Type 3 secretion system of Pseudomonas aeruginosa

Horna, Gertrudis; Ruiz, Joaquı́m

doi:10.1016/j.micres.2021.126719

Cited by 73 publications

(83 citation statements)

References 206 publications

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“…Four effector proteins, ExoS, ExoT, ExoU, and ExoY have been typically described as the effector proteins used by the P. aeruginosa type III secretion system [ 61 ]; however, two additional effectors, PemA and PemB, have recently been described [ 62 ]. The most clinically relevant effectors may be ExoS and ExoU, which are thought to be mutually exclusive when found in P. aeruginosa strains [ 63 ]. ExoS impairs cell-to-cell adhesion through disruption of the actin cytoskeleton of host respiratory epithelial cells [ 63 ], while also inducing apoptosis of host cells [ 64 ].…”

Section: Mechanisms Of Infection Virulence and Resistancementioning

confidence: 99%

“…The most clinically relevant effectors may be ExoS and ExoU, which are thought to be mutually exclusive when found in P. aeruginosa strains [ 63 ]. ExoS impairs cell-to-cell adhesion through disruption of the actin cytoskeleton of host respiratory epithelial cells [ 63 ], while also inducing apoptosis of host cells [ 64 ]. ExoU is thought to be responsible for the greatest virulence due to its cytotoxic activity that induces host cell death and is more often found in patients in ICUs or burn units [ 63 , 65 , 66 ].…”

Section: Mechanisms Of Infection Virulence and Resistancementioning

confidence: 99%

“…Previous studies have demonstrated that the presence of a type III secretion system in P. aeruginosa is associated with poor outcomes including a larger burden of bacteria, persistence of infection and increased mortality [ 61 , 63 , 67 – 70 ]. Chronic infection with P. aeruginosa , such as in patients with CF, may select against type III secretion system, as many CF patients have antibodies directed against effector proteins and the conversion to a mucoid phenotype leading to downregulation of type III secretion proteins [ 61 , 71 , 72 ].…”

Section: Mechanisms Of Infection Virulence and Resistancementioning

confidence: 99%

See 2 more Smart Citations

The Epidemiology and Pathogenesis and Treatment of Pseudomonas aeruginosa Infections: An Update

Reynolds

Kollef

2021

Drugs

283

204

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Section: Mechanisms Of Infection Virulence and Resistancementioning

confidence: 99%

Section: Mechanisms Of Infection Virulence and Resistancementioning

confidence: 99%

Section: Mechanisms Of Infection Virulence and Resistancementioning

confidence: 99%

See 1 more Smart Citation

The Epidemiology and Pathogenesis and Treatment of Pseudomonas aeruginosa Infections: An Update

Reynolds

Kollef

2021

Drugs

283

204

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“…Our study, which targets C. trachomatis T3SS tip protein CT584, adds to the growing evidence that the injectosome tip is a useful antigen for antibody-mediated immunotherapy. As we show for C. trachomatis, antibody against the T3SS tip protein of other bacterial pathogens is particularly useful in generating passive protection: passive antibody blockade of the Pseudomonas aeruginosa T3SS tip protein, PcrV, was shown to be protective in multiple small animal models [45][46][47][48][49][50]. Progress has also been made with targeting the T3SS injectosome tip of Chlamydia spp., often in multivalent formulations.…”

Section: Discussionmentioning

confidence: 94%

Immunogenicity and Protective Capacity of a Virus-like Particle Vaccine against Chlamydia trachomatis Type 3 Secretion System Tip Protein, CT584

et al. 2022

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An effective vaccine against Chlamydia trachomatis is urgently needed as infection rates continue to rise and C. trachomatis causes reproductive morbidity. An obligate intracellular pathogen, C. trachomatis employs a type 3 secretion system (T3SS) for host cell entry. The tip of the injectosome is composed of the protein CT584, which represents a potential target for neutralization with vaccine-induced antibody. Here, we investigate the immunogenicity and efficacy of a vaccine made of CT584 epitopes coupled to a bacteriophage virus-like particle (VLP), a novel platform for Chlamydia vaccines modeled on the success of HPV vaccines. Female mice were immunized intramuscularly, challenged transcervically with C. trachomatis, and assessed for systemic and local antibody responses and bacterial burden in the upper genital tract. Immunization resulted in a 3-log increase in epitope-specific IgG in serum and uterine homogenates and in the detection of epitope-specific IgG in uterine lavage at low levels. By contrast, sera from women infected with C. trachomatis and virgin controls had similarly low titers to CT584 epitopes, suggesting these epitopes are not systemically immunogenic during natural infection but can be rendered immunogenic by the VLP platform. C. trachomatis burden in the upper genital tract of mice varied after active immunization, yet passive protection was achieved when immune sera were pre-incubated with C. trachomatis prior to inoculation into the genital tract. These data demonstrate the potential for antibody against the T3SS to contribute to protection against C. trachomatis and the value of VLPs as a novel platform for C. trachomatis vaccines.

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“…Type III secretion system (T3SS) is the major contributor to P. aeruginosa-induced virulence [78][79][80][81]. Epithelial cells are especially sensitive to the effects of T3SS toxins [25,[80][81][82][83].…”

Section: Regulation Of Lung Permeability By Virulence Factors Belonging To P Aeruginosa Type III Secretion Systemmentioning

confidence: 99%

The Role of Pseudomonas aeruginosa Virulence Factors in Cytoskeletal Dysregulation and Lung Barrier Dysfunction

Wagener

et al. 2021

Toxins

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Pseudomonas (P.) aeruginosa is an opportunistic pathogen that causes serious infections and hospital-acquired pneumonia in immunocompromised patients. P. aeruginosa accounts for up to 20% of all cases of hospital-acquired pneumonia, with an attributable mortality rate of ~30–40%. The poor clinical outcome of P. aeruginosa-induced pneumonia is ascribed to its ability to disrupt lung barrier integrity, leading to the development of lung edema and bacteremia. Airway epithelial and endothelial cells are important architecture blocks that protect the lung from invading pathogens. P. aeruginosa produces a number of virulence factors that can modulate barrier function, directly or indirectly, through exploiting cytoskeleton networks and intercellular junctional complexes in eukaryotic cells. This review summarizes the current knowledge on P. aeruginosa virulence factors, their effects on the regulation of the cytoskeletal network and associated components, and molecular mechanisms regulating barrier function in airway epithelial and endothelial cells. A better understanding of these processes will help to lay the foundation for new therapeutic approaches against P. aeruginosa-induced pneumonia.

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Type 3 secretion system of Pseudomonas aeruginosa

Cited by 73 publications

References 206 publications

The Epidemiology and Pathogenesis and Treatment of Pseudomonas aeruginosa Infections: An Update

The Epidemiology and Pathogenesis and Treatment of Pseudomonas aeruginosa Infections: An Update

Immunogenicity and Protective Capacity of a Virus-like Particle Vaccine against Chlamydia trachomatis Type 3 Secretion System Tip Protein, CT584

The Role of Pseudomonas aeruginosa Virulence Factors in Cytoskeletal Dysregulation and Lung Barrier Dysfunction

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