Hydrophobic Interaction and Sorbact Wound Dressings

Åsa Ljungh, MD, PhD, and Torkel Wadström, MD, PhD, Department of Medical Microbiology, Dermatology and Infection, Lund University, Sölvegatan 23, SE-223 62 Lund, Sweden

The hydrophobic principle
According to the laws of nature, a system will always struggle to achieve the lowest possible energy consumption. When two water-repellent (hydrophobic) molecules collide with one another, they increase the entropy, create disorder. The water molecules that surround the two hydrophobic molecules will force them together by hydrogen bonds between the water molecules. Although there is no force of attraction between the hydrophobic molecules, they will associate with each other through what we call hydrophobic interaction and expel water molecules (Figure 1,1).

Microbial cell surface hydrophobins
Numerous studies during the last few decades have shown that bacteria, such as Staphylococcus aureus and Group A streptococci, both common wound pathogens, and the yeast Candida albicans commonly express profound cell surface hydrophobicity, CSH (2-5). Several structures that render the cell surface hydrophobic have been defined; they include the hair-like protein appendages, fimbriae, of E. coli which mediate adhesion to the intestinal wall (6,7), proteins on C. albicans, which have been called "hydrophobins" (8), and lipoteichoic acid in the cell wall of gram-positive bacteria (4). Fimbriae often have hydrophobic properties and are classified as lectins, i.e. sugar-binding proteins (6).

Cell surface hydrophobicity as a virulence trait
The initial step in infections of the skin and mucosal surfaces is microbial adhesion to wounded tissues. Several adhesins binding to specific receptors, such as fimbriae of gram-negative enteric bacteria, have been identified. Initial adhesion can be mediated by hydrophobic interactions between microbes and host tissue structures and also by charge interactions. The binding of extracellular matrix (ECM) and serum proteins, like fibronectin, collagen and fibrinogen, may further enhance the colonisation of deeper wounded tissue (11).

Growth conditions influence expression of cell surface hydrophobicity
It is well known that growth conditions influence the expression of CSH (5,12). Using the SAT, we showed that culture conditions mimicking a wound, i.e. the presence of serum on a rich microbial culture substrate (hematin agar), and incubation in 5% CO2 enhanced the expression of CSH of S. aureus, coagulase-negative staphylococci, E. coli, Enterobacter cloacae, Pseudomonas aeruginosa, C. albicans and some other bacterial species (13). We and others have previously shown that growth on nutrient-poor media, simulating "starvation" on the skin, promotes the expression of molecules which mediate the binding of ECM proteins (14,15).

Wound infections
After tissue colonisation, wound microbes multiply, cause local tissue damage through the release of toxins and enzymes and even spread to the blood stream.

The human body has multiple defence mechanisms, such as the complement system, phagocytosis, antimicrobial peptides (defensins) and other structures of the so-called innate immune system. Moreover, specific antibodies directed against the colonising micro-organism may be active to reduce the number of micro-organisms. Numerous studies have shown that high tissue counts of micro-organisms delay wound healing. The infectious dose is significantly reduced in patients with diabetes mellitus, receiving corticosteroid or immunosuppressive therapy, or with an impaired peripheral blood supply.

The presence of a foreign material, like surgical sutures, also reduces the infectious dose (11). Bacterial counts above 105/g tissue in an otherwise healthy tissue have been correlated to poor wound healing and hampered skin transplantation (16). On the other hand, small numbers of bacteria were shown to enhance the wound healing process in rodents by stimulating the production of collagen-hydroxyproline (17,18). Many bacterial products like lipoteichoic acid and staphylococcal enterotoxins are potent mitogens (19).

Wound treatment
The conventional treatment of wounds consists of mechanical cleansing with water, buffer solutions or disinfectants to remove bacteria and debris (20,21). This is of the utmost importance as debris hampers wound healing. Microbiologists disapprove of the use of local antibiotics as this is known to induce antibiotic resistance. We are now encountering significant problems with multiple antibiotic-resistant wound pathogens, like S. aureus, Enterococcus species and P. aeruginosa, as well as coagulase-negative staphylococci and streptococci (22-24). When signs of local spread, e.g. erysipelas, or spread to the blood stream develop, the systemic administration of antibiotics is indicated.

The Sorbact principle
The Sorbact wound dressing consists of an acetate or cotton fabric coated with a fatty ester, DACC (diacylcarbamoyl chloride), which gives Sorbact a strong hydrophobic property. Microbes in a wound will adhere to Sorbact as a result of hydrophobic interaction and will be removed from the wound when the dressing is changed. As a result, the number of micro-organisms decreases to a level that the body can control, thereby enabling the wound to heal. As microbes adhere to the dressing through hydrophobic interaction, the spread of micro-organisms to the environment during dressing changes is limited.

Hydrophobic interaction results in the expulsion of water. Sorbact is therefore designed for wet-moist wounds.

Sorbact has been shown to enhance wound healing in pigs infected with S. aureus (25) and in patients with wound infections caused by various micro-organisms, as well as enhancing the effectiveness of skin transplantation (26-28).

The use of Sorbact with or without systemic antibiotic therapy reduces the number of infectious micro-organisms but does not eliminate all bacteria, which is an advantage, as  a small number of micro-organisms stimulate wound healing (17). The use of Sorbact replaces the use of topical antibiotics and thereby the spread of antibiotic-resistant organisms.

References

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