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      Autophagy and inflammation in chronic respiratory disease

      1 , 2 , 1 , 1 , 2 , 1
      Autophagy
      Informa UK Limited

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          Abstract

          <p id="d1625664e186">Persistent inflammation within the respiratory tract underlies the pathogenesis of numerous chronic pulmonary diseases including chronic obstructive pulmonary disease, asthma and pulmonary fibrosis. Chronic inflammation in the lung may arise from a combination of genetic susceptibility and environmental influences, including exposure to microbes, particles from the atmosphere, irritants, pollutants, allergens, and toxic molecules. To this end, an immediate, strong, and highly regulated inflammatory defense mechanism is needed for the successful maintenance of homeostasis within the respiratory system. Macroautophagy/autophagy plays an essential role in the inflammatory response of the lung to infection and stress. At baseline, autophagy may be critical for inhibiting spontaneous pulmonary inflammation and fundamental for the response of pulmonary leukocytes to infection; however, when not regulated, persistent or inefficient autophagy may be detrimental to lung epithelial cells, promoting lung injury. This perspective will discuss the role of autophagy in driving and regulating inflammatory responses of the lung in chronic lung diseases with a focus on potential avenues for therapeutic targeting. </p><p id="d1625664e188"> <div class="def-list"> <a class="named-anchor" id="d1625664e190"> <!-- named anchor --> </a> <h6 class="subsection-title" id="d1625664e191">Abbreviations</h6> <table class="def-list"> <tr id="d1625664e193"> <td class="def-term" id="d1625664e194"> <p>AR</p> </td> <td id="d1625664e196"> <p class="first" id="d1625664e197">allergic rhinitis</p> </td> </tr> <tr id="d1625664e199"> <td class="def-term" id="d1625664e200"> <p>AM</p> </td> <td id="d1625664e202"> <p class="first" id="d1625664e203">alveolar macrophage</p> </td> </tr> <tr id="d1625664e205"> <td class="def-term" id="d1625664e206"> <p>ATG</p> </td> <td id="d1625664e208"> <p class="first" id="d1625664e209">autophagy-related</p> </td> </tr> <tr id="d1625664e211"> <td class="def-term" id="d1625664e212"> <p>CF</p> </td> <td id="d1625664e214"> <p class="first" id="d1625664e215">cystic fibrosis</p> </td> </tr> <tr id="d1625664e217"> <td class="def-term" id="d1625664e218"> <p>CFTR</p> </td> <td id="d1625664e220"> <p class="first" id="d1625664e221">cystic fibrosis transmembrane conductance regulator</p> </td> </tr> <tr id="d1625664e223"> <td class="def-term" id="d1625664e224"> <p>COPD</p> </td> <td id="d1625664e226"> <p class="first" id="d1625664e227">chronic obstructive pulmonary disease</p> </td> </tr> <tr id="d1625664e229"> <td class="def-term" id="d1625664e230"> <p>CS</p> </td> <td id="d1625664e232"> <p class="first" id="d1625664e233">cigarette smoke</p> </td> </tr> <tr id="d1625664e235"> <td class="def-term" id="d1625664e236"> <p>CSE</p> </td> <td id="d1625664e238"> <p class="first" id="d1625664e239">cigarette smoke extract</p> </td> </tr> <tr id="d1625664e241"> <td class="def-term" id="d1625664e242"> <p>DC</p> </td> <td id="d1625664e244"> <p class="first" id="d1625664e245">dendritic cell</p> </td> </tr> <tr id="d1625664e247"> <td class="def-term" id="d1625664e248"> <p>IH</p> </td> <td id="d1625664e250"> <p class="first" id="d1625664e251">intermittent hypoxia</p> </td> </tr> <tr id="d1625664e254"> <td class="def-term" id="d1625664e255"> <p>IPF</p> </td> <td id="d1625664e257"> <p class="first" id="d1625664e258">idiopathic pulmonary fibrosis</p> </td> </tr> <tr id="d1625664e260"> <td class="def-term" id="d1625664e261"> <p>ILD</p> </td> <td id="d1625664e263"> <p class="first" id="d1625664e264">interstitial lung disease</p> </td> </tr> <tr id="d1625664e266"> <td class="def-term" id="d1625664e267"> <p>MAP1LC3B</p> </td> <td id="d1625664e269"> <p class="first" id="d1625664e270">microtubule associated protein 1 light chain 3 beta</p> </td> </tr> <tr id="d1625664e272"> <td class="def-term" id="d1625664e273"> <p>MTB</p> </td> <td id="d1625664e275"> <p class="first" id="d1625664e276"> <i>Mycobacterium tuberculosis</i> </p> </td> </tr> <tr id="d1625664e281"> <td class="def-term" id="d1625664e282"> <p>MTOR</p> </td> <td id="d1625664e284"> <p class="first" id="d1625664e285">mechanistic target of rapamycin kinase</p> </td> </tr> <tr id="d1625664e287"> <td class="def-term" id="d1625664e288"> <p>NET</p> </td> <td id="d1625664e290"> <p class="first" id="d1625664e291">neutrophil extracellular traps</p> </td> </tr> <tr id="d1625664e293"> <td class="def-term" id="d1625664e294"> <p>OSA</p> </td> <td id="d1625664e296"> <p class="first" id="d1625664e297">obstructive sleep apnea</p> </td> </tr> <tr id="d1625664e299"> <td class="def-term" id="d1625664e300"> <p>PAH</p> </td> <td id="d1625664e302"> <p class="first" id="d1625664e303">pulmonary arterial hypertension</p> </td> </tr> <tr id="d1625664e305"> <td class="def-term" id="d1625664e306"> <p>PH</p> </td> <td id="d1625664e308"> <p class="first" id="d1625664e309">pulmonary hypertension</p> </td> </tr> <tr id="d1625664e311"> <td class="def-term" id="d1625664e312"> <p>ROS</p> </td> <td id="d1625664e314"> <p class="first" id="d1625664e315">reactive oxygen species</p> </td> </tr> <tr id="d1625664e317"> <td class="def-term" id="d1625664e318"> <p>TGFB1</p> </td> <td id="d1625664e320"> <p class="first" id="d1625664e321">transforming growth factor beta 1</p> </td> </tr> <tr id="d1625664e324"> <td class="def-term" id="d1625664e325"> <p>TNF</p> </td> <td id="d1625664e327"> <p class="first" id="d1625664e328">tumor necrosis factor</p> </td> </tr> </table> </div> </p>

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          Most cited references86

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          Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines-2016 revision.

          Allergic rhinitis (AR) affects 10% to 40% of the population. It reduces quality of life and school and work performance and is a frequent reason for office visits in general practice. Medical costs are large, but avoidable costs associated with lost work productivity are even larger than those incurred by asthma. New evidence has accumulated since the last revision of the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines in 2010, prompting its update.
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            Inflammation and immunity in the pathogenesis of pulmonary arterial hypertension.

            This review summarizes an expanding body of knowledge indicating that failure to resolve inflammation and altered immune processes underlie the development of pulmonary arterial hypertension. The chemokines and cytokines implicated in pulmonary arterial hypertension that could form a biomarker platform are discussed. Pre-clinical studies that provide the basis for dysregulated immunity in animal models of the disease are reviewed. In addition, we present therapies that target inflammatory/immune mechanisms that are currently enrolling patients, and discuss others in development. We show how genetic and metabolic abnormalities are inextricably linked to dysregulated immunity and adverse remodeling in the pulmonary arteries.
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              Human IRGM induces autophagy to eliminate intracellular mycobacteria.

              Immunity-related p47 guanosine triphosphatases (IRG) play a role in defense against intracellular pathogens. We found that the murine Irgm1 (LRG-47) guanosine triphosphatase induced autophagy and generated large autolysosomal organelles as a mechanism for the elimination of intracellular Mycobacterium tuberculosis. We also identified a function for a human IRG protein in the control of intracellular pathogens and report that the human Irgm1 ortholog, IRGM, plays a role in autophagy and in the reduction of intracellular bacillary load.
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                Author and article information

                Journal
                Autophagy
                Autophagy
                Informa UK Limited
                1554-8627
                1554-8635
                January 29 2018
                February 2018
                February 08 2018
                February 2018
                : 14
                : 2
                : 221-232
                Affiliations
                [1 ] Division of Pulmonary and Critical Care Medicine, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medical College, New York, NY, USA
                [2 ] New York-Presbyterian Hospital, New York, NY, USA
                Article
                10.1080/15548627.2017.1389823
                5902194
                29130366
                005914c3-bc1c-4e05-a242-5a8f5022cb32
                © 2018

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