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Updated: Apr 29, 2026
NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
Published on: January 12, 2020
Nucleoside diphosphate kinase and flagellin from Pseudomonas aeruginosa induce interleukin 1 expression via the
Yong-Jae Kim1, Jung-Hoon Lee1, Yeji Lee1
1Department of Biotechnology and Bioinformatics, Korea University, Sejong, Republic of Korea.
Abstract:
Inflammatory responses are a first line of host defense against a range of invading pathogens, consisting of the release of proinflammatory cytokines followed by attraction of polymorphonuclear neutrophils (PMNs) to the site of inflammation. Among the many virulence factors that contribute to the pathogenesis of infections, nucleoside diphosphate kinase (Ndk) mediates bacterially induced toxicity against eukaryotic cells. However, no study has examined how Ndk affects inflammatory responses. The present study examined the mechanisms by which Pseudomonas aeruginosa activates inflammatory responses upon infection of cells. The results showed that bacterial Ndk, with the aid of an additional bacterial factor, flagellin, induced expression of the proinflammatory cytokines interleukin-1α (IL-1α) and IL-1β. Cytokine induction appeared to be dependent on the kinase activity of Ndk and was mediated via the NF-κB signaling pathway. Notably, Ndk activated the Akt signaling pathway, which acts upstream of NF-κB, as well as caspase-1, which is a key component of inflammasome. Thus, this study demonstrated that P. aeruginosa, through the combined effects of Ndk and flagellin, upregulates the expression of proinflammatory cytokines via the Akt/NF-κB signaling pathways.
Insights
Pseudomonas aeruginosa uses nucleoside diphosphate kinase (Ndk) and flagellin to trigger inflammatory cytokine release. This process involves the Akt and NF-κB signaling pathways, crucial for host defense against bacterial infection.
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Inflammatory responses are critical for host defense against pathogens.
- Bacterial virulence factors, like nucleoside diphosphate kinase (Ndk) from Pseudomonas aeruginosa, contribute to infection pathogenesis.
- The impact of Ndk on host inflammatory responses remained unexamined.
Purpose of the Study:
- To investigate the mechanisms by which Pseudomonas aeruginosa Ndk influences host inflammatory responses.
- To elucidate the role of Ndk and flagellin in activating inflammatory pathways.
- To determine the signaling cascades involved in bacterial-induced inflammation.
Main Methods:
- Infection of cells with Pseudomonas aeruginosa.
- Analysis of cytokine expression (IL-1α, IL-1β).
- Investigation of signaling pathways including Akt, NF-κB, and caspase-1 activation.
Main Results:
- Bacterial Ndk, with flagellin, induced the expression of proinflammatory cytokines IL-1α and IL-1β.
- Cytokine induction was dependent on Ndk's kinase activity and mediated through the NF-κB signaling pathway.
- Ndk activated the upstream Akt signaling pathway and caspase-1, a key inflammasome component.
Conclusions:
- Pseudomonas aeruginosa utilizes Ndk and flagellin to upregulate proinflammatory cytokine expression.
- The Akt and NF-κB signaling pathways are central to Ndk-mediated inflammatory responses.
- This study reveals a novel mechanism of bacterial-induced inflammation involving Ndk.
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