Virulence factors in Pseudomonas aeruginosa: mechanisms and modes of regulation

Pseudomonas aeruginosa is a bacterium responsible for severe nosocomial infections, life-threatening infections in immunocompromised persons, and chronic infections in cystic fibrosis patients. The bacterium's virulence depends on a large number of cell-associated and extracellular factors. The virulence factors play an important pathological role in the colonization, the survival of the bacteria and the invasion of tissues. There are two types of virulence factors: (1) factors involved in the acute infection: these factors are either on the surface of P. aeruginosa, either secreted. The pili allow adherence to the epithelium. The exoenzyme S and other adhesins reinforce the adherence to epithelial cells. The exotoxin A is responsible of tissue necrosis. Phospholipase C is a thermolabile haemolysin. The pathogenic role of exoenzyme S is attributable to the disruption of normal cytoskeletal organization, the destruction of immunoglobulin G and A, leads to depolymerization of actin filaments and contributes to the resistance to macrophages. P. aeruginosa produces at least four proteases causing bleeding and tissue necrosis; (2) factors involved in the chronic infection: siderophores (pyoverdin and pyochelin), allow the bacteria to multiply in the absence of ferrous ions. The strains isolated from patients with cystic fibrosis have a pseudocapsule of alginate that protects the bacterium from phagocytosis, dehydration and antibiotics. Moreover, it improves adherence to epithelial cells forming a biofilm. Two different types of regulation systems control the expression of the majority of these virulence factors: the two-component transcriptional regulatory system and the quorum sensing system. These two mechanisms are necessary to the survival and the proliferation of this microorganism in the host.