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10.1016/j.jaci.2015.09.033 http://scihub22266oqcxt.onion/10.1016/j.jaci.2015.09.033 C4860134!4860134 !26589586     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26589586 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26589586 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Allergy+Clin+Immunol 2016 ; 137 (5 ): 1382-1389.e9 Nephropedia Template TP {{tp|p=26589586 |t=2016. Lack of autophagy induces steroid-resistant airway inflammation |pdf=|usr=}}{{26589586 }} gab.com Text Lack of autophagy induces steroid-resistant airway inflammation JO: J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26589586 #FOAvip BACKGROUND: Neutrophilic corticosteroid-resistant asthma accounts for a significant proportion of asthma; however, little is known about the mechanisms that underlie the pathogenesis of the disease. OBJECTIVE: We sought to address the role of autophagy in lung inflammation and the pathogenesis of corticosteroid-resistant neutrophilic asthma. METHODS: We developed CD11c-specific autophagy-related gene 5 (Atg5)(-/-) mice and used several murine models to investigate the role of autophagy in asthmatic patients. RESULTS: For the first time, we found that deletion of the Atg5 gene specifically in CD11c(+) cells, which leads to impairment of the autophagy pathway, causes unprovoked spontaneous airway hyperreactivity and severe neutrophilic lung inflammation in mice. We found that severe lung inflammation impairs the autophagy pathway, particularly in pulmonary CD11c(+) cells in wild-type mice. We further found that adoptive transfer of Atg5(-/-), but not wild-type, bone marrow-derived dendritic cells augments lung inflammation with increased IL-17A levels in the lungs. Our data indicate that neutrophilic asthma in Atg5(-/-) mice is glucocorticoid resistant and IL-17A dependent. CONCLUSION: Our results suggest that lack of autophagy in pulmonary CD11c(+) cells induces neutrophilic airway inflammation and hyperreactivity. Twit Text FOAVip Lack of autophagy induces steroid-resistant airway inflammation ????J Allergy Clin Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26589586 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26589586 #FOAvip English Wikipedia <ref>{{Cite pmid|26589586 }}</ref> Lack of autophagy induces steroid-resistant airway inflammation #MMPMID26589586 Suzuki Y ; Maazi H ; Sankaranarayanan I ; Lam J ; Khoo B ; Soroosh P ; Barbers RG ; James Ou JH ; Jung JU ; Akbari O J Allergy Clin Immunol 2016[May]; 137 (5 ): 1382-1389.e9 PMID26589586 show ga BACKGROUND: Neutrophilic corticosteroid-resistant asthma accounts for a significant proportion of asthma; however, little is known about the mechanisms that underlie the pathogenesis of the disease. OBJECTIVE: We sought to address the role of autophagy in lung inflammation and the pathogenesis of corticosteroid-resistant neutrophilic asthma. METHODS: We developed CD11c-specific autophagy-related gene 5 (Atg5)(-/-) mice and used several murine models to investigate the role of autophagy in asthmatic patients. RESULTS: For the first time, we found that deletion of the Atg5 gene specifically in CD11c(+) cells, which leads to impairment of the autophagy pathway, causes unprovoked spontaneous airway hyperreactivity and severe neutrophilic lung inflammation in mice. We found that severe lung inflammation impairs the autophagy pathway, particularly in pulmonary CD11c(+) cells in wild-type mice. We further found that adoptive transfer of Atg5(-/-), but not wild-type, bone marrow-derived dendritic cells augments lung inflammation with increased IL-17A levels in the lungs. Our data indicate that neutrophilic asthma in Atg5(-/-) mice is glucocorticoid resistant and IL-17A dependent. CONCLUSION: Our results suggest that lack of autophagy in pulmonary CD11c(+) cells induces neutrophilic airway inflammation and hyperreactivity. |*Asthma/drug therapy/immunology [MESH] |*Autophagy [MESH] |*Drug Resistance [MESH] |Animals [MESH] |Anti-Inflammatory Agents/therapeutic use [MESH] |Autophagy-Related Protein 5/genetics [MESH] |Bronchoalveolar Lavage Fluid/cytology/immunology [MESH] |Cell Count [MESH] |Cytokines/immunology [MESH] |Dexamethasone/*therapeutic use [MESH] |Female [MESH] |Lung/cytology/immunology [MESH] |Mice, Inbred BALB C [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH]Lack of autophagy induces steroid-resistant airway inflammation (epmc).pdf DeepDyve Pubget Overpricing