Detection of Pseudomonas aeruginosa quorum sensing signals in an infected ischemic wound: an experimental study in rats.

Abstract

Quorum sensing is a cell-to-cell communication that occurs via autoinducers, regulating a number of bacterial virulence factors including the opportunistic wound pathogen Pseudomonas aeruginosa, which uses the N-(3-oxododecanoyl)-homoserine lactone as one of the two main autoinducers; however, little is known about its role in chronic wound infection. This study was designed to quantify this autoinducer from P. aeruginosa-infected wounds with the aim of examining the possible use of autoinducers as an indicator of chronic wound infection. Pressure-induced ischemic wounds were infected with P. aeruginosa (N=12) or uninfected as a control (N=12). The autoinducer was quantified by bioassay method employing Escherichia coli DH5 alpha (pJN105L, pSC11) or Agrobacterium tumefaciens NTL4 (pZLR4) reporter, which expresses beta-galactosidase when exposed to P. aeruginosa quorum sensing signals. The average concentration of autoinducer was 0.33 pmol/g at day 3 and 0.49 pmol/g at day 7 in the infected wounds, as detected from tissue samples. A linear correlation between autoinducer concentration and bacterial counts was observed. No autoinducer was detected in tissue samples from the uninfected control group. Our findings indicate that the quantification of autoinducers is possible and quorum sensing system could play a role in in vivo wound infection models, and also suggest possible clinical implications of autoinducer signal quantification in diagnosis of chronic wound infection.