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Recombinant Treponema pallidum protein Tp0136 promotes fibroblast migration by modulating MCP-1/CCR2 through TLR4.
J Eur Acad Dermatol Venereol. 2020 Apr; 34(4):862-872.JE

Abstract

BACKGROUND

Chancre self-healing is an important clinical feature in the early stages of syphilis infection. Wound healing may involve an important mechanism by the migration of fibroblasts filling the injured lesion. However, the specific mechanism underlying this process is still unknown.

OBJECTIVES

We aimed to analyse the role of Tp0136 in the migration of fibroblasts and the related mechanism.

METHODS

The migration ability of fibroblasts was detected by a wound-healing assay. RT-PCR and ELISA detected the expression of MCP-1, IL-6 and MMP-9. TLR4 expression was detected by RT-PCR. The protein levels of CCR2 and relevant signalling pathway molecules were measured by Western blotting.

RESULTS

Tp0136 significantly promoted fibroblast migration. Subsequently, the levels of MCP-1 and its receptor CCR2 were increased in this process. The migration of fibroblasts was significantly inhibited by an anti-MCP-1 neutralizing antibody or CCR2 inhibitors. Furthermore, studies demonstrated that Tp0136 could activate the ERK/JNK/PI3K/NF-κB signalling pathways through TLR4 activity and that signalling pathways inhibitors could weaken MCP-1 secretion and fibroblast migration.

CONCLUSIONS

These findings demonstrate that Tp0136 promotes the migration of fibroblasts by inducing MCP-1/CCR2 expression through signalling involving the TLR4, ERK, JNK, PI3K and NF-κB signalling pathways, which could contribute to the mechanism of chancre self-healing in syphilis.

Authors+Show Affiliations

Center of Clinical Laboratory, Zhongshan Hospital, School of Medicine, Xiamen University, Xiamen, China.Center of Clinical Laboratory, Zhongshan Hospital, School of Medicine, Xiamen University, Xiamen, China.Center of Clinical Laboratory, Zhongshan Hospital, School of Medicine, Xiamen University, Xiamen, China.Center of Clinical Laboratory, Zhongshan Hospital, School of Medicine, Xiamen University, Xiamen, China. Institute of Infectious Disease, School of Medicine, Xiamen University, Xiamen, China.Center of Clinical Laboratory, Zhongshan Hospital, School of Medicine, Xiamen University, Xiamen, China. Institute of Infectious Disease, School of Medicine, Xiamen University, Xiamen, China.Center of Clinical Laboratory, Zhongshan Hospital, School of Medicine, Xiamen University, Xiamen, China. Institute of Infectious Disease, School of Medicine, Xiamen University, Xiamen, China.Dermatology Hospital, Southern Medical University, Guangzhou, China.Center of Clinical Laboratory, Zhongshan Hospital, School of Medicine, Xiamen University, Xiamen, China. Institute of Infectious Disease, School of Medicine, Xiamen University, Xiamen, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31856347

Citation

Luo, X, et al. "Recombinant Treponema Pallidum Protein Tp0136 Promotes Fibroblast Migration By Modulating MCP-1/CCR2 Through TLR4." Journal of the European Academy of Dermatology and Venereology : JEADV, vol. 34, no. 4, 2020, pp. 862-872.
Luo X, Gao ZX, Lin SW, et al. Recombinant Treponema pallidum protein Tp0136 promotes fibroblast migration by modulating MCP-1/CCR2 through TLR4. J Eur Acad Dermatol Venereol. 2020;34(4):862-872.
Luo, X., Gao, Z. X., Lin, S. W., Tong, M. L., Liu, L. L., Lin, L. R., Ke, W. J., & Yang, T. C. (2020). Recombinant Treponema pallidum protein Tp0136 promotes fibroblast migration by modulating MCP-1/CCR2 through TLR4. Journal of the European Academy of Dermatology and Venereology : JEADV, 34(4), 862-872. https://doi.org/10.1111/jdv.16162
Luo X, et al. Recombinant Treponema Pallidum Protein Tp0136 Promotes Fibroblast Migration By Modulating MCP-1/CCR2 Through TLR4. J Eur Acad Dermatol Venereol. 2020;34(4):862-872. PubMed PMID: 31856347.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Recombinant Treponema pallidum protein Tp0136 promotes fibroblast migration by modulating MCP-1/CCR2 through TLR4. AU - Luo,X, AU - Gao,Z-X, AU - Lin,S-W, AU - Tong,M-L, AU - Liu,L-L, AU - Lin,L-R, AU - Ke,W-J, AU - Yang,T-C, Y1 - 2020/01/19/ PY - 2019/08/12/received PY - 2019/11/12/accepted PY - 2019/12/20/pubmed PY - 2019/12/20/medline PY - 2019/12/20/entrez SP - 862 EP - 872 JF - Journal of the European Academy of Dermatology and Venereology : JEADV JO - J Eur Acad Dermatol Venereol VL - 34 IS - 4 N2 - BACKGROUND: Chancre self-healing is an important clinical feature in the early stages of syphilis infection. Wound healing may involve an important mechanism by the migration of fibroblasts filling the injured lesion. However, the specific mechanism underlying this process is still unknown. OBJECTIVES: We aimed to analyse the role of Tp0136 in the migration of fibroblasts and the related mechanism. METHODS: The migration ability of fibroblasts was detected by a wound-healing assay. RT-PCR and ELISA detected the expression of MCP-1, IL-6 and MMP-9. TLR4 expression was detected by RT-PCR. The protein levels of CCR2 and relevant signalling pathway molecules were measured by Western blotting. RESULTS: Tp0136 significantly promoted fibroblast migration. Subsequently, the levels of MCP-1 and its receptor CCR2 were increased in this process. The migration of fibroblasts was significantly inhibited by an anti-MCP-1 neutralizing antibody or CCR2 inhibitors. Furthermore, studies demonstrated that Tp0136 could activate the ERK/JNK/PI3K/NF-κB signalling pathways through TLR4 activity and that signalling pathways inhibitors could weaken MCP-1 secretion and fibroblast migration. CONCLUSIONS: These findings demonstrate that Tp0136 promotes the migration of fibroblasts by inducing MCP-1/CCR2 expression through signalling involving the TLR4, ERK, JNK, PI3K and NF-κB signalling pathways, which could contribute to the mechanism of chancre self-healing in syphilis. SN - 1468-3083 UR - https://www.unboundmedicine.com/medline/citation/31856347/Recombinant_Treponema_pallidum_protein_Tp0136_promotes_fibroblast_migration_by_modulating_MCP-1/CCR2_through_TLR4 L2 - https://doi.org/10.1111/jdv.16162 DB - PRIME DP - Unbound Medicine ER -
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