Compartmentalization of Immune Responses during Staphylococcus aureus Cranial Bone Flap Infection
| Autor: | Joseph T. Cheatle, William E. Thorell, Michael D. Boska, Tammy Kielian, Amy Aldrich |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Methicillin-Resistant Staphylococcus aureus
Staphylococcus aureus Chemokine Pathology medicine.medical_specialty Neutrophils medicine.medical_treatment Inflammation medicine.disease_cause Surgical Flaps Pathology and Forensic Medicine Mice Immune system Immunity Parenchyma medicine Animals Humans Surgical Wound Infection Immunity Cellular biology Skull Brain Regular Article Staphylococcal Infections Magnetic Resonance Imaging Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure Myeloid Differentiation Factor 88 biology.protein Decompressive craniectomy Chemokines medicine.symptom |
| Zdroj: | The American Journal of Pathology. 183:450-458 |
| ISSN: | 0002-9440 |
| DOI: | 10.1016/j.ajpath.2013.04.031 |
| Popis: | Decompressive craniectomy is often required after head trauma, stroke, or cranial bleeding to control subsequent brain swelling and prevent death. The infection rate after cranial bone flap replacement ranges from 0.8% to 15%, with an alarming frequency caused by methicillin-resistant Staphylococcus aureus , which is problematic because of recalcitrance to antibiotic therapy. Herein we report the establishment of a novel mouse model of S. aureus cranial bone flap infection that mimics several aspects of human disease. Bacteria colonized bone flaps for up to 4 months after infection, as revealed by scanning electron microscopy and quantitative culture, demonstrating the chronicity of the model. Analysis of a human cranial bone flap with confirmed S. aureus infection by scanning electron microscopy revealed similar structural attributes as the mouse model, demonstrating that it closely parallels structural facets of human disease. Inflammatory indices were most pronounced within the subcutaneous galeal compartment compared with the underlying brain parenchyma. Specifically, neutrophil influx and chemokine expression (CXCL2 and CCL5) were markedly elevated in the galea, which demonstrated substantial edema on magnetic resonance images, whereas the underlying brain parenchyma exhibited minimal involvement. Evaluation of immune mechanisms required for bacterial containment and inflammation revealed critical roles for MyD88-dependent signaling and neutrophils. This novel mouse model of cranial bone flap infection can be used to identify key immunologic and therapeutic mechanisms relevant to persistent bone flap infection in humans. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|