EspF acts as a molecular scaffold to facilitate TRIM25-mediated NLRP3 inflammasome activation during mycobacterial infection
BCG strains overexpressing EspF exhibited exacerbated lung lesions, increased inflammatory cell infiltration, and higher bacterial burdens. Collectively, these findings reveal EspF-TRIM25-NLRP3 axis is a novel mechanism of mycobacterial pathogenesis that drives hyperinflammation to facilitate bacterial survival and dissemination.
Authors
- Luqing Cui (ORCID: https://orcid.org/0000-0003-0922-541X)
- Yunjie Li (ORCID: https://orcid.org/0000-0003-3721-0178)
- Houhui Song (ORCID: https://orcid.org/0000-0001-6530-5794)
- Ahui Xu
- Xu We (ORCID: https://orcid.org/0009-0005-2230-929X)
- Hexiang Jiang
- Xinxin Zang
- Yang Yang (ORCID: https://orcid.org/0000-0002-6103-0292)
- Jingyan Fan
- Longjian Wu
- Yixin Han
- Bei Huang
- Guiqing He
Institutions
- Zhejiang A & F University (CN)
- Wenzhou Medical University (CN)
Publication Details
- Journal
- Virulence
- Published
- 2026-09-08
- DOI
- https://doi.org/10.1080/21505594.2026.2723678
- Primary Topic
- Inflammasome and immune disorders
- Type
- article
- Field-Weighted Citation Impact
- 0.00