cIn individuals with polymicrobial infections, microbes often display synergistic interactions that can enhance their colonization, virulence, or persistence. One of the most prevalent types of polymicrobial infection occurs in chronic wounds, where Pseudomonas aeruginosa and Staphylococcus aureus are the two most common causes. Although they are the most commonly associated microbial species in wound infections, very little is known about their interspecies relationship. Evidence suggests that P. aeruginosa-S. aureus coinfections are more virulent than monoculture infection with either species; however, difficulties in growing these two pathogens together in vitro have hampered attempts to uncover the mechanisms involved. Here we describe a simple and clinically relevant in vitro wound model that supported concomitant growth of P. aeruginosa and S. aureus. We observed that the ability of P. aeruginosa and S. aureus to survive antibiotic treatment increased when they were grown together in planktonic cocultures and that antibiotic tolerance was further enhanced when they were grown together in the wound model. We attributed this enhanced tolerance to both the "host-derived" and "bacterium-derived" matrix components. Taken together, our data indicate that P. aeruginosa and S. aureus may benefit each other by coinfecting wounds and that the host-derived matrix may serve as important a role as the bacterium-derived matrix in protecting bacteria from some antibiotics.
Chronic wounds are a growing medical problem that cause high rates of morbidity and mortality, costing the healthcare industry in the United States millions of dollars annually. Chronic wound healing is hampered by the presence of bacterial infections that form biofilms, in which the bacteria are encased in exopolysaccharide (EPS) and are less metabolically active than their free-living counterparts. Bacterial biofilms make chronic wounds more refractory to treatment and slow tissue repair by stimulating chronic inflammation at the wound site. Bacterial species communicate through a mechanism known as quorum sensing (QS) to regulate and coordinate the gene expression that is important for virulence-factor production, including biofilm formation. This review focuses on the relationships between chronic wounds, biofilms, and QS in the virulence of chronic-wound pathogens.
Diabetes affects 25.8 million people in the United States, or 8.3% of the population, and these numbers are even higher in developing countries. Diabetic patients are more susceptible to the development of chronic wounds with debilitating bacterial infections than nondiabetics. Previously, we compared the ability of the opportunistic pathogen Pseudomonas aeruginosa to cause biofilm-associated infections in chronic wounds of diabetic and nondiabetic mice (C. Watters, K. DeLeon, U. Trivedi, J. A. Griswold, M. Lyte, K. J. Hampel, M. J. Wargo, and K. P. Rumbaugh, Med. Microbiol. Immunol. 202:131-141, 2013). Unexpectedly, we observed that insulin-treated diabetic mice had significantly more biofilm in their wounds, which correlated with higher antibiotic tolerance. Here, we investigated whether insulin treatment modulates the diabetic immune system to favor P. aeruginosa biofilm formation. Utilizing a murine chronic wound model, we found that DNA protected P. aeruginosa in the wounds of insulin-treated diabetic mice from antibiotic treatment. We also observed increased numbers of neutrophils, reduced numbers of macrophages, and increased cell death in the wounds of diabetic mice on insulin therapy. Taken together, these data suggest that high levels of lysed neutrophils in the wounds of diabetic mice on insulin, combined with fewer macrophages to remove the cellular debris, contribute to increased DNA levels, which enhance P. aeruginosa biofilms.
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