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A Pseudomonas aeruginosa quorum-sensing system, which produces N-(3-oxododecanoyl)- l-homoserine lactone (3-oxo- C12-HSL) and N-butanoyl- l-homoserine lactone ( C4-HSL), regulates the virulence factors. In our previous study, 3-oxo- C12-HSL, encoded by lasI gene, was shown to promote wound healing. However, the effect of C4-HSL, encoded by rhlI gene, remains to be elucidated. We addressed the effect of C4-HSL on wounds in P. aeruginosa infection. Wounds were created on the backs of Sprague-Dawley SD rats, and P. aeruginosa PAO1 ( PAO1) or its rhlI deletion mutant (Δ rhlI) or lasI deletion mutant (Δ lasI) was inoculated onto the wound. Rats were injected intraperitoneally with anti- C4-HSL antiserum or treated with C4-HSL at the wound surface. PAO1 inoculation led to significant acceleration of wound healing, which was associated with neutrophil infiltration and TNF-α synthesis. These responses were reversed, except for TNF-α production, when Δ rhlI was inoculated instead of PAO1 or when rats were co-treated with PAO1 and anti-C4-HSL . In contrast, the healing process and neutrophil infiltration, but not TNF-α synthesis, were accelerated when C4-HSL was administered in the absence of PAO1. This acceleration was not affected by anti- TNF-α antibody. These results suggest that C4-HSL may be involved in the acceleration of acute wound healing in P. aeruginosa infection by modifying the neutrophilic inflammation. [ABSTRACT FROM AUTHOR]

A Pseudomonas aeruginosa quorum-sensing system, which produces N-(3-oxododecanoyl)-l-homoserine lactone (3-oxo-C 12 -HSL) and N-butanoyl-l-homoserine lactone (C 4 -HSL), regulates the virulence factors. In our previous study, 3-oxo-C 12 -HSL, encoded by lasI gene, was shown to promote wound healing. However, the effect of C 4 -HSL, encoded by rhlI gene, remains to be elucidated. We addressed the effect of C 4 -HSL on wounds in P. aeruginosa infection. Wounds were created on the backs of Sprague-Dawley SD rats, and P. aeruginosa PAO1 (PAO1) or its rhlI deletion mutant (ΔrhlI) or lasI deletion mutant (ΔlasI) was inoculated onto the wound. Rats were injected intraperitoneally with anti-C 4 -HSL antiserum or treated with C 4 -HSL at the wound surface. PAO1 inoculation led to significant acceleration of wound healing, which was associated with neutrophil infiltration and TNF-α synthesis. These responses were reversed, except for TNF-α production, when ΔrhlI was inoculated instead of PAO1 or when rats were co-treated with PAO1 and anti-C 4 -HSL antiserum. In contrast, the healing process and neutrophil infiltration, but not TNF-α synthesis, were accelerated when C 4 -HSL was administered in the absence of PAO1. This acceleration was not affected by anti-TNF-α antibody. These results suggest that C 4 -HSL may be involved in the acceleration of acute wound healing in P. aeruginosa infection by modifying the neutrophilic inflammation., (© 2015 Medicalhelplines.com Inc and John Wiley & Sons Ltd.)