ArticleBMC infectious diseases2018
Development of tissue inflammation accompanied by NLRP3 inflammasome activation in rabbits infected with Treponema pallidum strain Nichols.
Article in BMC infectious diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Treponema pallidum induces pathological injury of the rabbit testis and sperm through NLRP3 inflammasome activation-mediated pyroptosis.BMC immunology · 2026Article
- HIF-1α regulated GLUT1-mediated glycolysis enhances Treponema pallidum-induced cytokine responses.Cell communication and signaling : CCS · 2025Article
- Article
- Lacrimal Gland Epithelial Cells Shape Immune Responses through the Modulation of Inflammasomes and Lipid Metabolism.International journal of molecular sciences · 2023Article
- Association between treatment failure in patients with early syphilis and penicillin resistance-related gene mutations ofFrontiers in medicine · 2023Article
- YTHDF1 Negatively RegulatesFrontiers in immunology · 2022Article
- MiR-223-3p inhibits rTp17-induced inflammasome activation and pyroptosis by targeting NLRP3.Journal of cellular and molecular medicine · 2020Article
- Article
- The N-terminal D1 domain of Treponema pallidum flagellin binding to TLR5 is required but not sufficient in activation of TLR5.Journal of cellular and molecular medicine · 2019Article
- Treponema pallidum promotes macrophage polarization and activates the NLRP3 inflammasome pathway to induce interleukin-1β production.BMC immunology · 2018Article
- NLRP3 in somatic non-immune cells of rodent and primate testes.Reproduction (Cambridge, England) · 2018Article
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Authors and funding
16 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe inflammasome responses in Treponema pallidum infection have been poorly understood to date. This study aimed to investigate the expression of the nucleotide-binding leucine-rich receptor protein 3 (NLRP3) inflammasome in the development of tissue inflammation in rabbits infected with T. pallidum.
methodsForty-five rabbits were randomly assigned to a blank group or an infection group, and the latter was divided into no benzathine penicillin G (BPG) and BPG treatment subgroups. Rabbits in the infection group were injected intradermally with 0.1 mL of a 10
resultsRabbits infected with T. pallidum (both the BPG treatment and no BPG treatment subgroups), exhibited NLRP3 inflammasome activation and IL-1β secretion in cutaneous lesions, showing a trend in elevation to decline; NLRP3 mRNA expression reached a peak at 18 d in the BPG treatment subgroup and 21 d in the no BPG treatment subgroup and returned to "normal" levels [vs. the blank group (P > 0.05)] at 42 d post-infection. The trend was similar to the change in cutaneous lesions in the infected rabbits, which reached a peak at 16 d in the BPG treatment subgroup and 18 d in the no BPG treatment subgroup. NLRP3, caspase-1, and IL-1β mRNA expression levels were slightly different in different organs. NLRP3 inflammasome activation was also observed in the kidney, liver, lung, spleen and testis. IL-1β expression was observed in the kidney, liver, lung and spleen; however, there was no detectable level of IL-1β in the testes of the infected rabbits.
conclusionsThis study established a clear link between NLRP3 inflammasome activation and the development of tissue inflammation in rabbits infected with T. pallidum. BPG therapy imperceptibly adjusted syphilitic inflammation.
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