No abstract

Pseudomonas aeruginosa infection is preceded by selective adhesion of the bacteria to the host target cells via diverse adhesins, including lectins. This step enables maximal damage to the target host cells by the bacterially secreted injurious toxins and enzymes. The production of both lectins and many of the virulence factors is positively controlled by transcription activators including signaling autoinducers (N-acyl-L-homoserine lactones). We show in this communication that erythromycin at subminimal growth inhibitory concentrations simultaneously suppresses the production of P. aeruginosa hemagglutinins (including lectins), protease, hemolysin and homoserine lactone autoinducers. The antibiotic-treated bacteria also show reduced virulence to mice, endorsing clinical observations that indicate the efficiency of low-dose erythromycin treatment of persistent drug-resistant P. aeruginosa infections.

The effects of PA-I lectin isolated from the human pathogen Pseudomonas aeruginosa upon cellular metabolism in vivo have been studied using the rat gut as a model system. Orally ingested PA-I lectin stimulated metabolic activity and induced polyamine accumulation and growth in the small intestine, caecum and colon. The nature and extent of the changes induced by PA-I lectin were similar to those caused by dietary kidney bean lectin and were likely to lead to impaired epithelial cell function and integrity. This finding contributes to our understanding of the possible roles of these lectins in Pseudomonas aeruginosa infection.