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The outer membrane protein Tp92 of Treponema pallidum induces human mononuclear cell death and IL-8 secretion.
J Cell Mol Med 2018; 22(12):6039-6054JC

Abstract

Treponema pallidum is the pathogen that causes syphilis, a sexually transmitted disease; however, the pathogenic mechanism of this organism remains unclear. Tp92 is the only T. pallidum outer membrane protein that has structural features similar to the outer membrane proteins of other Gram-negative bacteria, but the exact functions of this protein remain unknown. In the present study, we demonstrated that the recombinant Tp92 protein can induce human mononuclear cell death. Tp92 mediated the human monocytic cell line derived from an acute monicytic leukemia patient (THP-1) cell death by recognizing CD14 and/or TLR2 on cell surfaces. After the stimulation of THP-1 cells by the Tp92 protein, Tp92 may induce atypical pyroptosis of THP-1 cells via the pro-caspase-1 pathway. Meanwhile, this protein caused the apoptosis of THP-1 cells via the receptor-interacting protein kinase 1/caspase-8/aspase-3 pathway. Tp92 reduced the number of monocytes among peripheral blood mononuclear cells. Interestingly, further research showed that Tp92 failed to increase the tumour necrosis factor-α, interleukin (IL)-1β, IL-6, IL-10, IL-18 and monocyte chemotactic protein 1 (MCP)-1 levels but slightly elevated the IL-8 levels via the Nuclear Factor (NF)-κB pathway in THP-1 cells. The data suggest that Tp92 recognizes CD14 and TLR2, transfers the signal to a downstream pathway, and activates NF-κB to mediate the production of IL-8. This mechanism may help T. pallidum escape recognition and elimination by the host innate immune system.

Authors+Show Affiliations

Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China. Department of Histology and Embryology, School of Medicine, University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China. Department of Clinical Laboratory, The First Affiliated Hospital of University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China. Department of Clinical Laboratory, The Second Affiliated Hospital of University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China.Institute of Pathogenic Biology and Key Laboratory of Special Pathogen Prevention and Control of Hunan Province, Collaborative Innovation Center for New Molecular Drug Research, University of South China, Hengyang, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30596396

Citation

Luo, Xi, et al. "The Outer Membrane Protein Tp92 of Treponema Pallidum Induces Human Mononuclear Cell Death and IL-8 Secretion." Journal of Cellular and Molecular Medicine, vol. 22, no. 12, 2018, pp. 6039-6054.
Luo X, Zhang X, Gan L, et al. The outer membrane protein Tp92 of Treponema pallidum induces human mononuclear cell death and IL-8 secretion. J Cell Mol Med. 2018;22(12):6039-6054.
Luo, X., Zhang, X., Gan, L., Zhou, C., Zhao, T., Zeng, T., ... Zhao, F. (2018). The outer membrane protein Tp92 of Treponema pallidum induces human mononuclear cell death and IL-8 secretion. Journal of Cellular and Molecular Medicine, 22(12), pp. 6039-6054. doi:10.1111/jcmm.13879.
Luo X, et al. The Outer Membrane Protein Tp92 of Treponema Pallidum Induces Human Mononuclear Cell Death and IL-8 Secretion. J Cell Mol Med. 2018;22(12):6039-6054. PubMed PMID: 30596396.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The outer membrane protein Tp92 of Treponema pallidum induces human mononuclear cell death and IL-8 secretion. AU - Luo,Xi, AU - Zhang,Xiaohong, AU - Gan,Lin, AU - Zhou,Chenglong, AU - Zhao,Tie, AU - Zeng,Tiebing, AU - Liu,Shuangquan, AU - Xiao,Yongjian, AU - Yu,Jian, AU - Zhao,Feijun, Y1 - 2018/09/14/ PY - 2018/02/12/received PY - 2018/07/30/accepted PY - 2019/1/1/entrez PY - 2019/1/1/pubmed PY - 2019/1/1/medline KW - Treponema pallidum KW - CD14 KW - IL‐8 KW - TLR2 KW - Tp92 KW - apoptosis KW - membrane protein KW - pyroptosis SP - 6039 EP - 6054 JF - Journal of cellular and molecular medicine JO - J. Cell. Mol. Med. VL - 22 IS - 12 N2 - Treponema pallidum is the pathogen that causes syphilis, a sexually transmitted disease; however, the pathogenic mechanism of this organism remains unclear. Tp92 is the only T. pallidum outer membrane protein that has structural features similar to the outer membrane proteins of other Gram-negative bacteria, but the exact functions of this protein remain unknown. In the present study, we demonstrated that the recombinant Tp92 protein can induce human mononuclear cell death. Tp92 mediated the human monocytic cell line derived from an acute monicytic leukemia patient (THP-1) cell death by recognizing CD14 and/or TLR2 on cell surfaces. After the stimulation of THP-1 cells by the Tp92 protein, Tp92 may induce atypical pyroptosis of THP-1 cells via the pro-caspase-1 pathway. Meanwhile, this protein caused the apoptosis of THP-1 cells via the receptor-interacting protein kinase 1/caspase-8/aspase-3 pathway. Tp92 reduced the number of monocytes among peripheral blood mononuclear cells. Interestingly, further research showed that Tp92 failed to increase the tumour necrosis factor-α, interleukin (IL)-1β, IL-6, IL-10, IL-18 and monocyte chemotactic protein 1 (MCP)-1 levels but slightly elevated the IL-8 levels via the Nuclear Factor (NF)-κB pathway in THP-1 cells. The data suggest that Tp92 recognizes CD14 and TLR2, transfers the signal to a downstream pathway, and activates NF-κB to mediate the production of IL-8. This mechanism may help T. pallidum escape recognition and elimination by the host innate immune system. SN - 1582-4934 UR - https://www.unboundmedicine.com/medline/citation/30596396/The_outer_membrane_protein_Tp92_of_Treponema_pallidum_induces_human_mononuclear_cell_death_and_IL_8_secretion_ L2 - https://doi.org/10.1111/jcmm.13879 DB - PRIME DP - Unbound Medicine ER -