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10.1152/ajplung.00297.2015 http://scihub22266oqcxt.onion/10.1152/ajplung.00297.2015 C4824163!4824163 !26851260     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26851260 &cmd=llinks): Failed to open stream: HTTP request failed! 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Treatment with intranasal iloprost reduces disease manifestations in a murine model of previously established COPD |pdf=|usr=}}{{26851260 }} gab.com Text Treatment with intranasal iloprost reduces disease manifestations in a murine model of previously established COPD JO: Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26851260 #FOAvip Pulmonary endothelial prostacyclin appears to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). The effect of treatment with a prostacyclin analog in animal models of previously established COPD is unknown. We evaluated the short- and long-term effect of iloprost on inflammation and airway hyperresponsiveness (AHR) in a murine model of COPD. Nineteen mice were exposed to LPS/elastase, followed by either three doses of intranasal iloprost or saline. In the long-term treatment experiment, 18 mice were exposed to LPS/elastase and then received 6 wk of iloprost or were left untreated as controls. In the short-term experiment, iloprost did not change AHR but significantly reduced serum IL-5 and IFN-?. Long-term treatment with iloprost for both 2 and 6 wk significantly improved AHR. After 6 wk of iloprost, there was a reduction in bronchoalveolar lavage (BALF) neutrophils, serum IL-1? (30.0 ± 9.2 vs. 64.8 ± 7.4 pg/ml, P = 0.045), IL-2 (36.5 ± 10.6 vs. 83.8 ± 0.4 pg/ml, P = 0.01), IL-10 (75.7 ± 9.3 vs. 96.5 ± 3.5 pg/ml, P = 0.02), and nitrite (15.1 ± 5.4 vs. 30.5 ± 10.7 ?mol, P = 0.01). Smooth muscle actin (SMA) in the lung homogenate was also significantly reduced after iloprost treatment (P = 0.02), and SMA thickness was reduced in the small and medium blood vessels after iloprost (P < 0.001). In summary, short- and long-term treatment with intranasal iloprost significantly reduced systemic inflammation in an LPS/elastase COPD model. Long-term iloprost treatment also reduced AHR, serum nitrite, SMA, and BALF neutrophilia. These data encourage future investigations of prostanoid therapy as a novel treatment for COPD patients. Twit Text FOAVip Treatment with intranasal iloprost reduces disease manifestations in a murine model of previously established COPD ????Am J Physiol Lung Cell Mol Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26851260 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26851260 #FOAvip English Wikipedia <ref>{{Cite pmid|26851260 }}</ref> Treatment with intranasal iloprost reduces disease manifestations in a murine model of previously established COPD #MMPMID26851260 Lammi MR ; Ghonim MA ; Pyakurel K ; Naura AS ; Ibba SV ; Davis CJ ; Okpechi SC ; Happel KI ; deBoisblanc BP ; Shellito J ; Boulares AH Am J Physiol Lung Cell Mol Physiol 2016[Apr]; 310 (7 ): L630-8 PMID26851260 show ga Pulmonary endothelial prostacyclin appears to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). The effect of treatment with a prostacyclin analog in animal models of previously established COPD is unknown. We evaluated the short- and long-term effect of iloprost on inflammation and airway hyperresponsiveness (AHR) in a murine model of COPD. Nineteen mice were exposed to LPS/elastase, followed by either three doses of intranasal iloprost or saline. In the long-term treatment experiment, 18 mice were exposed to LPS/elastase and then received 6 wk of iloprost or were left untreated as controls. In the short-term experiment, iloprost did not change AHR but significantly reduced serum IL-5 and IFN-?. Long-term treatment with iloprost for both 2 and 6 wk significantly improved AHR. After 6 wk of iloprost, there was a reduction in bronchoalveolar lavage (BALF) neutrophils, serum IL-1? (30.0 ± 9.2 vs. 64.8 ± 7.4 pg/ml, P = 0.045), IL-2 (36.5 ± 10.6 vs. 83.8 ± 0.4 pg/ml, P = 0.01), IL-10 (75.7 ± 9.3 vs. 96.5 ± 3.5 pg/ml, P = 0.02), and nitrite (15.1 ± 5.4 vs. 30.5 ± 10.7 ?mol, P = 0.01). Smooth muscle actin (SMA) in the lung homogenate was also significantly reduced after iloprost treatment (P = 0.02), and SMA thickness was reduced in the small and medium blood vessels after iloprost (P < 0.001). In summary, short- and long-term treatment with intranasal iloprost significantly reduced systemic inflammation in an LPS/elastase COPD model. Long-term iloprost treatment also reduced AHR, serum nitrite, SMA, and BALF neutrophilia. These data encourage future investigations of prostanoid therapy as a novel treatment for COPD patients. |Administration, Intranasal [MESH] |Animals [MESH] |Anti-Inflammatory Agents/*administration & dosage [MESH] |Cytokines/metabolism [MESH] |Disease Models, Animal [MESH] |Drug Evaluation, Preclinical [MESH] |Iloprost/*administration & dosage [MESH] |Lipopolysaccharides/pharmacology [MESH] |Male [MESH] |Mice, Inbred C57BL [MESH] |Neutrophil Infiltration [MESH] |Pulmonary Disease, Chronic Obstructive/*drug therapy/immunology [MESH]Treatment with intranasal iloprost reduces disease manifestations in a(epmc).pdf DeepDyve Pubget Overpricing