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1.
Artículo en Inglés | MEDLINE | ID: mdl-31138566

RESUMEN

Surgical site infections (SSIs) are commonly caused by Staphylococcus aureus We report that a combination of three monoclonal antibodies (MEDI6389) that neutralize S. aureus alpha-toxin, clumping factor A, and four leukocidins (LukSF, LukED, HlgAB, and HlgCB) plus vancomycin had enhanced efficacy compared with control antibody plus vancomycin in two mouse models of S. aureus SSI. Therefore, monoclonal antibody-based neutralization of multiple S. aureus virulence factors may provide an adjunctive perioperative approach to combat S. aureus SSIs.


Asunto(s)
Antibacterianos/farmacología , Anticuerpos Monoclonales/farmacología , Infecciones Estafilocócicas/tratamiento farmacológico , Infección de la Herida Quirúrgica/tratamiento farmacológico , Animales , Anticuerpos Monoclonales Humanizados/farmacología , Proteínas Bacterianas/inmunología , Anticuerpos ampliamente neutralizantes/farmacología , Coagulasa/inmunología , Leucocidinas/inmunología , Staphylococcus aureus Resistente a Meticilina/patogenicidad , Ratones Endogámicos C57BL , Ratones Endogámicos , Infecciones Estafilocócicas/microbiología , Infección de la Herida Quirúrgica/microbiología , Vancomicina/farmacología
2.
J Orthop Res ; 38(8): 1800-1809, 2020 08.
Artículo en Inglés | MEDLINE | ID: mdl-31975434

RESUMEN

Orthopedic implant-associated infection (OIAI) is a major complication that leads to implant failure. In preclinical models of Staphylococcus aureus OIAI, osteomyelitis and septic arthritis, interleukin-1α (IL-1α), IL-1ß, and tumor necrosis factor (TNF) are induced, but whether they have interactive or distinctive roles in host defense are unclear. Herein, a S. aureus OIAI model was performed in mice deficient in IL-1α, IL-1ß, or TNF. Mice deficient in IL-1ß or TNF (to a lesser extent) but not IL-1α had increased bacterial burden at the site of the OIAI throughout the 28-day experiment. IL-1ß and TNF had a combined and critical role in host defense as mice deficient in both IL-1R and TNF (IL-1R/TNF-deficient mice) had a 40% mortality rate, which was associated with markedly increased bacterial burden at the site of the OIAI infection. Finally, IL-1α- and IL-1ß-deficient mice had impaired neutrophil recruitment whereas IL-1ß-, TNF-, and IL-1R/TNF-deficient mice all had impaired recruitment of both neutrophils and monocytes. Therefore, IL-1ß and TNF contributed to host defense against S. aureus OIAI and neutrophil recruitment was primarily mediated by IL-1ß and monocyte recruitment was mediated by both IL-1ß and TNF.


Asunto(s)
Interleucina-1beta/metabolismo , Infiltración Neutrófila , Infecciones Relacionadas con Prótesis/metabolismo , Factor de Necrosis Tumoral alfa/metabolismo , Animales , Interleucina-1alfa/metabolismo , Masculino , Ratones Endogámicos C57BL , Infecciones Relacionadas con Prótesis/inmunología , Infecciones Estafilocócicas/inmunología , Infecciones Estafilocócicas/metabolismo
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