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Bazley Trust"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2015,2]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    Chronic rhinosinusitis with nasal polyps (\n                    <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>\n                    w\n                    <jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>\n                    ) is a complex inflammatory condition that affects a large proportion of the population world\u2010wide and is associated with high cost of management and significant morbidity. Yet, there is a lack of population\u2010based epidemiologic studies using current definitions of\n                    <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>\n                    w\n                    <jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>\n                    , and the mechanisms that drive pathogenesis in this disease remain unclear. In this review, we summarize the current evidence for the plethora of factors that likely contribute to\n                    <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>\n                    w\n                    <jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>\n                    pathogenesis. Defects in the innate function of the airway epithelial barrier, including diminished expression of antimicrobial products and loss of barrier integrity, combined with colonization by fungi and bacteria likely play a critical role in the development of chronic inflammation in\n                    <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>\n                    w\n                    <jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>\n                    . This chronic inflammation is characterized by elevated expression of many key inflammatory cytokines and chemokines, including\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20105, thymic stromal lymphopoietin and\n                    <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>\n                    11, that help to initiate and perpetuate this chronic inflammatory response. Together, these factors likely combine to drive the influx of a variety of immune cells, including eosinophils, mast cells, group 2 innate lymphoid cells and lymphocytes, which participate in the chronic inflammatory response within the nasal polyps. Importantly, however, future studies are needed to demonstrate the necessity and sufficiency of these potential drivers of disease in\n                    <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>\n                    w\n                    <jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>\n                    . In addition to the development of new tools and models to aid mechanistic studies, the field of\n                    <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>\n                    w\n                    <jats:styled-content style=\"fixed-case\">NP<\/jats:styled-content>\n                    research also needs the type of robust epidemiologic data that has served the asthma community so well. Given the high prevalence, costs and morbidity, there is a great need for continued research into\n                    <jats:styled-content style=\"fixed-case\">CRS<\/jats:styled-content>\n                    that could facilitate the development of novel therapeutic strategies to improve treatment for patients who suffer from this disease.\n                  <\/jats:p>","DOI":"10.1111\/cea.12472","type":"journal-article","created":{"date-parts":[[2014,12,9]],"date-time":"2014-12-09T01:31:52Z","timestamp":1418088712000},"page":"328-346","source":"Crossref","is-referenced-by-count":210,"title":["Pathogenesis of nasal polyposis"],"prefix":"10.1111","volume":"45","author":[{"given":"K. E.","family":"Hulse","sequence":"first","affiliation":[{"name":"Division of Allergy\u2010Immunology Department of Medicine Northwestern University Feinberg School of Medicine Chicago IL USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W. 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