Effect of Pseudomonas aeruginosa alginate on Escherichia coli- and Staphylococcus aureus-induced inflammatory mediator release from human cells.

We analyzed the role of soluble purified Pseudomonas aeruginosa alginate on Escherichia coli K-12 (pANN5211) as well as on Staphylococcus aureus 121c-induced inflammatory mediator release from human platelets, granulocytes, and basophils. In the presence of alginate (1-4 mg/ml), the mucoid exopolysaccharide of P. aeruginosa, the bacteria-induced inflammatory mediator release was modulated as follows: (1) the E. coli- as well as S. aureus-induced chemiluminescence response from human neutrophils increased 2- to 3-fold and 5- to 6-fold, respectively; (2) the E. coli-induced leukotriene B4 formation from human neutrophils was enhanced (from 29.17 +/- 1.8 up to 36.9 +/- 4 ng/10(7) cells) as was also observed for the E. coli- and S. aureus-induced histamine release (3- to 4-fold) and the 12-hydroxyeicosatetraenoic acid generation from human platelets (2-fold), and (3) prolonged duration of the E. coli-induced increase in CD11b expression was observed. Alginate by itself was inactive. Our results provide evidence that alginate interacts with hemolysin-producing E. coli and S. aureus bacteria and thus leads to a modulation of the cellular response pattern, which leads to the local destruction of the lung in cystic fibrosis.