Functional Consequences of Calcium Influx Promoted by Bacterial Pore-Forming Toxins.

Bacterial pore-forming toxins induce a rapid and massive increase in cytosolic Ca concentration due to the formation of pores in the plasma membrane and/or activation of Ca-channels. As Ca is an essential messenger in cellular signaling, a sustained increase in Ca concentration has dramatic consequences on cellular behavior, eventually leading to cell death. However, host cells have adapted mechanisms to protect against Ca intoxication, such as Ca efflux and membrane repair.

Corrigendum: Takes a Multi-Target Approach to Achieve Junction Breach.

[This corrects the article on p. 532 in vol. 7, PMID: 29379773.

Takes a Multi-Target Approach to Achieve Junction Breach.

is an opportunistic pathogen which uses a number of strategies to cross epithelial and endothelial barriers at cell-cell junctions. In this review, we describe how the coordinated actions of 's virulence factors trigger various molecular mechanisms to disarm the junctional gate responsible for tissue integrity.

Exolysin Shapes the Virulence of Pseudomonas aeruginosa Clonal Outliers.

Bacterial toxins are important weapons of toxicogenic pathogens. Depending on their origin, structure and targets, they show diverse mechanisms of action and effects on eukaryotic cells. Exolysin is a secreted 170 kDa pore-forming toxin employed by clonal outliers of providing to some strains a hyper-virulent behaviour.

Pseudomonas aeruginosa ExlA and Serratia marcescens ShlA trigger cadherin cleavage by promoting calcium influx and ADAM10 activation.

Pore-forming toxins are potent virulence factors secreted by a large array of bacteria. Here, we deciphered the action of ExlA from Pseudomonas aeruginosa and ShlA from Serratia marcescens on host cell-cell junctions. ExlA and ShlA are two members of a unique family of pore-forming toxins secreted by a two-component secretion system.

Pseudomonas aeruginosa Exolysin promotes bacterial growth in lungs, alveolar damage and bacterial dissemination.

Exolysin (ExlA) is a recently-identified pore-forming toxin secreted by a subset of Pseudomonas aeruginosa strains identified worldwide and devoid of Type III secretion system (T3SS), a major virulence factor. Here, we characterized at the ultrastructural level the lesions caused by an ExlA-secreting strain, CLJ1, in mouse infected lungs. CLJ1 induced necrotic lesions in pneumocytes and endothelial cells, resulting in alveolo-vascular barrier breakdown.

Pseudomonas aeruginosa Pore-Forming Exolysin and Type IV Pili Cooperate To Induce Host Cell Lysis.

Unlabelled: Clinical strains of Pseudomonas aeruginosa lacking the type III secretion system genes employ a toxin, exolysin (ExlA), for host cell membrane disruption. Here, we demonstrated that ExlA export requires a predicted outer membrane protein, ExlB, showing that ExlA and ExlB define a new active two-partner secretion (TPS) system of P. aeruginosa In addition to the TPS signals, ExlA harbors several distinct domains, which include one hemagglutinin domain, five arginine-glycine-aspartic acid (RGD) motifs, and a C-terminal region lacking any identifiable sequence motifs.

Pseudomonas aeruginosa renews its virulence factors.

Highly divergent strains of the major human opportunistic pathogen Pseudomonas aeruginosa have been isolated around the world by different research laboratories. They came from patients with various types of infectious diseases or from the environment. These strains are devoid of the major virulence factor used by classical strains, the Type III secretion system, but possess additional putative virulence factors, including a novel two-partner secretion system, ExlBA, responsible for the hypervirulent behavior of some clinical isolates.

Phenotype and toxicity of the recently discovered exlA-positive Pseudomonas aeruginosa strains collected worldwide.

We recently identified a hypervirulent strain of Pseudomonas aeruginosa, differing significantly from the classical strains in that it lacks the type 3 secretion system (T3SS), a major determinant of P. aeruginosa virulence. This new strain secretes a novel toxin, called ExlA, which induces plasma membrane rupture in host cells.