{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T22:35:50Z","timestamp":1792708550866,"version":"4.5.0"},"reference-count":68,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2017,7,1]],"date-time":"2017-07-01T00:00:00Z","timestamp":1498867200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,7,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The polysaccharide-rich fungal cell wall provides pathogen-specific targets for antifungal therapy and distinct molecular patterns that stimulate protective or detrimental host immunity. The echinocandin antifungal caspofungin inhibits synthesis of cell wall \u03b2-1,3-glucan and is used for prophylactic therapy in immune-suppressed individuals. However, breakthrough infections with fungal pathogen Aspergillus fumigatus are associated with caspofungin prophylaxis. In this study, we report in vitro and in vivo increases in fungal surface chitin in A. fumigatus induced by caspofungin that was associated with airway eosinophil recruitment in neutropenic mice with invasive pulmonary aspergillosis (IA). More importantly, caspofungin treatment of mice with IA resulted in a pattern of increased fungal burden and severity of disease that was reversed in eosinophil-deficient mice. Additionally, the eosinophil granule proteins major basic protein and eosinophil peroxidase were more frequently detected in the bronchoalveolar lavage fluid of lung transplant patients diagnosed with IA that received caspofungin therapy when compared with azole-treated patients. Eosinophil recruitment and inhibition of fungal clearance in caspofungin-treated mice with IA required RAG1 expression and \u03b3\u03b4 T cells. These results identify an eosinophil-mediated mechanism for paradoxical caspofungin activity and support the future investigation of the potential of eosinophil or fungal chitin-targeted inhibition in the treatment of IA.<\/jats:p>","DOI":"10.4049\/jimmunol.1700078","type":"journal-article","created":{"date-parts":[[2017,6,1]],"date-time":"2017-06-01T00:50:17Z","timestamp":1496278217000},"page":"624-632","source":"Crossref","is-referenced-by-count":21,"title":["Caspofungin Increases Fungal Chitin and Eosinophil and \u03b3\u03b4 T Cell\u2013Dependent Pathology in Invasive Aspergillosis"],"prefix":"10.1093","volume":"199","author":[{"given":"Nansalmaa","family":"Amarsaikhan","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, Indiana University School of Medicine\u2013Terre Haute , Terre Haute, IN 47809"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ethan M","family":"Sands","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Indiana University School of Medicine\u2013Terre Haute , Terre Haute, IN 47809"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anand","family":"Shah","sequence":"additional","affiliation":[{"name":"Fungal Pathogens Laboratory, National Heart and Lung Institute, Imperial College London , London SW7 2AZ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ali","family":"Abdolrasouli","sequence":"additional","affiliation":[{"name":"Fungal Pathogens Laboratory, National Heart and Lung Institute, Imperial College London , London SW7 2AZ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7826-9101","authenticated-orcid":false,"given":"Anna","family":"Reed","sequence":"additional","affiliation":[{"name":"Lung Transplant Unit, Royal Brompton and Harefield National Health Service Trust , London UB9 6JH,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James E","family":"Slaven","sequence":"additional","affiliation":[{"name":"Department of Biostatistics, Indiana University School of Medicine , Indianapolis, IN 46202"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darius","family":"Armstrong-James","sequence":"additional","affiliation":[{"name":"Fungal Pathogens Laboratory, National Heart and Lung Institute, Imperial College London , London SW7 2AZ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven P","family":"Templeton","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, Indiana University School of Medicine\u2013Terre Haute , Terre Haute, IN 47809"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2017,7,15]]},"reference":[{"key":"2025030614173730600_r1","doi-asserted-by":"crossref","first-page":"1953","DOI":"10.1128\/EC.00274-07","article-title":"Aspergillus fumigatus: principles of pathogenesis and host defense","volume":"6","author":"Hohl","year":"2007","journal-title":"Eukaryot. 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