Pseudomonas aeruginosa wound infection involves activation of its iron acquisition system in response to fascial contact.

BACKGROUND: Wound infections are traditionally thought to occur when microbial burden exceeds the innate clearance capacity of host immune system. Here, we introduce the idea that the wound environment itself plays a significant contributory role to wound infection.
METHODS: We developed a clinically relevant murine model of soft tissue infection to explore the role of activation of microbial virulence in response to tissue factors as a mechanism by which pathogenic bacteria cause wound infections. Mice underwent abdominal skin incision and light muscle injury with a crushing forceps versus skin incision alone followed by topical inoculation of Pseudomonas aeruginosa. Mice were sacrificed on postoperative Day 6, and abdominal tissues were analyzed for clinical signs of wound infection. To determine if specific wound tissue components induce bacterial virulence, P. aeruginosa was exposed to the skin, fascia, and muscle.
RESULTS: Gross wound infection caused by P. aeruginosa was observed to be significantly increased in injured tissues versus noninjured (80% vs.10%) tissues (n = 20 per group, p < 0.0001). Exposure of P. aeruginosa to individual tissue components demonstrated that fascia significantly induced bacterial virulence as judged by the production of pyocyanin, a redox-active phenazine compound known to kill immune cells. Whole-genome transcriptional profiling of P. aeruginosa exposed to the fascia demonstrated activation of multiple genes responsible for the synthesis of the iron scavenging molecule pyochelin.
CONCLUSION: We conclude that wound elements, in particular fascia, may play a significant role in enhancing the virulence of P. aeruginosa and may contribute to the pathogenesis of clinical wound infection.