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Background   Legionella pneumophila  ( L .  pneumophila ) is a causative agent of severe pneumonia. It is highly adapted to intracellular replication and manipulates host cell functions like vesicle trafficking and mRNA translation to its own advantage. However, it is still unknown to what extent microRNAs (miRNAs) are involved in the  Legionella -host cell interaction.    Methods  WT and  MyD88  -/-  murine bone marrow-derived macrophages (BMM) were infected with  L .  pneumophila , the transcriptome was analyzed by high throughput qPCR array (microRNAs) and conventional qPCR (mRNAs), and mRNA-miRNA interaction was validated by luciferase assays with 3´-UTR mutations and western blot.    Results   L .  pneumophila  infection caused a pro-inflammatory reaction and significant miRNA changes in murine macrophages. In  MyD88  -/-  cells, induction of inflammatory markers, such as  Ccxl1/Kc ,  Il6  and miR-146a-5p was reduced. Induction of miR-125a-3p was completely abrogated in  MyD88  -/-  cells. Target prediction analyses revealed N-terminal asparagine amidase 1 (NTAN1), a factor from the n-end rule pathway, to be a putative target of miR-125a-3p. This interaction could be confirmed by luciferase assay and western blot.    Conclusion  Taken together, we characterized the miRNA regulation in  L .  pneumophila  infection with regard to MyD88 signaling and identified NTAN1 as a target of miR-125a-3p. This finding unravels a yet unknown feature of  Legionella -host cell interaction, potentially relevant for new treatment options.

microRNA-125a-3p is regulated by MyD88 in Legionella pneumophila infection and targets NTAN1