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Detection of Pseudomonas aeruginosa quorum sensing signals in an infected ischemic wound: An experimental study in rats
Author(s) -
Nakagami Gojiro,
Sanada Hiromi,
Sugama Junko,
Morohoshi Tomohiro,
Ikeda Tsukasa,
Ohta Yasunori
Publication year - 2008
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1111/j.1524-475x.2007.00329.x
Subject(s) - autoinducer , quorum sensing , pseudomonas aeruginosa , microbiology and biotechnology , bacteria , wound healing , homoserine , virulence , biology , chemistry , biofilm , immunology , biochemistry , gene , genetics
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 DH5α (pJN105L, pSC11) or Agrobacterium tumefaciens NTL4 (pZLR4) reporter, which expresses β‐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.