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Treponema pallidum promotes macrophage polarization and activates the NLRP3 inflammasome pathway to induce interleukin-1β production.
BMC Immunol 2018; 19(1):28BI

Abstract

BACKGROUND

The involvement of inflammasome activation and macrophage polarization during the process of syphilis infection remains unknown. In this study, A series of experiments were performed using human macrophages to research the role of NLRP3 inflammasome regulation in interleukin (IL)-1β production and its influence on macrophage polarization triggered by T. pallidum.

RESULTS

The results showed that in M0 macrophages treated with T. pallidum, the M1-associated markers inducible nitric oxide synthase (iNOS), IL-1β and TNF-α were upregulated, and the M2-associated markers CD206 and IL-10 were downregulated. In addition, we observed NLRP3 inflammasome activation and IL-1β secretion in T. pallidum-treated macrophages, and the observed production of IL-1β occurred in a dose- and time-dependent manner. Moreover, the secretion of IL-1β by macrophages after T. pallidum treatment was notably reduced by anti-NLRP3 siRNA and caspase-1 inhibitor treatment. NAC, KCl, and CA074-ME treatment also suppressed IL-1β release from T. pallidum-treated macrophages.

CONCLUSIONS

These findings showed that T. pallidum induces M0 macrophages to undergo M1 macrophage polarization and elevate IL-1β secretion through NLRP3. Moreover, the process of NLRP3 inflammasome activation and IL-1β production in macrophages in response to T. pallidum infection involves K+ efflux, mitochondrial ROS production and cathepsin release. This study provides a new insight into the innate immune response to T. pallidum infection.

Authors+Show Affiliations

Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China.Xiamen Fifth Hospital, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China.Xiamen Hospital of Traditional Chinese Medicine, Xiamen, Fujian Province, China.Xiamen Huli District Maternity and Child Care Hospital, Xiamen, Fujian Province, China.Xiamen Huli District Maternity and Child Care Hospital, Xiamen, Fujian Province, China.Xiamen Huli District Maternity and Child Care Hospital, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. niujianjun211@xmu.edu.cn. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China. niujianjun211@xmu.edu.cn.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. mikhail929@163.com. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China. mikhail929@163.com.Zhongshan Hospital, Medical College of Xiamen University, Xiamen, Fujian Province, China. yangtianci@xmu.edu.cn. Institute of Infectious Disease, Medical College of Xiamen University, Xiamen, Fujian Province, China. yangtianci@xmu.edu.cn.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

30217146

Citation

Lin, Li-Rong, et al. "Treponema Pallidum Promotes Macrophage Polarization and Activates the NLRP3 Inflammasome Pathway to Induce Interleukin-1β Production." BMC Immunology, vol. 19, no. 1, 2018, p. 28.
Lin LR, Liu W, Zhu XZ, et al. Treponema pallidum promotes macrophage polarization and activates the NLRP3 inflammasome pathway to induce interleukin-1β production. BMC Immunol. 2018;19(1):28.
Lin, L. R., Liu, W., Zhu, X. Z., Chen, Y. Y., Gao, Z. X., Gao, K., ... Yang, T. C. (2018). Treponema pallidum promotes macrophage polarization and activates the NLRP3 inflammasome pathway to induce interleukin-1β production. BMC Immunology, 19(1), p. 28. doi:10.1186/s12865-018-0265-9.
Lin LR, et al. Treponema Pallidum Promotes Macrophage Polarization and Activates the NLRP3 Inflammasome Pathway to Induce Interleukin-1β Production. BMC Immunol. 2018 09 14;19(1):28. PubMed PMID: 30217146.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Treponema pallidum promotes macrophage polarization and activates the NLRP3 inflammasome pathway to induce interleukin-1β production. AU - Lin,Li-Rong, AU - Liu,Wei, AU - Zhu,Xiao-Zhen, AU - Chen,Yu-Yan, AU - Gao,Zheng-Xiang, AU - Gao,Kun, AU - Tong,Man-Li, AU - Zhang,Hui-Lin, AU - Xiao,Yao, AU - Li,Wen-Dong, AU - Li,Shu-Lian, AU - Lin,Hui-Ling, AU - Liu,Li-Li, AU - Fang,Zan-Xi, AU - Niu,Jian-Jun, AU - Lin,Yong, AU - Yang,Tian-Ci, Y1 - 2018/09/14/ PY - 2018/05/02/received PY - 2018/08/16/accepted PY - 2018/9/16/entrez PY - 2018/9/16/pubmed PY - 2018/9/16/medline KW - IL-1β KW - Macrophage KW - NLRP3 KW - Polarization KW - Treponema pallidum SP - 28 EP - 28 JF - BMC immunology JO - BMC Immunol. VL - 19 IS - 1 N2 - BACKGROUND: The involvement of inflammasome activation and macrophage polarization during the process of syphilis infection remains unknown. In this study, A series of experiments were performed using human macrophages to research the role of NLRP3 inflammasome regulation in interleukin (IL)-1β production and its influence on macrophage polarization triggered by T. pallidum. RESULTS: The results showed that in M0 macrophages treated with T. pallidum, the M1-associated markers inducible nitric oxide synthase (iNOS), IL-1β and TNF-α were upregulated, and the M2-associated markers CD206 and IL-10 were downregulated. In addition, we observed NLRP3 inflammasome activation and IL-1β secretion in T. pallidum-treated macrophages, and the observed production of IL-1β occurred in a dose- and time-dependent manner. Moreover, the secretion of IL-1β by macrophages after T. pallidum treatment was notably reduced by anti-NLRP3 siRNA and caspase-1 inhibitor treatment. NAC, KCl, and CA074-ME treatment also suppressed IL-1β release from T. pallidum-treated macrophages. CONCLUSIONS: These findings showed that T. pallidum induces M0 macrophages to undergo M1 macrophage polarization and elevate IL-1β secretion through NLRP3. Moreover, the process of NLRP3 inflammasome activation and IL-1β production in macrophages in response to T. pallidum infection involves K+ efflux, mitochondrial ROS production and cathepsin release. This study provides a new insight into the innate immune response to T. pallidum infection. SN - 1471-2172 UR - https://www.unboundmedicine.com/medline/citation/30217146/Treponema_pallidum_promotes_macrophage_polarization_and_activates_the_NLRP3_inflammasome_pathway_to_induce_interleukin_1β_production_ L2 - https://bmcimmunol.biomedcentral.com/articles/10.1186/s12865-018-0265-9 DB - PRIME DP - Unbound Medicine ER -