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001-es BibID:BIBFORM003869
Első szerző:Elekes Krisztián
Cím:Inhibitory effects of synthetic somatostatin receptor subtype 4 agonists on acute and chronic airway inflammation and hyperreactivity in the mouse / Krisztián Elekes, Zsuzsanna Helyes, László Kereskai, Katalin Sándor, Erika Pintér, Gábor Pozsgai, Valéria Tékus, Ágnes Bánvölgyi, József Németh, Tamás Szűts, György Kéri, János Szolcsányi
Dátum:2008
Megjegyzések:Somatostatin released fromactivated capsaicin-sensitive afferents of the lung inhibits inflammation and related bronchial hyperreactivity presumably via somatostatin 4 receptors (sst4). The aim of this studywas to examine the effects of TT-232, a heptapeptide sst4/sst1 receptor agonist and J-2156, a high affinity sst4 receptor-selective peptidomimetic agonist in airway inflammation models. Acute pneumonitis was evoked by intranasal lipopolysaccharide 24 h before measurement. Chronic inflammation was induced by ovalbumin inhalation on days 28, 29 and 30 after i.p. sensitization on days 1 and 14. Semiquantitative histopathological scoring was based on perivascular/peribronchial oedema, neutrophil/macrophage infiltration, goblet cell hyperplasia in the acute model and eosinophil infiltration,mucosal oedema,mucus production and epithelial cell damage in chronic inflammation.Myeloperoxidase activity of the lung was measured spectrophotometrically to quantify granulocyte accumulation and the broncoalveolar lavage fluid was analysed by flow cytometry. Carbachol-induced bronchoconstriction was assessed by unrestrained whole body plethysmography and its calculated indicator, enhanced pause (Penh)was determined. TT-232 and J-2156 induced similar inhibition on granulocyte recruitment and histopathological changes in both models, although macrophage infiltration in LPS-induced inflammation was unaltered by either compounds. Both agonists diminished inflammatory airway hyperresponsiveness. Since their single administration after the development of the inflammatory reactions also inhibited carbachol-induced bronchoconstriction, somatostatin sst4 receptor activation on bronchial smooth muscle cells is likely to be involved in their anti-hyperreactivity effect. These results suggest that stable, somatostatin sst4 receptor-selective agonists could be potential candidates for the development of a completely novel group of anti-inflammatory drugs for the treatment of airway inflammation and hyperresponsiveness.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Somatostatin sst4 receptor
Interleukin-1beta
Whole body plethysmography
Ovalbumin
Lipopolysaccharide
Bronchial hyperreactivity
Airway inflammation
Megjelenés:European Journal of Pharmacology. - 578 : 2-3 (2008), p. 313-322. -
További szerzők:Helyes Zsuzsanna Kereskai László Sándor Katalin Pintér Erika Pozsgai Gábor Tékus Valéria Bánvölgyi Ágnes Németh József (1954-) (vegyész, analitikus) Szűts Tamás Kéri György Szolcsányi János (Pécs)
Internet cím:elektronikus változat
DOI
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001-es BibID:BIBFORM061062
Első szerző:Helyes Zsuzsanna
Cím:Pituitary Adenylate Cyclase-Activating Polypeptide Is Upregulated in Murine Skin Inflammation and Mediates Transient Receptor Potential Vanilloid-1-Induced Neurogenic Edema / Zsuzsanna Helyes, Jozsef Kun, Nora Dobrosi, Katalin Sándor, Jozsef Németh, Aniko Perkecz, Erika Pintér, Krisztina Szabadfi, Balazs Gaszner, Valeria Tékus, Janos Szolcsányi, Martin Steinhoff, Hitoshi Hashimoto, Dora Reglődi, Tamas Bíró
Dátum:2015
ISSN:0022-202X
Megjegyzések:Although pituitary adenylate cyclase-activating polypeptide (PACAP) was described as a key vasoregulator inhuman skin, little is known about its expression in mouse skin. As it is important to investigate PACAP signaling intranslational mouse dermatitis models, we determined its presence, regulation, and role in neurogenic and nonneurogeniccutaneous inflammatory mechanisms. The mRNA of PACAP and its specific receptor PAC1 wasdetected with real-time PCR in several skin regions at comparable levels. PACAP-38-immunoreactivity measuredwith radioimmunoassay was similar in plantar and dorsal paw skin and the ear but significantly smaller in theback skin. PACAP and PAC1 mRNA, as well as PACAP-38 and PAC1 protein expression, significantly increased in theplantar skin after intraplantar administration of capsaicin (50 ?l, 100 ?gml?1), an agonist of the transient receptorpotential vanilloid 1 (TRPV1) receptor, evoking chiefly neurogenic inflammation without inflammatory cellaccumulation. Intraplantar complete Freund's adjuvant (CFA; 50 ?l, 1mgml?1) also increased PACAP/PAC1 mRNAbut not the PACAP peptide. Capsaicin-induced neurogenic paw edema, but not CFA-evoked non-neurogenicswelling, was significantly smaller in PACAP-deficient mice throughout a 24-hour period. To our knowledge, weprovide previously unreported evidence for PACAP and PAC1 expression upregulation during skin inflammation ofdifferent mechanisms and for its pro-inflammatory function in neurogenic edema formation.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
cross-talk
sebaceous gland
sebocytes
skin homeostasis
Megjelenés:Journal Of Investigative Dermatology 135 : 9 (2015), p. 2209-2218. -
További szerzők:Kun József Dobrosi Nóra (1981-) (molekuláris biológus) Sándor Katalin Németh József (1954-) (vegyész, analitikus) Perkecz Anikó Pintér Erika Szabadfi Krisztina (Pécsi Egyetem) Gaszner Balázs (Neuroanatómia) Tékus Valéria Szolcsányi János (Pécs) Steinhoff, Martin Hashimoto, Hitoshi Reglődi Dóra (Idegtudományok) Bíró Tamás (1968-) (élettanász)
Pályázati támogatás:OTKA-104984
OTKA
OTKA-PD100706
OTKA
OTKA-101761
OTKA
OTKA105369
OTKA
TÁMOP-4.2.2./A-11/1/KONV-2012-0025
TÁMOP
TÁMOP-4.2.4.A/ 2- 11/1-2012-0001
TÁMOP
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