Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2017, Article ID 1592365, 8 pages
Research Article

Chlamydia muridarum Infection of Macrophages Stimulates IL-1β Secretion and Cell Death via Activation of Caspase-1 in an RIP3-Independent Manner

1Shanghai Public Health Clinical Center, Key Laboratory of Medical Molecular Virology, Ministry of Education and Health, Fudan University, Shanghai 201508, China
2Clinical Laboratory, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221002, China
3Huazhong Agricultural University, Wuhan 430070, China
4Unit of Innate Immunity, Key Laboratory of Molecular Virology & Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai 200031, China

Correspondence should be addressed to Shun Li; moc.621@68nuhsil and Xiaohui Zhou; gro.chpahs@iuhoaixuohz

Received 18 March 2017; Accepted 9 May 2017; Published 4 June 2017

Academic Editor: Nobuo Kanazawa

Copyright © 2017 Lixiang Chen 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.


Chlamydiae are Gram-negative bacteria, which replicate exclusively in the infected host cells. Infection of the host cells by Chlamydiae stimulates the innate immune system leading to an inflammatory response, which is manifested not only by secretion of proinflammatory cytokines such as IL-1 from monocytes, macrophages, and dendritic cells, but also possibly by cell death mediated by Caspase-1 pyroptosis. RIP3 is a molecular switch that determines the development of necrosis or inflammation. However, the involvement of RIP3 in inflammasome activation by Chlamydia muridarum infection has not been clarified. Here, we assessed the role of RIP3 in synergy with Caspase-1 in the induction of IL-1β production in BMDM after either LPS/ATP or Chlamydia muridarum stimulation. The possibility of pyroptosis and necroptosis interplays and the role of RIP3 in IL-1 production during Chlamydia muridarum infection in BMDM was investigated as well. The data indicated that RIP3 is involved in NLRP3 inflammasome activation in LPS/ATP-stimulated BMDMs but not in Chlamydia muridarum infection. Pyroptosis occurred in BMDM after LPS/ATP stimulation or Chlamydia muridarum infection. Moreover, the results also illuminated the important role of the Caspase-1-mediated pyroptosis process which does not involve RIP3. Taken together, these observations may help shed new light on details in inflammatory signaling pathways activated by Chlamydia muridarum infection.