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Propagation of multidrug‐resistant Pseudomonas aeruginosa, which causes endemic noso‐ comial infections, has become a major concern in various parts of the world. In patients with cystic fibrosis, a major cause of death is respiratory tract infections with antibiotic‐ resistant P. aeruginosa. This condition has prompted medical research aimed at develop‐ ing effective prophylaxis and treatments that do not rely on conventional antimicrobial agents. The pathogenesis that results in cytotoxicity and mortality in immunocompro‐ mised patients infected with P. aeruginosa is associated with the type III secretion sys‐ tem of this bacterium. Clinical isolates that are cytotoxic and drug‐resistant are involved in acute exacerbation of chronic infectious diseases. The P. aeruginosa V‐antigen PcrV, a Yersinia V‐antigen LcrV homolog, is involved as an indispensable component in the translocational process of type III secretory (TTS) toxins. Vaccination against PcrV ensures survival of infection‐challenged mice and decreases lung inflammation and injury. Furthermore, anti‐PcrV IgG can inhibit translocation of TTS toxins. These observa‐ tions support the hypothesis that anti‐PcrV strategies have the potential as nonantibiotic immune strategies for preventing aggravation of P. aeruginosa infections in patients with cystic fibrosis.

Anti‐PcrV Immunization for Pseudomonas aeruginosa Pneumonia in Cystic Fibrosis