{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T12:40:23Z","timestamp":1791031223564,"version":"4.1.0"},"reference-count":27,"publisher":"American Society for Microbiology","issue":"4","license":[{"start":{"date-parts":[[2011,4,1]],"date-time":"2011-04-01T00:00:00Z","timestamp":1301616000000},"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":[[2011,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Cerebral malaria (CM) is a major complication of<jats:italic>Plasmodium falciparum<\/jats:italic>infection, particularly in children. The pathogenesis of cerebral malaria involves parasitized red blood cell (RBC)-mediated vascular inflammation, immune stimulation, loss of blood-brain barrier integrity, and obstruction of cerebral capillaries. Therefore, blunting vascular inflammation and immune cell recruitment is crucial in limiting the disease course. Beta interferon (IFN-\u03b2) has been used in the treatment of diseases, such as multiple sclerosis (MS) but has not yet been explored in the treatment of CM. Therefore, we sought to determine whether IFN-\u03b2 also limits disease progression in experimental cerebral malaria (ECM).<jats:italic>Plasmodium berghei<\/jats:italic>-infected mice treated with IFN-\u03b2 died later and showed increased survival, with improved blood-brain barrier function, compared to infected mice. IFN-\u03b2 did not alter systemic parasitemia. However, we identified multiple action sites that were modified by IFN-\u03b2 administration.<jats:italic>P. berghei<\/jats:italic>infection resulted in increased expression of chemokine (C-X-C motif) ligand 9 (CXCL9) in brain vascular endothelial cells that attract T cells to the brain, as well as increased T-cell chemokine (C-X-C motif) receptor 3 (CXCR3) expression. The infection also increased the cellular content of intercellular adhesion molecule 1 (ICAM-1), a molecule important for attachment of parasitized RBCs to the endothelial cell. In this article, we report that IFN-\u03b2 treatment leads to reduction of CXCL9 and ICAM-1 in the brain, reduction of T-cell CXCR3 expression, and downregulation of serum tumor necrosis factor alpha (TNF-\u03b1). In addition, IFN-\u03b2-treated<jats:italic>P. berghei<\/jats:italic>-infected mice also had fewer brain T-cell infiltrates, further demonstrating its protective effects. Hence, IFN-\u03b2 has important anti-inflammatory properties that ameliorate the severity of ECM and prolong mouse survival.<\/jats:p>","DOI":"10.1128\/iai.00810-10","type":"journal-article","created":{"date-parts":[[2011,1,19]],"date-time":"2011-01-19T04:51:07Z","timestamp":1295412667000},"page":"1750-1758","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":46,"title":["Beta Interferon Suppresses the Development of Experimental Cerebral Malaria"],"prefix":"10.1128","volume":"79","author":[{"given":"Craig N.","family":"Morrell","sequence":"first","affiliation":[{"name":"Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kalyan","family":"Srivastava","sequence":"additional","affiliation":[{"name":"Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"AnneMarie","family":"Swaim","sequence":"additional","affiliation":[{"name":"Department of Molecular and Comparative Pathobiology, School of Medicine, The Johns Hopkins University, Baltimore, Maryland 21287"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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