{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T18:59:33Z","timestamp":1791140373042,"version":"4.1.0"},"reference-count":48,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2016,11,18]],"date-time":"2016-11-18T00:00:00Z","timestamp":1479427200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2016,12,1]],"date-time":"2016-12-01T00:00:00Z","timestamp":1480550400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100000265","name":"Medical Research Council","doi-asserted-by":"publisher","award":["G1001998"],"award-info":[{"award-number":["G1001998"]}],"id":[{"id":"10.13039\/501100000265","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","award":["094779"],"award-info":[{"award-number":["094779"]}],"id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2016,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Chronic pulmonary infection with\n                    <jats:named-content content-type=\"genus-species\">Pseudomonas aeruginosa<\/jats:named-content>\n                    is a feature of cystic fibrosis (CF) and other chronic lung diseases. Cytokines of the interleukin-17 (IL-17) family have been proposed as important in the host response to\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    infection through their role in augmenting antibacterial immune responses, although their proinflammatory effect may contribute to lung damage that occurs as a result of chronic infection. We set out to explore the role of IL-17 in the host response to chronic\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    infection. We used a murine model of chronic pulmonary infection with CF-related strains of\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    . We demonstrate that IL-17 cytokine signaling is essential for mouse survival and prevention of chronic infection at 2 weeks postinoculation using two different\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    strains. Following infection, there was a marked expansion of cells within mediastinal lymph nodes, comprised mainly of innate lymphoid cells (ILCs); \u223c90% of IL-17-producing (IL-17\n                    <jats:sup>+<\/jats:sup>\n                    ) cells had markers consistent with group 3 ILCs. A smaller percentage of IL-17\n                    <jats:sup>+<\/jats:sup>\n                    cells had markers consistent with a B1 phenotype. In lung homogenates harvested 14 days following infection, there was a significant expansion of IL-17\n                    <jats:sup>+<\/jats:sup>\n                    cells; about 50% of these were CD3\n                    <jats:sup>+<\/jats:sup>\n                    , split equally between CD4\n                    <jats:sup>+<\/jats:sup>\n                    Th17 cells and \u03b3\u03b4 T cells, while the CD3\n                    <jats:sup>\u2212<\/jats:sup>\n                    IL-17\n                    <jats:sup>+<\/jats:sup>\n                    cells were almost exclusively group 3 ILCs. Further experiments with B cell-deficient mice showed that B cell production of IL-17 or natural antibodies did not provide any defense against chronic\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    infection. Thus, IL-17 rather than antibody is a key element in host defense against chronic pulmonary infection with\n                    <jats:named-content content-type=\"genus-species\">P. aeruginosa<\/jats:named-content>\n                    .\n                  <\/jats:p>","DOI":"10.1128\/iai.00717-16","type":"journal-article","created":{"date-parts":[[2016,10,3]],"date-time":"2016-10-03T22:39:14Z","timestamp":1475534354000},"page":"3507-3516","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":75,"title":["Interleukin-17 Is Required for Control of Chronic Lung Infection Caused by Pseudomonas aeruginosa"],"prefix":"10.1128","volume":"84","author":[{"given":"Hannah K.","family":"Bayes","sequence":"first","affiliation":[{"name":"Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neil D.","family":"Ritchie","sequence":"additional","affiliation":[{"name":"Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4140-6352","authenticated-orcid":false,"given":"Thomas J.","family":"Evans","sequence":"additional","affiliation":[{"name":"Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jcf.2005.05.018"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro2907"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/s12016-007-8039-9"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1600-065X.2008.00699.x"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1186\/1465-9921-11-177"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.181.7.4965"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.smim.2007.10.009"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1586\/17476348.1.1.121"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0090263"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00011-007-6187-2"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1574-695X.2010.00764.x"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1258\/002367702320162405"},{"key":"e_1_3_3_14_2","article-title":"A murine model of early Pseudomonas aeruginosa lung disease with transition to chronic infection","author":"Bayes HK","unstructured":"Bayes HK, Ritchie ND, Irvine S, Evans TJ. 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