{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T20:46:32Z","timestamp":1761597992056,"version":"build-2065373602"},"reference-count":24,"publisher":"MDPI AG","issue":"3","license":[{"start":{"date-parts":[[2018,9,17]],"date-time":"2018-09-17T00:00:00Z","timestamp":1537142400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JoF"],"abstract":"<jats:p>Tissue from 13 autopsy cases with invasive gastrointestinal candidiasis was studied for the binding of the pentraxins, C-reactive protein (CRP), pentraxin 3 (PTX3), and serum amyloid P component (SAP) to fungal surfaces. Invasive candidal infection was demonstrated using a hematoxylin and eosin stain and a Gomori methenamine silver stain (GMS). Immunohistochemistry was performed with CRP and PTX3 monoclonal antibodies and did not demonstrate CRP or PTX3 bound to fungi (0 of 13 cases), although CRP was extensively deposited on human tissue. A polyclonal antibody to SAP showed that SAP was bound to fungi in 12 of 13 cases. Although all three pentraxins have been reported to bind to fungi or bacteria, only SAP was bound to filamentous and yeast forms of Candida in human tissue, as detected by immunohistochemistry. SAP was abundantly present on fungi and may have affected the host innate immune response to the invading fungi.<\/jats:p>","DOI":"10.3390\/jof4030111","type":"journal-article","created":{"date-parts":[[2018,9,17]],"date-time":"2018-09-17T10:42:20Z","timestamp":1537180940000},"page":"111","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Do Pentraxins Bind to Fungi in Invasive Human Gastrointestinal Candidiasis?"],"prefix":"10.3390","volume":"4","author":[{"given":"Umamaheshwari","family":"Golconda","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Arizona College of Medicine, Tucson, AZ 85724, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard E.","family":"Sobonya","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Arizona College of Medicine, Tucson, AZ 85724, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stephen A.","family":"Klotz","sequence":"additional","affiliation":[{"name":"Division of Infections Diseases, Department of Medicine, University of Arizona College of Medicine, Tucson, AZ 85724, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2018,9,17]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Du Clos, T.W. 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