MicroRNA-155 induction by Mycobacterium bovis BCG enhances ROS production through targeting SHIP1

Jinli Wang, Minhao Wu, Jinsheng Wen, Kun Yang, Miao Li, Xiaoxia Zhan, Lianqiang Feng, Meiyu Li, Xi Huang

Research output: Contribution to journalArticlepeer-review

54 Scopus citations


mycobacterial infection. Macrophages play a critical role in the host immune response against mycobacterial infection. Our previous study has demonstrated that microRNA-155 (miR-155), one of the most important small non-coding RNAs in the immune system, promotes oxygen-independent mycobacterial killing in macrophages. However, little is known regarding the role of miR-155 in modulating oxygen-dependent mycobactericidal response in macrophages, including the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). In the present study, we demonstrated that miR-155 was increased in macrophages after Mycobacterium bovis bacille Calmette-Guérin (BCG) infection. Moreover, the BCG-induced upregulation of miR-155 in macrophages was dependent on TLR2, NF-κB and JNK signaling pathways. More importantly, our study explored that miR-155 significantly elevated ROS production in macrophages, although miR-155 had no influence on the inducible nitric oxide synthase (iNOS) expression or nitric oxide (NO) production. In addition, our study demonstrated that miR-155 repressed the expression of src homology 2 (SH2) containing inositol 5-phosphatase1 (SHIP1), and knockdown of SHIP1 greatly increased ROS production in BCG-infected macrophages. Collectively, these data indicate that miR-155 modulates ROS but not RNS production by targeting SHIP1, which may provide a better understanding of the host anti-mycobacterial response.

Original languageEnglish (US)
Pages (from-to)29-36
Number of pages8
JournalMolecular Immunology
Issue number1
StatePublished - Nov 2014
Externally publishedYes


  • MicroRNA
  • Mycobacteria
  • Nitric oxide
  • Reactive oxygen species

ASJC Scopus subject areas

  • Immunology
  • Molecular Biology


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