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001-es BibID:BIBFORM002464
Első szerző:Helyes Zsuzsanna
Cím:Role of transient receptor potential vanilloid 1 receptors in endotoxin-induced / Zsuzsanna Helyes, Krisztián Elekes, József Németh, Gábor Pozsgai, Katalin Sándor, László Kereskai, Rita Börzsei, Erika Pintér, Árpád Szabó, János Szolcsányi
Dátum:2007
Megjegyzések:Airways are densely innervated by capsaicin-sensitive sensory neurons expressing transient receptor potential vanilloid 1 (TRPV1) receptors/ion channels, which play an important regulatory role in inflammatory processes via the release of sensory neuropeptides. The aim of the present study was to investigate the role of TRPV1 receptors in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity with functional, morphological, and biochemical techniques using receptor gene-deficient mice. Inflammation was evoked by intranasal administration of Escherichia coli lipopolysaccharide (60 gammal, 167 gammag/ml) in TRPV1 knockout (TRPV1-/-) mice and their wild-type counterparts (TRPV1+/+) 24 h before measurement. Airway reactivity was assessed by unrestrained whole body plethysmography, and its quantitative indicator, enhanced pause (Penh), was calculated after inhalation of the bronchoconstrictor carbachol. Histological examination and spectrophotometric myeloperoxidase measurement was performed from the lung. Somatostatin concentration was measured in the lung and plasma with radioimmunoassay. Bronchial hyperreactivity, histological lesions (perivascular/peribronchial edema, neutrophil/ macrophage infiltration, goblet cell hyperplasia), and myeloperoxidase activity were significantly greater in TRPV-/- mice. Inflammation markedly elevated lung and plasma somatostatin concentrations in TRPV1+/+ but not TRPV1-/- animals. In TRPV1-/- mice, exogenous administration of somatostatin-14 (4 x 100 gamma g/kg ip) diminished inflammation and hyperreactivity. Furthermore, in wildtype mice, antagonizing somatostatin receptors by cyclo-somatostatin (4 x 250 gamma g/kg ip) increased these parameters. This study provides the first evidence for a novel counterregulatory mechanism during endotoxin-induced airway inflammation, which is mediated by somatostatin released from sensory nerve terminals in response to activation of TRPV1 receptors of the lung. It reaches the systemic circulation and inhibits inflammation and consequent bronchial hyperreactivity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
capsaicin-sensitive afferents
inflammatory airway hyperreactivity
Megjelenés:American journal of physiology. Lung cellular and molecular physiology. - 292 (2007), p. L1173-L1181. -
További szerzők:Sándor Katalin Szolcsányi János (Pécs) Szabó Árpád Pintér Erika Börzsei Rita Kereskai László Pozsgai Gábor Elekes Krisztián Németh József (1954-) (vegyész, analitikus)
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001-es BibID:BIBFORM020438
Első szerző:Szilvássy Judit (fül- orr- gégész)
Cím:Feeble bronchomotor responses in diabetic rats in association with decreased sensory neuropeptide release / Judit Szilvássy, Istvan Sziklai, Peter Horvath, Maria Szilasi, József Németh, Péter Kovács, Zoltán Szilvássy
Dátum:2002
Megjegyzések:AbstractType I diabetes is associated with a low incidence of asthma. We tested whether a decrease in sensory neuropeptide release is associated with an attenuated bronchoconstrictive response to field stimulation (FS; 100 stimuli, 20 V, 0.1 ms, 20 Hz) in streptozotocin (STZ)-induced diabetes. The organ fluid of the preparations were also tested for substance P, calcitonin gene-related peptide (CGRP), and somatostatin concentrations by RIA. Preparations were from either normal rats or those pretreated with 50 mg/kg STZ iv 8 wk before experiment. A group of STZ-treated animals was supplied with insulin delivery (4 IU/day sc) implants between 4 and 8 wk. A subgroup was formed to study the effect of capsaicin desensitization. The atropine-resistant contraction was attenuated by diabetes without capsaicin-sensitive relaxation response. Exogenous CGRP and substance P potentiated, whereas somatostatin inhibited (1 nM-10 microM) the FS-induced contractions in rings from either group. FS released somatostatin, CGRP, and substance P from 0.17 +/- 0.024, 0.15 +/- 0.022, and 1.65 +/- 0.093 to 0.58 +/- 0.032, 0.74 +/- 0.122, and 5.34 +/- 0.295 in preparations from normal, and from 0.19 +/- 0.016, 0.11 +/- 0.019, and 0.98 +/- 0.116 to 0.22 +/- 0.076, 0.34 +/- 0.099, and 1.84 +/- 0.316 fmol/mg wet wt in preparations from diabetic rats. Insulin supplementation restored neuropeptide release in rings from STZ-treated rats. The results show that the decreased FS-induced contractions occurred with a decrease in sensory neuropeptide release in STZ-diabetic rats.
Tárgyszavak:Orvostudományok Gyógyszerészeti tudományok idegen nyelvű folyóiratközlemény külföldi lapban
bronchomotor responses
decreased sensory
neuropeptide
Megjelenés:American Journal of Physiology. - 282 : 5 (2002), p. 1023-1030. -
További szerzők:Sziklai István (1954-) (fül-orr-gégész) Horváth Péter Szilasi Mária (1953-) (tüdőgyógyász, klinikai immunológus, allergológus, belgyógyász) Németh József (Pécs) Kovács Péter (1939-) (farmakológus) Szilvássy Zoltán (1957-) (belgyógyász, farmakológus, klinikai farmakológus)
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