ArticleBMC microbiology2025
Dual RNA-seq analysis reveals the interaction between multidrug-resistant Klebsiella pneumoniae and host in a mouse model of pneumonia.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Comparative analysis of virulence factors and two-component systems expression in carbapenem-resistant and carbapenem-susceptibleMicrobiology spectrum · 2026Article
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
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9 authors.
Funding
Abstract
backgroundMultidrug-resistant Klebsiella pneumoniae (MDR-KP) poses a significant global health threat, associated with high morbidity and mortality rates among hospitalized patients. The interaction between MDR-KP and its host is highly complex, and few studies have investigated these interactions from both the pathogen and host perspectives. Here, we explored these interactions in a mouse model of pneumonia using dual RNA-seq analysis.
methodsPCR identification and antimicrobial susceptibility test were employed to screen for MDR-KP strains. A mouse model of pneumonia was established through aerosolized intratracheal inoculation with high-dose or low-dose bacteria. Bacterial loads, pathological changes, inflammatory cytokine expression, and immune cell infiltration were assessed post-challenge. Dual RNA-seq analysis was conducted on lung tissues following infection.
resultsNY13307 was identified as an MDR-KP strain with minimal virulence factor genes and broad-spectrum drug resistance. High-dose bacteria induced more severe pulmonary pathological changes, a significant increase in bacterial load, and notably elevated secretion of inflammatory cytokines compared to low-dose bacteria. Alveolar macrophages and resident interstitial macrophages were identified as the primary sources of these cytokines. Further RNA-seq analysis revealed that, compared to the low-dose group, the high-dose group significantly upregulated hypoxia and pro-inflammatory cytokine-related genes in the host, and siderophore-related genes in the bacteria. Correlation analysis demonstrated a significant association between siderophore-related genes and clusters of genes related to pro-inflammatory cytokines and hypoxia.
conclusionsIn this mouse model of bacterial pneumonia, excessive siderophore expression may trigger the activation of hypoxia signaling pathways and the release of pro-inflammatory cytokines, ultimately reducing survival rates.
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