TY - JOUR
T1 - MicroRNA-155 induction by Mycobacterium bovis BCG enhances ROS production through targeting SHIP1
AU - Wang, Jinli
AU - Wu, Minhao
AU - Wen, Jinsheng
AU - Yang, Kun
AU - Li, Miao
AU - Zhan, Xiaoxia
AU - Feng, Lianqiang
AU - Li, Meiyu
AU - Huang, Xi
N1 - Funding Information:
This work was supported by grants National Natural Science Foundation of China ( 81172811 , 81261160323 , 31070143 ), the 111 Project (No. B13037 ), Guangdong Innovative Research Team Program ( 2009010058 ), Guangdong Natural Science Foundation ( 10251008901000013 , S2012040006680 ), the Natural Science Foundation of Zhejiang ( LY13H160035 ), Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme (No. 2009 ), National Science and Technology Key Projects for Major Infectious Diseases ( 2013ZX10003001 ).
PY - 2014/11
Y1 - 2014/11
N2 - 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.
AB - 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.
KW - MicroRNA
KW - Mycobacteria
KW - Nitric oxide
KW - Reactive oxygen species
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U2 - 10.1016/j.molimm.2014.05.012
DO - 10.1016/j.molimm.2014.05.012
M3 - Article
C2 - 24937178
AN - SCOPUS:84902274347
SN - 0161-5890
VL - 62
SP - 29
EP - 36
JO - Molecular Immunology
JF - Molecular Immunology
IS - 1
ER -