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Mediators of Inflammation
Volume 2016 (2016), Article ID 7369351, 13 pages
Research Article

mTORC1-Activated Monocytes Increase Tregs and Inhibit the Immune Response to Bacterial Infections

1Department of Hematology, The Second Affiliated Hospital of Nanchang University, Key Laboratory of Experimental Hematology in Jiangxi Province, Nanchang, Jiangxi, China
2Medical Department of Nanchang University Graduate School, Nanchang, Jiangxi, China
3Department of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China
4State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Disease, Chinese Academy of Medical Sciences, Tianjin, China
5Department of Medical Microbiology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China
6Department of Hematology and Oncology, The First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China

Received 25 April 2016; Revised 5 August 2016; Accepted 11 August 2016

Academic Editor: Anshu Agrawal

Copyright © 2016 Lijun Fang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The TSC1/2 heterodimer, a key upstream regulator of the mTOR, can inhibit the activation of mTOR, which plays a critical role in immune responses after bacterial infections. Monocytes are an innate immune cell type that have been shown to be involved in bacteremia. However, how the mTOR pathway is involved in the regulation of monocytes is largely unknown. In our study, TSC1 KO mice and WT mice were infected with E. coli. When compared to WT mice, we found higher mortality, greater numbers of bacteria, decreased expression of coactivators in monocytes, increased numbers of Tregs, and decreased numbers of effector T cells in TSC1 KO mice. Monocytes obtained from TSC1 KO mice produced more ROS, IL-6, IL-10, and TGF-β and less IL-1, IFN-γ, and TNF-α. Taken together, our results suggest that the inhibited immune functioning in TSC1 KO mice is influenced by mTORC1 activation in monocytes. The reduced expression of coactivators resulted in inhibited effector T cell proliferation. mTORC1-activated monocytes are harmful during bacterial infections. Therefore, inhibiting mTORC1 signaling through rapamycin administration could rescue the harmful aspects of an overactive immune response, and this knowledge provides a new direction for clinical therapy.