Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Differential microRNA expression in experimental cerebral and noncerebral malaria

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Antibiotic prescribing in paediatric inpatients in Ghana: a multi-centre point prevalence survey

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Population Pharmacokinetics of the Antimalarial Amodiaquine: a Pooled Analysis To Optimize Dosing

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Traffic flow and microbial air contamination in operating rooms at a major teaching hospital in Ghana

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer
MicroRNAs (miRNAs) are posttranscriptional regulatory molecules that have been implicated in the regulation of immune responses, but their role in the immune response to Plasmodium infection is unknown. We studied the expression of selected miRNAs following infection of CBA mice with Plasmodium berghei ANKA (PbA), which causes cerebral malaria (CM), or Plasmodium berghei K173 (PbK), which causes severe malaria but without cerebral complications, termed non-CM. The differential expression profiles of selected miRNAs (let-7i, miR-27a, miR-150, miR-126, miR-210, and miR-155) were analyzed in mouse brain and heart tissue by quantitative reverse transcription-PCR (qRT-PCR). We identified three miRNAs that were differentially expressed in the brain of PbA-infected CBA mice: let7i, miR-27a, and miR-150. In contrast, no miRNA changes were detected in the heart, an organ with no known pathology during acute malaria. To investigate the involvement of let-7i, miR-27a, and miR-150 in CM-resistant mice, we assessed the expression levels in gamma interferon knockout (IFN-γ(-/-)) mice on a C57BL/6 genetic background. The expression of let-7i, miR-27a, and miR-150 was unchanged in both wild-type (WT) and IFN-γ(-/-) mice following infection. Overexpression of these three miRNAs during PbA, but not PbK, infection in WT mice may be critical for the triggering of the neurological syndrome via regulation of their potential downstream targets. Our data suggest that in the CBA mouse at least, miRNA may have a regulatory role in the pathogenesis of severe malaria.
OriginalsprogEngelsk
TidsskriftInfection and Immunity
Vol/bind79
Udgave nummer6
Sider (fra-til)2379-84
Antal sider6
ISSN0019-9567
DOI
StatusUdgivet - 1 jun. 2011

ID: 32665872