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Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Health Sciences / Faculty of Health Sciences >
Peer-reviewed Journal Articles, etc >
Synergistic Costimulatory Effect of Chlamydia pneumoniae with Carbon Nanoparticles on NLRP3 Inflammasome-Mediated Interleukin-1 beta Secretion in Macrophages
| Title: | Synergistic Costimulatory Effect of Chlamydia pneumoniae with Carbon Nanoparticles on NLRP3 Inflammasome-Mediated Interleukin-1 beta Secretion in Macrophages |
| Authors: | Matsuo, Junji Browse this author →KAKEN DB | | Nakamura, Shinji Browse this author →KAKEN DB | | Takeda, Seiji Browse this author →KAKEN DB | | Ishida, Kasumi Browse this author | | Yamazaki, Tomohiro Browse this author | | Yoshida, Mitsutaka Browse this author | | Chiba, Hitoshi Browse this author →KAKEN DB | | Hui, Shu-Ping Browse this author →KAKEN DB | | Yamaguchi, Hiroyuki Browse this author →KAKEN DB |
| Issue Date: | Jul-2015 |
| Publisher: | American Society for Microbiology |
| Journal Title: | Infection and immunity |
| Volume: | 83 |
| Issue: | 7 |
| Start Page: | 2917 |
| End Page: | 2925 |
| Publisher DOI: | 10.1128/IAI.02968-14 |
| PMID: | 25939513 |
| Abstract: | The obligate intracellular bacterium Chlamydia pneumoniae is not only a causative agent of community-acquired pneumonia but is also associated with a more serious chronic disease, asthma, which might be exacerbated by air pollution containing carbon nanoparticles. Although a detailed mechanism of exacerbation remains unknown, the proinflammatory cytokine interleukin- 1 beta (IL-1 beta) is a critical player in the pathogenesis of asthma. C. pneumoniae induces IL-1 beta in macrophages via NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome activation and Toll-like receptor 2/4 (TLR2/4) stimulation. Carbon nanoparticles, such as carbon nanotubes (CNTs), can also evoke the NLRP3 inflammasome to trigger IL-1 beta secretion from lipopolysaccharide-primed macrophages. This study assessed whether costimulation of C. pneumoniae with CNTs synergistically enhanced IL-1 beta secretion from macrophages, and determined the molecular mechanism involved. Enhanced IL-1 beta secretion from C. pneumoniae-infected macrophages by CNTs was dose and time dependent. Transmission electron microscopy revealed that C. pneumoniae and CNTs were engulfed concurrently by macrophages. Inhibitors of actin polymerization or caspase-1, a component of the inflammasome, significantly blocked IL-1 beta secretion. Gene silencing using small interfering RNA (siRNA) targeting the NLRP3 gene also abolished IL-1 beta secretion. Other inhibitors (K+ efflux inhibitor, cathepsin B inhibitor, and reactive oxygen species-generating inhibitor) also blocked IL-1 beta secretion. Taken together, these findings demonstrated that CNTs synergistically enhanced IL-1 beta secretion from C. pneumoniae-infected macrophages via the NLRP3 inflammasome and caspase-1 activation, providing novel insight into our understanding of how C. pneumoniae infection can exacerbate asthma. |
| Type: | article (author version) |
| URI: | http://hdl.handle.net/2115/60611 |
| Appears in Collections: | 保健科学院・保健科学研究院 (Graduate School of Health Sciences / Faculty of Health Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 山口 博之
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