Direct activation of human polymorphonuclear leukocytes by Pseudomonas aeruginosa.
Brief exposure of polymorphonuclear leukocytes (PMNs) to unopsonized Pseudomonas aeruginosa resulted in significant enhancement of PMN adherence and 3H-deoxyglucose uptake, two important indicators of PMN activation. Dose-response and time-course experiments show that maximal stimulation of PMNs occurred at a PMN: bacteria ratio of 10:1 and exposure time of 10 min. The PMN-stimulatory capacity of P. aeruginosa was completely or partially abolished by treatment with formalin, heat, ultrasonication and ultraviolet (UV) irradiation, all of which affect the integrity of ligands on the bacteria surface. The putative glycoprotein ligand(s) contains galactose rather than glucose as shown by the ability of galactose in the medium to abrogate PMN-stimulatory activity. This PMN-stimulatory activity was not mediated by soluble factor(s) released from either P. aeruginosa or PMNs as shown by experiments with appropriate supernatants. Finally, PMN-stimulating activity was also observed with P. maltophilia and P. pseudomallei, but not by the other Pseudomonas spp. such as P. cepacia and P. fluorescens. These results suggest that P. aeruginosa and other Pseudomonas spp. may have little capacity to circumvent PMN host defences. This may account in part for their limited pathogenic role as opportunistic micro-organisms, for the severe inflammatory lesions seen in Pseudomonas infections when they do occur, and is consistent with the fact that infection with these organisms is commonly associated with impaired quantity or function of PMNs.