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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Sigala, Ioanna Zacharatos, Panayiotis Boulia, Stavroula Toumpanakis, Dimitris Michailidou, Tatiana Parthenis, Dimitris Roussos, Charis Papapetropoulos, Andreas Hussain, Sabah N. Vassilakopoulos, Theodoros |
| Description | Country affiliation: Greece Author Affiliation: Sigala I ( Department of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, 45-47 Ipsilandou Str., Athens, Greece.) |
| Abstract | Resistive breathing (encountered in chronic obstructive pulmonary disease and asthma) results in cytokine upregulation and decreased nitric oxide (NO) levels in the strenuously contracting diaphragm. NO can regulate gene expression. We hypothesized that endogenously produced NO downregulates cytokine production triggered by strenuous diaphragmatic contraction. Wistar rats treated with vehicle, the nonselective NO synthase inhibitor NG-nitro-l-arginine-methylester (l-NAME), or the NO donor diethylenetriamine-NONOate (DETA) were subjected to inspiratory resistive breathing (IRB; 50% of maximal inspiratory pressure) for 6 h or sham operation. Additional groups of rats were subjected to IRB for 6 h with concurrent administration of l-NAME and inhibitors of NF-κB (BAY-11-7082), ERK1/2 (PD98059), or P38 (SB203580). Inhibition of NO production (with l-NAME) resulted in upregulation of IRB-induced diaphragmatic IL-6, IL-10, IL-2, TNF- , and IL-1ß levels by 50%, 53%, 60%, 47%, and 45%, respectively. In contrast, the NO donor (DETA) attenuated the IRB-induced cytokine upregulation to levels characteristic of quietly breathing animals. l-NAME augmented IRB-induced activation of MAPKs (P38 and ERK1/2) and NF-κB, whereas DETA triggered the opposite effect. NF-κB and ERK1/2 inhibition in l-NAME-treated animals blunted the l-NAME-induced cytokine upregulation except IL-6, whereas P38 inhibition blunted all (including IL-6) cytokine upregulation. NO downregulates IRB-induced cytokine production in the strenuously contracting diaphragm through its action on MAPKs and NF-κB. |
| File Format | HTM / HTML |
| ISSN | 87507587 |
| e-ISSN | 15221601 |
| Journal | Journal of Applied Physiology |
| Issue Number | 10 |
| Volume Number | 113 |
| Language | English |
| Publisher | American Physiological Society |
| Publisher Date | 2012-11-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Discipline Physiology Cytokines Metabolism Diaphragm Inflammation Inhalation Lung Diseases, Obstructive Muscle Contraction Nitric Oxide Animals Drug Effects Immunology Enzyme Inhibitors Pharmacology Physiopathology Mitogen-activated Protein Kinases Antagonists & Inhibitors Nf-kappa B Nitric Oxide Donors Nitric Oxide Synthase Oxidation-reduction Protein Carbonylation Rats, Wistar Signal Transduction Time Factors Work Of Breathing Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Physiology Physiology (medical) Sports Science |
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