Phagocytosis of Pseudomonas aeruginosa fails to elicit heat shock protein expression in human monocytes.

Phagocytosis represents a powerful stress for the phagocytic cells. Phagocytosis of Staphylococcus aureus induces a stress response associated with the synthesis of specific heat shock/stress proteins (HSP). Here we investigated the stress response of human monocyte-macrophages (m phi) to Pseudomonas aeruginosa, a bacterium found, as for S. aureus, in the airways of patients suffering cystic fibrosis. P. aeruginosa activated in m phi the production of both extra- and intracellular O2-; increased Interleukin-1 beta and actin, but failed to induce host HSP. Neither S. aureus' exotoxins nor the scavenging property of P. aeruginosa's alginate, but the lower toxicity of P. aeruginosa and/or differential activation of proteine kinase C (PKC) by the two bacteria, might explain their differences in host HSP induction. While O2- is insufficient to induce HSP synthesis in m phi, hydroxyl radicals, generated in the presence of exogenous iron, is a likely additional signal, along with PKC activation, for HSP induction during bacterial phagocytosis.