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Article

UspF Regulates Type III Pili-Mediated Adhesion, Oxidative Stress Resistance, and Virulence in Klebsiella pneumoniae

1
School of Basic Medical Sciences & School of Public Health, Faculty of Medicine, Yangzhou University, Yangzhou 225009, China
2
Key Laboratory of the Jiangsu Higher Education Institutions for Nucleic Acid & Cell Fate Regulation (Yangzhou University), Yangzhou 225009, China
3
Jiangsu Key Laboratory of Zoonosis, Yangzhou University, Yangzhou 225009, China
4
Jiangsu Interdisciplinary Center for Zoonoses and Biosafety, Yangzhou University, Yangzhou 225009, China
5
International Research Laboratory of Prevention and Control of Important Animal Infectious Diseases and Zoonotic Diseases of Jiangsu Higher Education Institutions, Yangzhou University, Yangzhou 225009, China
6
College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, China
7
Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Microorganisms 2026, 14(2), 478; https://doi.org/10.3390/microorganisms14020478
Submission received: 8 January 2026 / Revised: 5 February 2026 / Accepted: 12 February 2026 / Published: 15 February 2026
(This article belongs to the Section Medical Microbiology)

Abstract

Klebsiella pneumoniae (K. pneumoniae, KP) is a significant opportunistic pathogen responsible for both nosocomial and community-acquired infections. Bacterial adhesion is the critical initial step for host colonization and the establishment of disease. In this study, we utilized a mariner transposon mutagenesis system to construct a mutant library from the clinical KP strain KP20, identifying a mutant with significantly impaired epithelial cell adhesion due to an insertion in the uspF gene. Genetic knockout experiments confirmed that uspF deletion markedly reduced the adhesion to human airway epithelial cells (Calu-3) and downregulated the transcription of type III pili-encoding genes (mrkABDF). Furthermore, uspF deficiency compromised antioxidant stress and serum resistance and increased susceptibility to dendritic cell and macrophage phagocytosis. In vivo challenge experiments further demonstrated that uspF deletion significantly attenuated K. pneumoniae virulence in mice. These findings provide important insights into the molecular pathogenesis of K. pneumoniae and identify UspF as a potential target for therapeutic intervention.
Keywords: Klebsiella pneumoniae; transposon; adhesion; universal stress protein UspF; pathogenicity Klebsiella pneumoniae; transposon; adhesion; universal stress protein UspF; pathogenicity

Share and Cite

MDPI and ACS Style

Yin, Y.; Jiang, Y.; Wu, W.; Zhu, J.; Zhang, F.; Luo, W.; Meng, C.; Yang, Y.; Miao, X.; Qin, T.; et al. UspF Regulates Type III Pili-Mediated Adhesion, Oxidative Stress Resistance, and Virulence in Klebsiella pneumoniae. Microorganisms 2026, 14, 478. https://doi.org/10.3390/microorganisms14020478

AMA Style

Yin Y, Jiang Y, Wu W, Zhu J, Zhang F, Luo W, Meng C, Yang Y, Miao X, Qin T, et al. UspF Regulates Type III Pili-Mediated Adhesion, Oxidative Stress Resistance, and Virulence in Klebsiella pneumoniae. Microorganisms. 2026; 14(2):478. https://doi.org/10.3390/microorganisms14020478

Chicago/Turabian Style

Yin, Yinyan, Yiran Jiang, Wangxin Wu, Jing Zhu, Feng Zhang, Wenqing Luo, Chuang Meng, Yang Yang, Xinyu Miao, Tao Qin, and et al. 2026. "UspF Regulates Type III Pili-Mediated Adhesion, Oxidative Stress Resistance, and Virulence in Klebsiella pneumoniae" Microorganisms 14, no. 2: 478. https://doi.org/10.3390/microorganisms14020478

APA Style

Yin, Y., Jiang, Y., Wu, W., Zhu, J., Zhang, F., Luo, W., Meng, C., Yang, Y., Miao, X., Qin, T., & Gao, Q. (2026). UspF Regulates Type III Pili-Mediated Adhesion, Oxidative Stress Resistance, and Virulence in Klebsiella pneumoniae. Microorganisms, 14(2), 478. https://doi.org/10.3390/microorganisms14020478

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