{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,15]],"date-time":"2026-05-15T03:17:30Z","timestamp":1778815050237,"version":"3.51.4"},"reference-count":23,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2016,4,1]],"date-time":"2016-04-01T00:00:00Z","timestamp":1459468800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"name":"nih rr","award":["P41-GM103422"],"award-info":[{"award-number":["P41-GM103422"]}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["20579"],"award-info":[{"award-number":["20579"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["56341"],"award-info":[{"award-number":["56341"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["99514"],"award-info":[{"award-number":["99514"]}],"id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100006492","name":"Division of Intramural Research, National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["40196"],"award-info":[{"award-number":["40196"]}],"id":[{"id":"10.13039\/100006492","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2016,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Trypanosoma cruzi<\/jats:named-content>\n            infection, which is the etiological agent of Chagas disease, is associated with intense inflammation during the acute and chronic phases. The pathological progression of Chagas disease is influenced by the infiltration and transmigration of inflammatory cells across the endothelium to infected tissues, which are carefully regulated processes involving several molecular mediators, including adhesion molecules and platelet-activating factor (PAF). We have shown that PAF production is dependent upon calcium-independent group VIA phospholipase A\n            <jats:sub>2<\/jats:sub>\n            \u03b2 (iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2) following infection of human coronary artery endothelial cells (HCAECs) with\n            <jats:named-content content-type=\"genus-species\">T. cruzi<\/jats:named-content>\n            , suggesting that the absence of iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2 may decrease the recruitment of inflammatory cells to the heart to manage parasite accumulation. Cardiac endothelial cells isolated from iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2-knockout (iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2-KO) mice infected with\n            <jats:named-content content-type=\"genus-species\">T. cruzi<\/jats:named-content>\n            demonstrated decreased PAF production compared to that by cells isolated from wild-type (WT) mice but demonstrated increases in adhesion molecule expression similar to those seen in WT mice. Myocardial inflammation in iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2-KO mice infected with\n            <jats:named-content content-type=\"genus-species\">T. cruzi<\/jats:named-content>\n            was similar in severity to that in WT mice, but the iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2-KO mouse myocardium contained more parasite pseudocysts. Upon activation, macrophages from iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2-KO mice produced significantly less nitric oxide (NO) and caused less\n            <jats:named-content content-type=\"genus-species\">T. cruzi<\/jats:named-content>\n            inhibition than macrophages from wild-type mice. Thus, the absence of iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2 activity does not influence myocardial inflammation, but iPLA\n            <jats:sub>2<\/jats:sub>\n            \u03b2 is essential for\n            <jats:named-content content-type=\"genus-species\">T. cruzi<\/jats:named-content>\n            clearance.\n          <\/jats:p>","DOI":"10.1128\/iai.01564-15","type":"journal-article","created":{"date-parts":[[2016,2,9]],"date-time":"2016-02-09T04:29:23Z","timestamp":1454992163000},"page":"1137-1142","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":15,"title":["Mice with Genetic Deletion of Group VIA Phospholipase A\n            <sub>2<\/sub>\n            \u03b2 Exhibit Impaired Macrophage Function and Increased Parasite Load in Trypanosoma cruzi-Induced Myocarditis"],"prefix":"10.1128","volume":"84","author":[{"given":"Janhavi","family":"Sharma","sequence":"first","affiliation":[{"name":"Department of Pathology, Saint Louis University School of Medicine, St. Louis, Missouri, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jennifer R.","family":"Blase","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, Missouri, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel F.","family":"Hoft","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, Missouri, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John O.","family":"Marentette","sequence":"additional","affiliation":[{"name":"Department of Pathology, Saint Louis University School of Medicine, St. Louis, Missouri, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John","family":"Turk","sequence":"additional","affiliation":[{"name":"Division of Endocrinology, Metabolism, and Lipid Research, Department of Medicine, Washington University in St. Louis, St. Louis, Missouri, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane","family":"McHowat","sequence":"additional","affiliation":[{"name":"Department of Pathology, Saint Louis University School of Medicine, St. Louis, Missouri, 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