Wound inflammation

Chronic wounds are an important problem worldwide. These wounds are characterized by a persistent inflammatory stage associated with excessive accumulation and elevated cell activity of neutrophils, suggesting that there must be a persistent stimulus that attracts and recruits neutrophils of the wound. The cellular inflammatory response against the bacteria in the chronic wounds, the amount of neutrophils accumulated at the site of infection, was evaluated through differential neutrophil counting on the tissue sections from wounds containing either P. aeruginosa or Staphylococcus aureus. Such bacteria are morphologically and physiologically different from free-living planktonic bacteria and have been implicated in numerous chronic infections ranging from cystic fibrosis to prostatitis (Costerton et al., 1995, 1999). The existence of biofilms in an acute partial-thickness wound (Serralta et al., 2001) and in chronic human wounds (Bello et al., 2001) has been documented.

Wound healing and infection is influenced by the relationship between the ability of bacteria to create a stable, prosperous community within a wound environment and the ability of the host to control the bacterial community. Within a stable, climax biofilm community, interactions between aerobic and anerobic bacteria are likely to increase their net pathogenic effect, enhancing their potential to cause infection and delay healing. Chronic wounds are invariably polymicrobial, yet most research to date has focused on the role of specific potential pathogens in wounds (e.g., P. aeruginosa) rather than the effect of interactions between different species (Percival and Bowler, 2004).

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