作者: A S Bayer , D P Speert , S Park , J Tu , M Witt
DOI: 10.1128/IAI.59.1.302-308.1991
关键词:
摘要: We evaluated in vitro the functional role of mucoid exopolysaccharide (MEP) Pseudomonas aeruginosa blocking antibiotic-induced and polymorphonuclear leukocyte (PMN)-mediated pseudomonal killing. The serum-resistant P. isolates used were strain 144MR its nonmucoid revertant, 144NM. By timed kill curves, early bacterial effects amikacin against substantially less than those observed with 144NM; this effect was reversible enzymatic hydrolysis MEP by alginase. Also, tobramycin uptake (15 to 30 min) cells that seen pretreatment alginase enhanced compared untreated (P = 0.08). In 144NM (but not 114MR) there a notable postantibiotic leukocidal enhancement manifested increased nonopsonic killing following brief exposure these supra-MIC amikacin; rendered more susceptible amikacin-induced enhancement. Similarly, direct PMN-mediated significantly 0.05); equal susceptibility addition, exogenous sodium alginate or extracted interfered effective PMNs. Studies also indicated phagocytosed well mate 0.00001), an reversed These data confirm MEPs functionally decrease bactericidal aminoglycosides interfere phagocytosis strains.