Literature DB >> 19840177

Production of cell-cell signalling molecules by bacteria isolated from human chronic wounds.

A H Rickard1, K R Colacino, K M Manton, R I Morton, E Pulcini, J Pfeil, D Rhoads, R D Wolcott, G James.   

Abstract

AIM: To (i) identify chronic wound bacteria and to test their ability to produce acyl-homoserine-lactones (AHLs) and autoinducer-2 (AI-2) cell-cell signalling molecules and (ii) determine whether chronic wound debridement samples might contain these molecules. METHODS AND
RESULTS: Partial 16S rRNA gene sequencing revealed the identity of 46 chronic wound strains belonging to nine genera. Using bio-reporter assays, 69.6% of the chronic wound strains were inferred to produce AI-2, while 19.6% were inferred to produce AHL molecules. At least one strain from every genus, except those belonging to the genera Acinetobacter and Pseudomonas, were indicated to produce AI-2. Production of AI-2 in batch cultures was growth-phase dependent. Cross-feeding assays demonstrated that AHLs were produced by Acinetobacter spp., Pseudomonas aeruginosa and Serratia marcescens. Independent from studies of the bacterial species isolated from wounds, AHL and/or AI-2 signalling molecules were detected in 21 of 30 debridement samples of unknown microbial composition.
CONCLUSION: Chronic wound bacteria produce cell-cell signalling molecules. Based on our findings, we hypothesize that resident species generally produce AI-2 molecules, and aggressive transient species associated with chronic wounds typically produce AHLs. Both these classes of cell-cell signals are indicated to be present in human chronic wounds. SIGNIFICANCE AND IMPACT OF THE STUDY: Interbacterial cell-cell signalling may be an important factor influencing wound development and if this is the case, the presence of AHLs and AI-2 could be used as a predictor of wound severity. Manipulation of cell-cell signalling may provide a novel strategy for improving wound healing.

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Year:  2009        PMID: 19840177      PMCID: PMC2902276          DOI: 10.1111/j.1365-2672.2009.04554.x

Source DB:  PubMed          Journal:  J Appl Microbiol        ISSN: 1364-5072            Impact factor:   3.772


  71 in total

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