Cytokine stimulation by Pseudomonas aeruginosa--strain variation and modulation by pulmonary surfactant

Pulmonary surfactant and its components are part of the first-line immune defense within the lung. Here the authors show that the surfactant protein (SP) SP-D, but not SP-A, agglutinates some clinical isolates of Pseudomonas aeruginosa and Stenotrophomonas maltophilia. No agglutination of Staphylococcus aureus or Burkholderia cepacia was observed. The SP-D-induced agglutination of P. aeruginosa was not dependent on a specific lipopolysaccharide (LPS) serotype. The authors also show that SP-D, but not SP-A, increased the tumor necrosis factor (TNF alpha) release from human monocytic cells in response to a subset of P. aeruginosa and P. aeruginosa LPS. A clinical preparation of surfactant (Alveofact) blocked the TNF alpha release from monocytic cells induced by P. aeruginosa or its LPS. SP-A reversed the inhibitory effect of Alveofact in 6/8 strains of P. aeruginosa and 2/9 preparations of P. aeruginosa LPS. SP-D did not significantly alter the TNF alpha production induced by vital P. aeruginosa in the presence of Alveofact but markedly increased the TNF alpha release induced by a preparation of rough and smooth P. aeruginosa LPS. In summary, this study shows that the immunomodulatory properties of SP-A and SP-D specifically depend on the colonizing strain of P. aeruginosa. In addition, the authors show that the function of SP-A and SP-D is modulated in the presence of surfactant lipids.