NDLI: Compartmentalization of immune responses during Staphylococcus aureus cranial bone flap infection.

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Compartmentalization of immune responses during Staphylococcus aureus cranial bone flap infection.

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Compartmentalization of immune responses during Staphylococcus aureus cranial bone flap infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cheatle, Joseph Aldrich, Amy Thorell, William E. Boska, Michael D. Kielian, Tammy
Description	Country affiliation: United States Author Affiliation: Cheatle J ( Division of Neurosurgery, Department of Surgery, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA.)
Abstract	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.
File Format	HTM / HTML
ISSN	00029440
e-ISSN	15252191
DOI	10.1016/j.ajpath.2013.04.031
Journal	The American Journal of Pathology
Issue Number	2
Volume Number	183
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2013-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Research Support, N.i.h., Extramural Surgical Flaps Brain Research Support, Non-u.s. Gov't Surgical Wound Infection Immunology Staphylococcus Aureus Physiology Diagnosis Disease Models, Animal Adverse Effects Mice, Inbred C57bl Deficiency Neutrophils Discipline Pathology Inflammation Myeloid Differentiation Factor 88 Metabolism Staphylococcal Infections Magnetic Resonance Imaging Methicillin-resistant Staphylococcus Aureus Animals Skull Mice Immunity, Cellular Chemokines
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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