A Skin Chamber To Investigate Wound Infection and Healing in the Mouse

Author(s): 
Peter M. Geerlings, Bsc(Hons); Wendy C. Ugarte, Bsc; William J. Penhale, BVsc, Ph

Abstract: The development of a simple, convenient, and reliable polypropylene screw-capped skin chamber, which can be inserted into mice, is described. All implanted chambers of normal immuno-competent mice (n = 10), or immuno-suppressed mice (n = 10) remained in-situ for 15 days. Wound infection was established by a clinical isolate of Pseudomonas aeruginosa in immuno-competent mice (n = 10) 1 day after chamber implantation and chambers remained in-situ for 10 days. Similar infections of wounds among mice immuno-suppressed with cyclophosphamide resulted in the mouse becoming moribund due to systemic invasion by the bacterium. The authors conclude that this mouse skin chamber will be of potential value for studying wound healing during the inflammatory and early proliferative phases, and the influence of infection and treatments on these processes in immuno-suppressed and immuno-competent mice.



Address correspondence to:
Peter M. Geerlings, Bsc,(Hons)
Murdoch University
South Street
Murdoch 6150
Western Australia
E-mail: p.geerlings@murdoch.edu.au
Phone: (08) 9360 2684






     The skin is the body’s primary protective barrier and serves a significant role in body fluid homeostasis, thermoregulation, and host defense. Once the integrity of the skin has been breached by traumatic injury, the healing process commences and involves both removal and repair of the damaged tissue. Augmented innate and specific immune reactivity against potential infections occurs.1 Healing is a progressive process of inflammation, proliferation, and re-modeling that involves an array of cells and cell signals. This process can be adversely affected by the extent of the injury, the immune status of the patient, and the presence of bacterial or other infection.2 Much remains to be learned regarding the early phases of healing and its influence by infectious agents. Several animal models of severe skin trauma were previously developed for this purpose that used sterile chambers either attached to, or inserted through the epidermis.3,4 These systems maintain sterility at the trauma site or permit the establishment of monoculture infections and allow for sampling of exudate and tissue, as well as application of therapy. Effective epidermal chamber applications have been previously described in pigs3 and rats,4 but to our knowledge, has not yet been attempted in the mouse. This is most likely due to the difficulties resulting from its small size and thinness, and therefore, more fragile nature of the mouse epidermis. While pig skin more closely resembles human skin, rodents have been used extensively to elucidate the genes involved in wound healing and as models of infection, wounding, and immunity.5–10 The availability of genetically defined strains plus the abundance of biomarkers and reagents for mouse experimentation adds to the value of mice as an in-vivo research tool to study wound healing and infection.

     A device was developed that is suitable for use in mice with normal immune function or in mice that have been treated with an immunosuppressant, to mimic a reduction in immune function much like what is observed following a severe burn. The following describes a simple and reliable full-thickness murine skin wound chamber and will discuss potential uses in studies of healing and infection.

Materials and Methods


     Chamber. The chamber has an overall height of 10 mm, an outer diameter (OD) of 18 mm at its base, weighs 1.8 g with a capacity of 400 µL ex-vivo, and can be autoclaved at 121˚C for 15 minutes and re-used.

References: 

1. Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clin Microbiol Rev. 2006;19(2):403–434.
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10. Toliver-Kinsky TE, Varma TK, Lin CY, Herndon DN, Sherwood ER. Interferon-gamma production is suppressed in thermally injured mice: decreased production of regulatory cytokines and corresponding receptors. Shock. 2002;18(4):322–330.










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