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Published on: August 31, 2015
Pycnogenol reduces the expression of P. aeruginosa T3SS and inflammatory response in NCI-H292 cells
Seung-Ho Kim1,2, Da Yun Seo3, Sang-Bae Han4
1Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Chungbuk 28116, Republic of Korea.
Abstract:
Nosocomial infections caused by Pseudomonas aeruginosa (P. aeruginosa) have become increasingly common, particularly among immunocompromised individuals, who experience high mortality rates and prolonged treatment durations due to the limited availability of effective therapies. In this study, we screened for anti-ExoS compounds targeting P. aeruginosa and identified pycnogenol (PYC) as a potent inhibitor of the type III secretion system (T3SS), a major virulence mechanism responsible for the translocation of effectors such as ExoS. Using ELISA, western blotting, and real-time PCR analyses in both P. aeruginosa and infected H292 cells, we found that PYC significantly reduced T3SS activity. Mechanistically, PYC suppressed the transcription of T3SS-related genes by downregulating exsA expression in P. aeruginosa. Furthermore, pretreatment with PYC attenuated the cytotoxic effects and reduced the expression of proinflammatory cytokines, including interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-18 (IL-18), in P. aeruginosa-infected H292 cells. These effects were associated with the inhibition of NF-κB signaling and inflammasome activation. Taken together, our findings suggest that PYC may serve as a promising therapeutic candidate against P. aeruginosa infections by targeting T3SS-mediated virulence and modulating host inflammatory responses.
Insights
Pycnogenol (PYC) effectively inhibits Pseudomonas aeruginosa virulence by targeting the type III secretion system (T3SS). This compound reduces bacterial cytotoxicity and host inflammation, offering a potential new therapy for P. aeruginosa infections.
Area of Science:
- Microbiology
- Immunology
- Pharmacology
Background:
- Nosocomial Pseudomonas aeruginosa infections pose significant risks, especially to immunocompromised individuals, due to limited effective treatments.
- The type III secretion system (T3SS) is a key virulence factor in P. aeruginosa, facilitating effector translocation and host cell damage.
Purpose of the Study:
- To identify compounds that inhibit P. aeruginosa ExoS delivery.
- To investigate the potential of pycnogenol (PYC) as an anti-virulence agent against P. aeruginosa.
Main Methods:
- Screening for anti-ExoS compounds.
- Utilizing ELISA, western blotting, and real-time PCR to assess T3SS activity and gene expression.
- Evaluating the effects of PYC on bacterial cytotoxicity and host inflammatory responses in infected H292 cells.
Main Results:
- Pycnogenol (PYC) was identified as a potent inhibitor of P. aeruginosa T3SS activity.
- PYC suppressed T3SS-related gene transcription by downregulating exsA expression.
- PYC pretreatment reduced cytotoxicity and pro-inflammatory cytokine expression (IL-1β, IL-6, IL-8, IL-18) in infected cells by inhibiting NF-κB signaling and inflammasome activation.
Conclusions:
- Pycnogenol (PYC) demonstrates significant anti-virulence properties against Pseudomonas aeruginosa.
- PYC targets T3SS-mediated virulence and modulates host inflammatory responses, suggesting its therapeutic potential for P. aeruginosa infections.
