Effect of<i>Pseudomonas aeruginosa</i>Elastase B on Level and Activity of Immune Proteins/Peptides of<i>Galleria mellonella</i>Hemolymph

Andrejko, Mariola; Mizerska-Dudka, Magdalena

doi:10.1673/031.012.8801

Cited by 18 publications

(6 citation statements)

References 53 publications

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“…While the crucial role of QS in the P. aeruginosa infection to insects is often documented (Chugani et al ., ; D'Argenio et al ., ), the responsible virulence effectors regulated by QS were not fully clarified. Some studies have suggested that the factors related with twitching motility that is under the control of QS are important in the Pseudomonas virulence in Drosophila model system (Glessner et al ., ; D'Argenio et al ., ), and elastase B (LasB), another QS‐regulated exoprotease of P. aeruginosa can stimulate the humoral immune response at early stage of infection, and then degrade some immune components at later stage in G. mellonella model system (Andrejko and Mizerska‐Dudka, 2011; 2012). However, it was reported that the twitching motility is not directly related to the fly killing (D'Argenio et al ., ), and our result showed that LasB is not crucially involved in the virulence to T. molitor (Fig.…”

Section: Discussionmentioning

confidence: 99%

Protease IV, a quorum sensing‐dependent protease of Pseudomonas aeruginosa modulates insect innate immunity

Park

Kim

et al. 2014

Molecular Microbiology

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SummaryIn Pseudomonas aeruginosa, quorum sensing (QS) plays an essential role in pathogenesis and the QS response controls many virulence factors. Using a mealworm, Tenebrio molitor as a host model, we found that Protease IV, a QS-regulated exoprotease of P. aeruginosa functions as a key virulence effector causing the melanization and death of T. molitor larvae. Protease IV was able to degrade zymogens of spätzle processing enzyme (SPE) and SPE-activating enzyme (SAE) without the activation of the antimicrobial peptide (AMP) production. Since SPE and SAE function to activate spätzle, a ligand of Toll receptor in the innate immune system of T. molitor, we suggest that Protease IV may interfere with the activation of the Toll signaling. Independently of the Toll pathway, the melanization response, another innate immunity was still generated, since Protease IV directly converted Tenebrio prophenoloxidase into active phenoloxidase. Protease IV also worked as an important factor in the virulence to brine shrimp and nematode. These results suggest that Protease IV provides P. aeruginosa with a sophisticated way to escape the immune attack of host by interfering with the production of AMPs.

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Section: Discussionmentioning

confidence: 99%

Protease IV, a quorum sensing‐dependent protease of Pseudomonas aeruginosa modulates insect innate immunity

Park

Kim

et al. 2014

Molecular Microbiology

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“…Elastase A and B have been shown to drive host invasion by reducing the action of exotoxins, which delay the latter process. Elastase B acts against the host immune system by degrading complement proteins, immunoglobulins A and G, and inhibiting phagocytosis (Andrejko and Dudka, 2012). There have been reports suggesting a possible role of elastase B in mediating the degradation of surfactant proteins A and D in the lungs of cystic fibrosis patients (Mariencheck et al ., 2003).…”

Section: Virulence Factors Of P Aeruginosa: An Arsenal Of Sophisticat...mentioning

confidence: 99%

Revisiting the virulence hallmarks of Pseudomonas aeruginosa: a chronicle through the perspective of quorum sensing

Chadha

Harjai

Chhibber

2021

Environmental Microbiology

126

106

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Pseudomonas aeruginosa is an opportunistic pathogen and the leading cause of mortality among immunocompromised patients in clinical setups. The hallmarks of virulence in P. aeruginosa encompass six biologically competent attributes that cumulatively drive disease progression in a multistep manner. These multifaceted hallmarks lay the principal foundation for rationalizing the complexities of pseudomonal infections. They include factors for host colonization and bacterial motility, biofilm formation, production of destructive enzymes, toxic secondary metabolites, iron-chelating siderophores and toxins. This arsenal of virulence hallmarks is fostered and stringently regulated by the bacterial signalling system called quorum sensing (QS). The central regulatory functions of QS in controlling the timely expression of these virulence hallmarks for adaptation and survival drive the disease outcome. This review describes the intricate mechanisms of QS in P. aeruginosa and its role in shaping bacterial responses, boosting bacterial fitness. We summarize the virulence hallmarks of P. aeruginosa, relating them with the QS circuitry in clinical infections. We also examine the role of QS in the development of drug resistance and propose a novel antivirulence therapy to combat P. aeruginosa infections. This can prove to be a next-generation therapy that may eventually become refractory to the use of conventional antimicrobial treatments.

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“…Larvae were surfaced sterilised with 70% ethanol (Thermo Fisher Scientific), sacrificed using a sterile disposable surgical scalpel (Swann-Morton) and hemolymph collected into a pre-chilled eppendorf tube containing 10-20 crystals of N-phenylthiourea (Alfa Aesar) to prevent further melanisation. 40 Optical density (OD) was measured at 450nm using an ELx800 plate reader (Biotek).…”

Section: Galleria Mellonella Melanisation Assaymentioning

confidence: 99%

Comparative virulence of urinary and bloodstream isolates of extra-intestinal pathogenicEscherichia coliin aGalleria mellonellamodel

et al. 2015

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Extra-intestinal pathogenic Escherichia coli (ExPEC) are a significant cause of urinary tract infections and bacteraemia worldwide. Currently no single virulence factor or ExPEC lineage has been identified as the sole contributor to severe extra-intestinal infection and/or urosepsis. Galleria mellonella has recently been established as a simple model for studying the comparative virulence of ExPEC. In this study we investigated the virulence of 40 well-characterized ExPEC strains, in G. mellonella, by measuring mortality (larvae survival), immune recognition/response (melanin production) and cell damage (lactate dehydrogenase production). Although mortality was similar between urinary and bloodstream isolates, it was heightened for community-associated infections, complicated UTIs and urinary-source bacteraemia. Isolates of ST131 and those possessing afa/dra, ompT and serogroup O6 were also associated with heightened virulence.

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Effect ofPseudomonas aeruginosaElastase B on Level and Activity of Immune Proteins/Peptides ofGalleria mellonellaHemolymph

Cited by 18 publications

References 53 publications

Protease IV, a quorum sensing‐dependent protease of Pseudomonas aeruginosa modulates insect innate immunity

Protease IV, a quorum sensing‐dependent protease of Pseudomonas aeruginosa modulates insect innate immunity

Revisiting the virulence hallmarks of Pseudomonas aeruginosa: a chronicle through the perspective of quorum sensing

Comparative virulence of urinary and bloodstream isolates of extra-intestinal pathogenicEscherichia coliin aGalleria mellonellamodel

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