{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T15:40:15Z","timestamp":1791042015905,"version":"4.1.0"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"7","license":[{"start":{"date-parts":[[2005,7,1]],"date-time":"2005-07-01T00:00:00Z","timestamp":1120176000000},"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":[[2005,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Chemokines regulate the host immune response to a variety of infectious pathogens. Since the role of chemokines in regulating host immunity in children with\n            <jats:italic>Plasmodium falciparum<\/jats:italic>\n            malaria has not previously been reported, circulating levels of \u03b2-chemokines (MIP-1\u03b1, MIP-1\u03b2, and RANTES) and their respective transcriptional profiles in ex vivo peripheral blood mononuclear cells (PBMCs) were investigated. Peripheral blood MIP-1\u03b1 and MIP-1\u03b2 levels were significantly elevated in mild and severe malaria, while RANTES levels decreased with increasing disease severity. \u03b2-Chemokine gene expression profiles in blood mononuclear cells closely matched those of circulating \u03b2-chemokines, illustrating that PBMCs are a primary source for the observed pattern of \u03b2-chemokine production during acute malaria. Statistical modeling revealed that none of the chemokines was significantly associated with either parasitemia or anemia. Additional investigations in healthy children with a known history of malaria showed that children with prior severe malaria had significantly lower baseline RANTES production than children with a history of mild malaria, suggesting inherent differences in the ability to produce RANTES in these two groups. Baseline MIP-1\u03b1 and MIP-1\u03b2 did not significantly differ between children with prior severe malaria and those with mild malaria. Additional in vitro experiments in PBMCs from healthy, malaria-nai\u0308ve donors revealed that\n            <jats:italic>P. falciparum<\/jats:italic>\n            -derived hemozoin (Hz; malarial pigment) and synthetic Hz (\u03b2-hematin) promote a similar pattern of \u03b2-chemokine gene expression. Taken together, the results presented here demonstrate that children with severe malaria have a distinct profile of \u03b2-chemokines characterized by increased circulating levels of MIP-1\u03b1 and MIP-1\u03b2 and decreased RANTES. Altered patterns of circulating \u03b2-chemokines result, at least in part, from Hz-induced changes in \u03b2-chemokine gene expression in blood mononuclear cells.\n          <\/jats:p>","DOI":"10.1128\/iai.73.7.4190-4197.2005","type":"journal-article","created":{"date-parts":[[2005,6,22]],"date-time":"2005-06-22T02:15:26Z","timestamp":1119406526000},"page":"4190-4197","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":80,"title":["Differential Regulation of \u03b2-Chemokines in Children with\n            <i>Plasmodium falciparum<\/i>\n            Malaria"],"prefix":"10.1128","volume":"73","author":[{"given":"Daniel O.","family":"Ochiel","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gordon A.","family":"Awandare","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher C.","family":"Keller","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James B.","family":"Hittner","sequence":"additional","affiliation":[{"name":"Department of Psychology, College of Charleston, Charleston, South Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter G.","family":"Kremsner","sequence":"additional","affiliation":[{"name":"Department of Parasitology, Institute of Tropical Medicine, University of Tu\u0308bingen, Tu\u0308bingen, Germany"},{"name":"Research Unit, Albert Schweitzer Hospital, Lambare\u0301ne\u0301, Gabon"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. Brice","family":"Weinberg","sequence":"additional","affiliation":[{"name":"Department of Medicine, VA and Duke University Medical Centers, Durham, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas J.","family":"Perkins","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases and Microbiology, University of Pittsburgh, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.5.2759"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1089\/107999002760624305"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.4269\/ajtmh.2001.64.iv"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1471-4922(01)01902-X"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF02982544"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1006\/clin.1995.1084"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1038\/sj.onc.1205326"},{"key":"e_1_3_2_9_2","first-page":"631","volume":"10","year":"2003","unstructured":"Chaisavaneeyakorn, S., J. 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