{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,17]],"date-time":"2026-01-17T04:25:19Z","timestamp":1768623919461,"version":"3.49.0"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2014,2,1]],"date-time":"2014-02-01T00:00:00Z","timestamp":1391212800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2014,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:named-content content-type=\"genus-species\">Cryptococcus neoformans<\/jats:named-content>is an opportunistic fungal pathogen that initiates infection following inhalation. As a result, the pulmonary immune response provides a first line of defense against<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>. Surfactant protein D (SP-D) is an important regulator of pulmonary immune responses and is typically host protective against bacterial and viral respiratory infections. However, SP-D is not protective against<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>. This is evidenced by previous work from our laboratory demonstrating that SP-D-deficient mice infected with<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>have a lower fungal burden and live longer than wild-type (WT) control animals. We hypothesized that SP-D alters susceptibility to<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>by dysregulating the innate pulmonary immune response following infection. Thus, inflammatory cells and cytokines were compared in the bronchoalveolar lavage fluid from WT and SP-D<jats:sup>\u2212\/\u2212<\/jats:sup>mice after<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>infection. Postinfection, mice lacking SP-D have reduced eosinophil infiltration and interleukin-5 (IL-5) in lung lavage fluid. To further explore the interplay of SP-D, eosinophils, and IL-5, mice expressing altered levels of eosinophils and\/or IL-5 were infected with<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>to assess the role of these innate immune mediators. IL-5-overexpressing mice have increased pulmonary eosinophilia and are more susceptible to<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>infection than WT mice. Furthermore, susceptibility of SP-D<jats:sup>\u2212\/\u2212<\/jats:sup>mice to<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>infection could be restored to the level of WT mice by increasing IL-5 and eosinophils by crossing the IL-5-overexpressing mice with SP-D<jats:sup>\u2212\/\u2212<\/jats:sup>mice. Together, these studies support the conclusion that SP-D increases susceptibility to<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>infection by promoting<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>-driven pulmonary IL-5 and eosinophil infiltration.<\/jats:p>","DOI":"10.1128\/iai.00855-13","type":"journal-article","created":{"date-parts":[[2013,11,26]],"date-time":"2013-11-26T04:25:37Z","timestamp":1385439937000},"page":"683-693","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":33,"title":["Impact of Surfactant Protein D, Interleukin-5, and Eosinophilia on Cryptococcosis"],"prefix":"10.1128","volume":"82","author":[{"given":"Stephanie M.","family":"Holmer","sequence":"first","affiliation":[{"name":"Department of Cell Biology, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kathy S.","family":"Evans","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yohannes G.","family":"Asfaw","sequence":"additional","affiliation":[{"name":"Division of Laboratory Animal Resources, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Divey","family":"Saini","sequence":"additional","affiliation":[{"name":"Duke Human Vaccine Institute, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wiley A.","family":"Schell","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julie G.","family":"Ledford","sequence":"additional","affiliation":[{"name":"Department of Cell Biology, Duke University Medical Center, Durham, North Carolina, USA"},{"name":"Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard","family":"Frothingham","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA"},{"name":"Duke Human Vaccine Institute, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jo Rae","family":"Wright","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory D.","family":"Sempowski","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA"},{"name":"Department of Pathology, Duke University Medical Center, Durham, North Carolina, USA"},{"name":"Duke Human Vaccine Institute, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John R.","family":"Perfect","sequence":"additional","affiliation":[{"name":"Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1097\/QAD.0b013e328322ffac"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00809-09"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.179.8.5367"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2010.090634"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.01143-07"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.2353\/ajpath.2009.090530"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0006854"},{"key":"e_1_3_3_9_2","doi-asserted-by":"crossref","first-page":"2393","DOI":"10.4049\/jimmunol.160.5.2393","article-title":"IL-5 is required for eosinophil recruitment, crystal deposition, and mononuclear cell recruitment during a pulmonary Cryptococcus neoformans infection in genetically susceptible mice (C57BL\/6)","volume":"160","author":"Huffnagle GB","year":"1998","unstructured":"HuffnagleGBBoydMBStreetNELipscombMF. 1998. 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