC cultures with pertussis toxin (PTX; 1-100 ng/ml) for 16 hr resulted in significant inhibition of the agonist-stimulated eNOS activity, indicating the involvement of Gi proteins. These findings lend evidence of a 5-HT1B receptor/eNOS pathway, accounting in part for the activation of eNOS by 5-HT. Further investigation is needed to determine the role of other vascular 5-HT receptors in the stimulation of eNOS activity.
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PMID:5-hydroxytryptamine evokes endothelial nitric oxide synthase activation in bovine aortic endothelial cell cultures. 1046 Jul 2

The partially degraded lipopolysaccharide of Burkholderia cepacia (LPSdegr) and the ornithine-containing lipids were purified from some bacteria. The substances were developed as complex lipid adjuvants, because they have weak toxicity and are able to activate the immune systems of the living body. After various toxoid antigens such as pertussis toxoid, diphtheria toxoid and tetanus toxoid were mixed with the complex lipid adjuvants, the mixtures were administered to mice subcutaneously. Antitoxoid IgG antibody titers in the serum were measured several times over 3 months. The efficacy of the LPSdegr as adjuvant was almost as high as that of the ornithine-containing lipids, and it was almost equal to that of the aluminum hydroxide adjuvant (Alum), which is generally used as a vaccine adjuvant.
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PMID:The partially degraded lipopolysaccharide of Burkholderia cepacia and ornithine-containing lipids derived from some Gram-negative bacteria are useful complex lipid adjuvants. 1242 68

Using an isolated working heart preparation we show that angiotensin II (ANG II), at concentrations of 10(-10)-10(-7) mol l(-1), elicits negative chronotropism and inotropism in the freshwater eel Anguilla anguilla. The negative inotropism was insensitive to losartan and CGP42112 (AT(1) and AT(2) ANG II receptor antagonists, respectively), and was abrogated by the AT(1) receptor antagonist CV11974, the G protein blocker pertussis toxin (PTx) and the muscarinic antagonist atropine. In contrast, it was not affected by the adrenoceptor antagonists propanolol, sotalol and phentolamine. Using donors (L-arginine) and inhibitors [N(G)-monomethyl-(L)-arginine (L-NMMA), L-N(5)(1-iminoethyl)ornithine ((L)-NIO)] of nitric oxide synthase (NOS), and haemoglobin as NO scavenger, we demonstrate that NO signalling is involved in ANG II-mediated inotropism. Pretreatment with Triton X-100, a detergent that damages the endocardial endothelium (EE), or with 1H-(1,2,4)oxadiazolo-(4,3-a)quinoxalin-1-one (ODQ), a specific inhibitor of soluble guanylate cyclase, or with the cGMP-activated protein kinase (PKG) inhibitor KT5328, abolished ANG II-mediated inotropism. Thus, ANG II-mediated inotropism occurs via an EE-NO-cGMP-PKG mechanism. ANG II did not affect the mechanical performance influenced by preload changes (i.e. the Frank-Starling response), which in the eel heart is modulated by NO. This EE-paracrine-mediated cardio-suppressive action of endoluminal ANG II suggests that the hormone plays an important intracardiac role in the fish heart.
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PMID:Angiotensin II-induced inotropism requires an endocardial endothelium-nitric oxide mechanism in the in-vitro heart of Anguilla anguilla. 1281 73

Fluorescence microscopy and the NO-sensitive indicator 4,5-diaminofluorescein were used to determine the effects of acetylcholine (ACh) on intracellular NO (NOi) in cat atrial myocytes. Field stimulation (1 Hz) of cells or exposure of quiescent cells to ACh (1 to 10 micromol/L) had no effect on NOi. However, in field-stimulated cells, ACh exposure increased NOi, and ACh withdrawal elicited an additional, prominent increase in NOi production. During ACh exposure, addition of 1 micromol/L atropine increased NOi production similar to ACh withdrawal. ACh-induced increases in NOi were reduced by prior exposure to 1 mmol/L extracellular Ca2+ ([Ca2+]o) and prevented by 0.5 mmol/L [Ca2+]o, 1 micromol/L verapamil, 1 micromol/L atropine, 10 micromol/L L-N5-(1-iminoethyl)ornithine, 10 micromol/L W-7, or incubating cells in pertussis toxin or 10 micromol/L LY294002 (inhibits phosphatidylinositol 3-kinase). Switching to 0.5 mmol/L [Ca2+]o during ACh withdrawal prevented the additional increase in NOi. ACh exposure increased phosphorylation (Ser473) of protein kinase B (Akt), and this effect was blocked by LY294002 and unaffected in low (0.5 mmol/L) [Ca2+]o. Confocal microscopy revealed that ACh exposure increased NOi at local subsarcolemmal sites, and ACh withdrawal additionally increased NOi by recruiting additional subsarcolemmal release sites. Disruption of caveolae by 2 mmol/L methyl-beta-cyclodextrin abolished ACh-induced NOi production. We conclude that in cat atrial myocytes, ACh stimulates NOi release from local subsarcolemmal sites. ACh-induced increases in NOi requires both muscarinic receptor-mediated Gi protein/phosphatidylinositol 3-kinase/Akt signaling and voltage-activated Ca2+ influx for stimulation of calmodulin-dependent endothelial NO synthase activity. Increases in NOi elicited by ACh withdrawal result from the recovery of Ca2+ influx after ACh inhibition. NO signaling elicited by ACh withdrawal stimulates rapid recovery from cholinergic atrial inhibition.
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PMID:Signaling mechanisms that mediate nitric oxide production induced by acetylcholine exposure and withdrawal in cat atrial myocytes. 1461 86

Chromogranin A (CGA) N-terminal fragments corresponding to residues 1-76 and 1-113, named vasostatins for their inhibitory effects on vascular tension, have been postulated as important homeostatic regulators of the cardiovascular system. We have used an in vitro isolated working frog (Rana esculenta) heart as a bioassay to study the effects of exogenous human recombinant CGA 1-76 (VS-1) and human CGA 7-57 synthetic peptide on cardiac performance. Under basal conditions, the concentration-response curves of the two peptides exhibited a significant negative inotropism. This vasostatin response was unaffected by pretreatment with either Triton X-100 or two nitric oxide synthase inhibitors, i.e., N(G)-monomethyl-L-arginine and L-N5 (5)(1-iminoethyl) ornithine or the soluble guanylate cyclase inhibitor 1H-(1,2,4) oxadiazolo-(4,3-a) quinoxalin-1-one, indicating an endocardial endothelium-nitric oxide-cGMP-independent mechanism. The negative inotropism was also unaffected by either adrenergic (i.e., phentolamine and propranolol) or muscarinic (atropine) receptor or G proteins (pertussis toxin) inhibition. On the contrary, it was dependent from both extracellular Ca(2+) and K(+) channels, since it was abolished by pretreatment to either the Ca(2+) channel inhibitors lanthanum and diltiazem or the K(+) channel inhibitors Ba(2+), 4-aminopyridine, tetraethylammonium chloride, and glibenclamide. In conclusion, the findings that vasostatins exert an inhibitory modulation on basal cardiac performance and counteract, as previously reported, the adrenergic-mediated positive inotropism, strongly support a cardio-regulatory role for these peptides.
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PMID:Chromogranin A N-terminal fragments vasostatin-1 and the synthetic CGA 7-57 peptide act as cardiostatins on the isolated working frog heart. 1502 25

Neuroendocrine regulation of cardiac function involves a population of three types of beta-adrenoceptors (ARs). In various mammalian species, beta1- and beta2-AR stimulation produces an increase in contractility; whereas beta3-AR activation mediates negative inotropic effects. At the moment, nothing is known about the physiological role of beta3-AR in fish. Using an isolated working heart preparation, we show that a beta3-AR selective agonist BRL(37344) (0.1-100 nmol l(-1)) elicits a dose-dependent negative inotropism in the freshwater eel Anguilla anguilla. This effect was insensitive to the beta1/beta2-AR inhibitor nadolol (10 mumol l(-1)), but was blocked by the beta3-AR-specific antagonist SR(59230) (10 nmol l(-1)). The analysis of the percentage of stroke work (SW) variations, in terms of EC(50) values, induced by BRL(37344) alone (10 nmol l(-1)), and in presence of SR(59230) (10 nmol l(-1)), indicated a competitive antagonism of SR(59230). In addition to the classic positive inotropism, the non-specific beta agonist isoproterenol (100 nmol l(-1)) induced, in 30% of the preparations, a negative inotropic effect that was abrogated by pre-treatment with SR(59230), pointing to a beta3-mediated pathway. The BRL(37344)-induced negative inotropic effect was abolished by exposure to a G(i/o) proteins inhibitor pertussis toxin (PTx; 0.01 nmol l(-1)), suggesting a G(i/o)-dependent mechanism. Using L-N5(l-imino-ethyl)ornithine (L-NIO; 10 mumol l(-1)), as a nitric oxide (NO) synthase (NOS) blocker and haemoglobin (Hb; 1 mumol l(-1)), as a NO scavenger, we demonstrated that NO signalling is involved in the BRL(37344)-induced response. Pre-treatment with either an inhibitor of soluble guanylate cyclase (GC) 1H-(1,2,4) oxadiazolo-(4,3-a)quinoxalin-1-one (ODQ; 10 mumol l(-1)), or an inhibitor of the cGMP-activated protein kinase (PKG) KT(5823) (100 nmol l(-1)), abolished the beta3-dependent negative inotropism, indicating the cGMP-PKG component as a crucial target of NO signalling. Taken together, our findings provide functional evidence for the presence of beta3-like adrenoceptors in the eel Anguilla anguilla heart identifying, for the first time in a working fish heart, the beta3-AR-dependent negative inotropy discovered in mammals.
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PMID:Beta3-adrenoceptor in the eel (Anguilla anguilla) heart: negative inotropy and NO-cGMP-dependent mechanism. 1714 85


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