The Journal of infectious diseases · 2026
Phospholipid Transporter MlaFEDCB Regulates Klebsiella pneumoniae Virulence by Modulating Fimbriae Synthesis and Stress-adaptive Growth.
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Zhao Xiaoyu, Liu Haoqi, Guo Qinglan, Ju Mohan, Wang Minggui, Qin Xiaohua, Hao Min
Аннотация
BACKGROUND: Klebsiella pneumoniae is a key opportunistic pathogen, and its emerging hypervirulent strains pose a growing public health threat. An association exists between the phospholipid transporter MlaFEDCB and bacterial virulence; however, its regulatory role and underlying mechanisms remain elusive. Herein, we focused on K. pneumoniae virulence regulation via mlaFEDCB under in vitro and in vivo conditions.
METHODS AND RESULTS: Homology analysis showed that mlaFEDCB gene cluster is highly conservative among gram-negative bacterial strains and is contiguously arranged and co-transcribed within the genome. Experiment involving murine intraperitoneal infection revealed that mice infected with KP-ΔmlaFEDCB strain showed substantially prolonged survival (P = .0005). Furthermore, transcriptomic analysis showed altered expression of virulence-associated genes, especially fimH and fimD, which are involved in fimbrial structure and host cell adherence. Scanning electron and transmission electron microscopy showed that the WT-KP strain demonstrated a complex fibrous fimbrial network, with several long, thin structures interwoven with those of neighboring bacteria, whereas the KP-ΔmlaFEDCB strain showed markedly fewer fimbriae and lacked the fimbrial network. Furthermore, bladder epithelial cells adhesion assay showed an apparent reduction in the KP-ΔmlaFEDCB strain compared with the WT-KP strain. The growth of the KP-ΔmlaFEDCB strain was significantly compromised in comparison to the wild-type strain under stress conditions.
CONCLUSIONS: Thus, mlaFEDCB gene cluster increases the adhesion, invasion, and environmental adaptability of K. pneumoniae by modulating virulence-related gene expression, pilus synthesis, and growth under stress conditions.
METHODS AND RESULTS: Homology analysis showed that mlaFEDCB gene cluster is highly conservative among gram-negative bacterial strains and is contiguously arranged and co-transcribed within the genome. Experiment involving murine intraperitoneal infection revealed that mice infected with KP-ΔmlaFEDCB strain showed substantially prolonged survival (P = .0005). Furthermore, transcriptomic analysis showed altered expression of virulence-associated genes, especially fimH and fimD, which are involved in fimbrial structure and host cell adherence. Scanning electron and transmission electron microscopy showed that the WT-KP strain demonstrated a complex fibrous fimbrial network, with several long, thin structures interwoven with those of neighboring bacteria, whereas the KP-ΔmlaFEDCB strain showed markedly fewer fimbriae and lacked the fimbrial network. Furthermore, bladder epithelial cells adhesion assay showed an apparent reduction in the KP-ΔmlaFEDCB strain compared with the WT-KP strain. The growth of the KP-ΔmlaFEDCB strain was significantly compromised in comparison to the wild-type strain under stress conditions.
CONCLUSIONS: Thus, mlaFEDCB gene cluster increases the adhesion, invasion, and environmental adaptability of K. pneumoniae by modulating virulence-related gene expression, pilus synthesis, and growth under stress conditions.