Host Response to Pseudomonas aeruginosa

Abstract

Patients with cystic fibrosis (CF) do not reveal a primary immune defect and respond with high numbers of functional polymorphonuclear leukocytes (PMN) and specific antibodies to lung infection with Pseudomonas aeruginosa. The mucoid character of P. aeruginosa, an altered epithelial cell surface, and high concentrations of PMN‐derived lysosomal enzymes contribute to impaired bacterial lung clearance and result in chronic infection. Released PMN‐elastase inactivates exotoxin A, the major toxin of P. aeruginosa, thus reducing its virulence. The imbalance between PMN‐proteinases and their inhibitors leads to lung tissue damage, impaired opsonophagocytosis, and T‐cell and B‐cell imbalance. New therapeutical concepts in CF therefore combine anti‐inflammatory drugs with effective antibiotics.

Induction of inflammatory mediator release (serotonin and 12-hydroxyeicosatetraenoic acid) from human platelets by Pseudomonas aeruginosa glycolipid

“…Pseudomonas aeruginosa is an opportunistic pathogen which causes either localized infections, such as pneumonia in patients with cystic fibrosis, or generalized septicemia in immunocompromised hosts who are suffering from severe burns or cancer or receiving immunosuppressive therapy (17,23,42,47,48,56). Basically, the occurrence of such diverse clinical diseases may derive either from an altered host defense in these patients and/or a difference in virulence of taxonomically identical P. aeruginosa strains (1,18,30,32,41,57).…”