{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,9,27]],"date-time":"2025-09-27T08:33:34Z","timestamp":1758962014897},"reference-count":40,"publisher":"American Society for Microbiology","issue":"2","license":[{"start":{"date-parts":[[2016,2,1]],"date-time":"2016-02-01T00:00:00Z","timestamp":1454284800000},"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":[[2016,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Cerebral malaria (CM) is the most severe complication of human infection with<jats:named-content content-type=\"genus-species\">Plasmodium falciparum<\/jats:named-content>. The mechanisms predisposing to CM are still not fully understood. Proinflammatory immune responses are required for the control of blood-stage malaria infection but are also implicated in the pathogenesis of CM. A fine balance between pro- and anti-inflammatory immune responses is required for parasite clearance without the induction of host pathology. The most accepted experimental model to study human CM is<jats:named-content content-type=\"genus-species\">Plasmodium berghei<\/jats:named-content>ANKA (<jats:italic>Pb<\/jats:italic>ANKA) infection in C57BL\/6 mice that leads to the development of a complex neurological syndrome which shares many characteristics with the human disease. We applied this model to study the outcome of<jats:italic>Pb<\/jats:italic>ANKA infection in mice previously infected with<jats:named-content content-type=\"genus-species\">Mycobacterium tuberculosis<\/jats:named-content>, the causative agent of tuberculosis. Tuberculosis is coendemic with malaria in large regions in the tropics, and mycobacteria have been reported to confer some degree of unspecific protection against rodent<jats:named-content content-type=\"genus-species\">Plasmodium<\/jats:named-content>parasites in experimental coinfection models. We found that concomitant<jats:named-content content-type=\"genus-species\">M. tuberculosis<\/jats:named-content>infection did not change the clinical course of<jats:italic>Pb<\/jats:italic>ANKA-induced experimental cerebral malaria (ECM) in C57BL\/6 mice. The immunological environments in spleen and brain did not differ between singly infected and coinfected animals; instead, the overall cytokine and T cell responses in coinfected mice were comparable to those in animals solely infected with<jats:italic>Pb<\/jats:italic>ANKA. Our data suggest that<jats:named-content content-type=\"genus-species\">M. tuberculosis<\/jats:named-content>coinfection is not able to change the outcome of<jats:italic>Pb<\/jats:italic>ANKA-induced disease, most likely because the inflammatory response induced by the parasite rapidly dominates in mice previously infected with<jats:named-content content-type=\"genus-species\">M. tuberculosis<\/jats:named-content>.<\/jats:p>","DOI":"10.1128\/iai.01290-15","type":"journal-article","created":{"date-parts":[[2015,12,8]],"date-time":"2015-12-08T15:05:36Z","timestamp":1449587136000},"page":"502-510","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":9,"title":["Mycobacterium tuberculosis Coinfection Has No Impact on Plasmodium berghei ANKA-Induced Experimental Cerebral Malaria in C57BL\/6 Mice"],"prefix":"10.1128","volume":"84","author":[{"given":"Jannike","family":"Blank","sequence":"first","affiliation":[{"name":"Division of Coinfection, Priority Area Infections, Research Center Borstel, Borstel, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jochen","family":"Behrends","sequence":"additional","affiliation":[{"name":"Fluorescence Cytometry Core Facility, Research Center Borstel, Borstel, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Jacobs","sequence":"additional","affiliation":[{"name":"Department of Immunology, Bernhard Nocht Institute for Tropical Medicine, Hamburg, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bianca E.","family":"Schneider","sequence":"additional","affiliation":[{"name":"Division of Coinfection, Priority Area Infections, Research Center Borstel, Borstel, Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1017\/S0031182009991715"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.pt.2010.03.002"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1000944"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1003955"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1100241"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1200688"},{"key":"e_1_3_3_8_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.ppat.1000369"},{"key":"e_1_3_3_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00079-10"},{"key":"e_1_3_3_10_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.3306918"},{"key":"e_1_3_3_11_2","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20020128"},{"key":"e_1_3_3_12_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.169.11.6369"},{"key":"e_1_3_3_13_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0806727105"},{"key":"e_1_3_3_14_2","doi-asserted-by":"publisher","DOI":"10.1002\/emmm.201202273"},{"key":"e_1_3_3_15_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.01210-10"},{"key":"e_1_3_3_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijpara.2010.08.003"},{"key":"e_1_3_3_17_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.9.5645-5653.2005"},{"key":"e_1_3_3_18_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0048110"},{"key":"e_1_3_3_19_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.33.1.199-211.1981"},{"key":"e_1_3_3_20_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0264-410X(00)00257-7"},{"key":"e_1_3_3_21_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.73.12.8369-8380.2005"},{"key":"e_1_3_3_22_2","doi-asserted-by":"publisher","DOI":"10.1038\/259309a0"},{"key":"e_1_3_3_23_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri3259"},{"key":"e_1_3_3_24_2","doi-asserted-by":"publisher","DOI":"10.3791\/50829"},{"key":"e_1_3_3_25_2","first-page":"257","article-title":"Resistance to cerebral malaria in tumor necrosis factor-alpha\/beta-deficient mice is associated with a reduction of intercellular adhesion molecule-1 up-regulation and T helper type 1 response","volume":"150","author":"Rudin W","year":"1997","unstructured":"Rudin W, Eugster HP, Bordmann G, Bonato J, Muller M, Yamage M, Ryffel B. 1997. 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