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OmpK35/36 modulate the virulence of hypervirulent Klebsiella pneumoniae by regulating capsular polysaccharide export
Journal article   Open access   Peer reviewed

OmpK35/36 modulate the virulence of hypervirulent Klebsiella pneumoniae by regulating capsular polysaccharide export

Susu Wu, Ying Zhang, Ying Sheng, Xiaobo Ma, Xinyi Yang, Bin Ma and Dakang Hu
BMC microbiology, Vol.26(1), 553
2026
DOI: https://doi.org/10.1186/s12866-026-05212-3
PMID: 42243662
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Open Access CC BY-NC-ND V4.0

Abstract

Animals Bacterial Capsules - metabolism Bacterial Outer Membrane Proteins - genetics Bacterial Outer Membrane Proteins - metabolism Bacterial Proteins - genetics Bacterial Proteins - metabolism Disease Models, Animal Female Gene Expression Regulation, Bacterial Klebsiella Infections - microbiology Klebsiella Infections - pathology Klebsiella pneumoniae - genetics Klebsiella pneumoniae - growth & development Klebsiella pneumoniae - metabolism Klebsiella pneumoniae - pathogenicity Mice Moths - microbiology Phagocytosis Polysaccharides, Bacterial - metabolism Porins - genetics Porins - metabolism Virulence Virulence Factors - genetics Virulence Factors - metabolism
Objective: This study aimed to investigate the impact of outer membrane proteins 35 (OmpK35) and 36 on the virulence of Klebsiella pneumoniae and the corresponding mechanisms. Methods: Serotype K1 strain NTUH-K2044 was utilized to create single-deletion mutants (ΔompK35 and ΔompK36) and a double-deletion mutant (ΔompK35/36), alongside their complementation variants. Multiple analyses were performed, including capsule staining, transmission electron microscopy, serum resistance assays, phagocytosis tests, and infection models using mice and Galleria mellonella. Results: The mutants retained hypercapsules similar to NTUH-K2044, but looser capsule structures revealed by transmission electron microscopy. All mutants exhibited decreased virulence, with median lethal doses under 5×10⁴ colony forming units in mice. Specifically, only ΔompK35/36 showed reduced serum resistance compared to the wild strain, similar for the anti- phagocytosis capabilities. Additionally, ΔompK35 induced liver inflammation, whereas ΔompK36 and ΔompK35/36 exerted milder effects. Despite these differences, all mutants displayed normal growth rates and upregulated expression of gnd and wcaJ, crucial for capsular polysaccharide (CPS) biosynthesis. Conclusions: The hypercapsule, composed mainly of CPS, plays a crucial role in the hypervirulence of K. pneumoniae. OmpK35/36 may modulate the virulence of K. pneumoniae by regulating CPS export. Keywords: Klebsiella pneumoniae, Virulence, Hypercapsule, Outer membrane protein

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