Role of capsaicin-sensitive afferents and sensory neuropeptides in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity in the mouse. Export

@article{citeulike:5931401, abstract = {Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitive afferents induce neurogenic inflammation via NK(1), NK(2) and CGRP1 receptor activation. This study examines the role of capsaicin-sensitive fibres and sensory neuropeptides in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity with functional, morphological and biochemical techniques in mice. Carbachol-induced bronchoconstriction was measured with whole body plethysmography 24 h after intranasal lipopolysaccharide administration. SP and CGRP were determined with radioimmunoassay, myeloperoxidase activity with spectrophotometry, interleukin-1beta with ELISA and histopathological changes with semiquantitative scoring from lung samples. Treatments with resiniferatoxin for selective destruction of capsaicin-sensitive afferents, NK(1) antagonist SR 140333, NK(2) antagonist SR 48968, their combination, or CGRP1 receptor antagonist CGRP(8-37) were performed. Lipopolysaccharide significantly increased lung SP and CGRP concentrations, which was prevented by resiniferatoxin pretreatment. Resiniferatoxin-desensitization markedly enhanced inflammation, but decreased bronchoconstriction. CGRP(8-37) or combination of SR 140333 and SR 48968 diminished neutrophil accumulation, MPO levels and IL-1beta production, airway hyperresponsiveness was inhibited only by SR 48968. This is the first evidence that capsaicin-sensitive afferents exert a protective role in endotoxin-induced airway inflammation, but contribute to increased bronchoconstriction. Activation of CGRP1 receptors or NK(1)+NK(2) receptors participate in granulocyte accumulation, but NK(2) receptors play predominant role in enhanced airway resistance.}, author = {Elekes, Kriszti\'{a}n and Helyes, Zsuzsanna and N\'{e}meth, J\'{o}zsef and S\'{a}ndor, Katalin and Pozsgai, G\'{a}bor and Kereskai, L\'{a}szl\'{o} and B\"{o}rzsei, Rita and Pint\'{e}r, Erika and Szab\'{o}, Arp\'{a}d and Szolcs\'{a}nyi, J\'{a}nos}, citeulike-article-id = {5931401}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.regpep.2006.12.018}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/17291600}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=17291600}, day = {7}, doi = {10.1016/j.regpep.2006.12.018}, issn = {0167-0115}, journal = {Regulatory peptides}, month = {June}, number = {1-3}, pages = {44--54}, posted-at = {2009-10-13 00:22:50}, priority = {3}, title = {Role of capsaicin-sensitive afferents and sensory neuropeptides in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity in the mouse.}, url = {http://dx.doi.org/10.1016/j.regpep.2006.12.018}, volume = {141}, year = {2007} }

TY - JOUR ID - citeulike:5931401 L3 - citeulike-article-id:5931401 N2 - Substance P (SP) and calcitonin gene-related peptide (CGRP) released from capsaicin-sensitive afferents induce neurogenic inflammation via NK(1), NK(2) and CGRP1 receptor activation. This study examines the role of capsaicin-sensitive fibres and sensory neuropeptides in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity with functional, morphological and biochemical techniques in mice. Carbachol-induced bronchoconstriction was measured with whole body plethysmography 24 h after intranasal lipopolysaccharide administration. SP and CGRP were determined with radioimmunoassay, myeloperoxidase activity with spectrophotometry, interleukin-1beta with ELISA and histopathological changes with semiquantitative scoring from lung samples. Treatments with resiniferatoxin for selective destruction of capsaicin-sensitive afferents, NK(1) antagonist SR 140333, NK(2) antagonist SR 48968, their combination, or CGRP1 receptor antagonist CGRP(8-37) were performed. Lipopolysaccharide significantly increased lung SP and CGRP concentrations, which was prevented by resiniferatoxin pretreatment. Resiniferatoxin-desensitization markedly enhanced inflammation, but decreased bronchoconstriction. CGRP(8-37) or combination of SR 140333 and SR 48968 diminished neutrophil accumulation, MPO levels and IL-1beta production, airway hyperresponsiveness was inhibited only by SR 48968. This is the first evidence that capsaicin-sensitive afferents exert a protective role in endotoxin-induced airway inflammation, but contribute to increased bronchoconstriction. Activation of CGRP1 receptors or NK(1)+NK(2) receptors participate in granulocyte accumulation, but NK(2) receptors play predominant role in enhanced airway resistance. IS - 1-3 JF - Regulatory peptides SN - 0167-0115 EP - 54 TI - Role of capsaicin-sensitive afferents and sensory neuropeptides in endotoxin-induced airway inflammation and consequent bronchial hyperreactivity in the mouse. VL - 141 SP - 44 AU - Elekes, Krisztián AU - Helyes, Zsuzsanna AU - Németh, József AU - Sándor, Katalin AU - Pozsgai, Gábor AU - Kereskai, László AU - Börzsei, Rita AU - Pintér, Erika AU - Szabó, Arpád AU - Szolcsányi, János PY - 2007/06/07/ UR - http://dx.doi.org/10.1016/j.regpep.2006.12.018 ER -