Epicutaneous model of community-acquired Staphylococcus aureus skin infections.

Document Type

Article

Publication Date

4-2013

Keywords

Animals, Bacterial Load, Community-Acquired Infections, Cytokines, Disease Models, Animal, Ear, External, Female, Lymph Nodes, Methicillin-Resistant Staphylococcus aureus, Mice, Mice, Inbred BALB C, Neutrophils, Skin, Staphylococcal Skin Infections, Time Factors

JAX Source

Infect Immun 2013 Apr; 81(4):1306-1315

Volume

81

Issue

4

First Page

1306

Last Page

1315

ISSN

1098-5522

PMID

23381997

Abstract

Staphylococcus aureus is one of the most common etiological agents of community-acquired skin and soft tissue infection (SSTI). Although the majority of S. aureus community-acquired SSTIs are uncomplicated and self-clearing in nature, some percentage of these cases progress into life-threatening invasive infections. Current animal models of S. aureus SSTI suffer from two drawbacks: these models are a better representation of hospital-acquired SSTI than community-acquired SSTI, and they involve methods that are difficult to replicate. For these reasons, we sought to develop a murine model of community-acquired methicillin-resistant S. aureus SSTI (CA-MRSA SSTI) that can be consistently reproduced with a high degree of precision. We utilized this model to begin to characterize the host immune response to this type of infection. We infected mice via epicutaneous challenge of the skin on the outer ear pinna using Morrow-Brown allergy test needles coated in S. aureus USA300. When mice were challenged in this model, they developed small, purulent, self-clearing lesions with predictable areas of inflammation that mimicked a human infection. CFU in the ear pinna peaked at day 7 before dropping by day 14. The T(h)1 and T(h)17 cytokines gamma interferon (IFN-γ), interleukin-12 (IL-12) p70, tumor necrosis factor alpha (TNF-α), IL-17A, IL-6, and IL-21 were all significantly increased in the draining lymph node of infected mice, and there was neutrophil recruitment to the infection site. In vivo neutrophil depletion demonstrated that neutrophils play a protective role in preventing bacterial dissemination and fatal invasive infection. Infect Immun 2013 Apr; 81(4):1306-1315

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