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We hypothesized that IL-17 responses would be detrimental in this setting and tested the impact of IL-17 receptor deficiency or antibody-mediated neutralization of IL-17 in a murine model of<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Pseudomonas aeruginosa<\/jats:named-content>ulcerative keratitis after scratch injury. We found that, compared with infected corneas from wild-type mice, those from IL-17 receptor (IL-17R)-deficient mice had significantly lower corneal pathology scores, neutrophil influx, and intracellular bacterial levels. Infected IL-17R-deficient corneas had low intercellular adhesion molecule 1 (ICAM-1) expression, and ICAM-1-deficient mice were similarly resistant to infection. Topical treatment with polyclonal antibodies to IL-17 resulted in significant reductions in corneal pathology and also lowered bacterial counts after infection with six different laboratory or clinical<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">P. aeruginosa<\/jats:named-content>strains, including both invasive and cytotoxic strains. Thus, neutralization of IL-17 during<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">P. aeruginosa<\/jats:named-content>corneal infection reduces neutrophil influx and pathology without compromising bacterial clearance and offers a promising new avenue for therapy of these potentially sight-threatening infections.<\/jats:p>","DOI":"10.1128\/iai.00249-12","type":"journal-article","created":{"date-parts":[[2012,7,17]],"date-time":"2012-07-17T15:52:16Z","timestamp":1342540336000},"page":"3706-3712","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":33,"title":["Topical Neutralization of Interleukin-17 during Experimental Pseudomonas aeruginosa Corneal Infection Promotes Bacterial Clearance and Reduces Pathology"],"prefix":"10.1128","volume":"80","author":[{"given":"Tanweer S.","family":"Zaidi","sequence":"first","affiliation":[{"name":"Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA"},{"name":"Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tauqeer","family":"Zaidi","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA"},{"name":"Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerald B.","family":"Pier","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA"},{"name":"Harvard Medical School, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory P.","family":"Priebe","sequence":"additional","affiliation":[{"name":"Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA"},{"name":"Harvard Medical School, Boston, Massachusetts, USA"},{"name":"Department of Anesthesiology, Perioperative and Pain Medicine, Division of Critical Care Medicine, and Department of Medicine, Division of Infectious Diseases, Boston Children's Hospital, Boston, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"494","DOI":"10.4049\/jimmunol.162.1.494","article-title":"IL-17 is produced by nickel-specific T lymphocytes and regulates ICAM-1 expression and chemokine production in human keratinocytes: synergistic or antagonist effects with IFN-gamma and TNF-alpha","volume":"162","author":"Albanesi C","year":"1999","unstructured":"AlbanesiCCavaniAGirolomoniG. 1999. 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