Send to

Choose Destination
See comment in PubMed Commons below
Eur J Clin Microbiol Infect Dis. 2014 Aug;33(8):1457-65. doi: 10.1007/s10096-014-2087-x. Epub 2014 Mar 30.

MicroRNA expressions associated with eosinophilic meningitis caused by Angiostrongylus cantonensis infection in a mouse model.

Author information

Department of Parasitology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.


Angiostrongylus cantonensis (A. cantonensis) infection is the major cause of eosinophilic meningitis (EM). Severe cases or infant and child cases have poor prognosis. MicroRNAs (miRNAs) play important roles in inflammation; however, little is known about the roles in brain inflammation caused by A. cantonensis. In this study, Illumina deep sequencing and bioinformatics were used to determine the abundance and differential expression of miRNAs in the brain tissues of a mouse model. A total of 648 conserved miRNAs were identified, 157 of which were significantly differentially expressed between infected mice and normal mice. The five most fold-changed miRNAs were miR-511-5p, miR-511-3p, miR-223-3p, miR-155-5p and miR-206-3p. These expressions of miR-511, miR-223, miR-155, miR-206, miR-142 and miR-21a were validated by quantitative reverse transcription polymerase chain reaction (RT-PCR). The analysis of these miRNAs showed that miR-511-3p was more abundant than the miR-511-5p strand, and increased to a peak in 21 days after A. cantonensis infection, miR-223 might be a potential indicator of disease severity and the upregulation of miR-155-5p after stimulation with the somatic antigen of phase IV A. cantonensis implied its involvement in the central nervous system (CNS) inflammation induced by A. cantonensis infection. These observations suggest that miRNAs may play important roles in the regulation of EM caused by A. cantonensis infection.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Springer
    Loading ...
    Support Center