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Staphylococcus aureus infection of mouse or human osteoblasts induces high levels of interleukin-6 and interleukin-12 production.
Bost, K L; Ramp, W K; Nicholson, N C; Bento, J L; Marriott, I; Hudson, M C.
Afiliación
  • Bost KL; Department of Biology, University of North Carolina at Charlotte, Charlotte, NC 28223, USA. klbost@email.uncc.edu
J Infect Dis ; 180(6): 1912-20, 1999 Dec.
Article en En | MEDLINE | ID: mdl-10558948
Staphylococcus aureus is the principal causative agent of the inflammatory bone disease osteomyelitis. Unfortunately, the pathogenesis of this often chronic infection is poorly understood and is complicated by the recent observation that bone-forming osteoblasts can harbor S. aureus. Such an infection presents a significant challenge for the host immune response, because osteoblasts are not known to initiate protective cell-mediated immune responses. Cultured mouse and human osteoblasts infected with S. aureus were found to express high levels of interleukin (IL)-6 and IL-12p75, on the basis of complementary investigations demonstrating both S. aureus-induced up-regulation of expression of IL-6 and IL-12p40 mRNA and secretion of IL-6 and IL-12p75 by these cells. Additionally, a quantitative bioassay demonstrated that IL-12p75 secreted after infection was biologically active. These studies are the first to demonstrate induced IL-12p75 expression by osteoblasts and suggest a previously unrecognized role for osteoblasts in initiating immune responses after S. aureus infection.
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoblastos / Staphylococcus aureus / Interleucina-6 / Interleucina-12 Límite: Animals / Humans Idioma: En Revista: J Infect Dis Año: 1999 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoblastos / Staphylococcus aureus / Interleucina-6 / Interleucina-12 Límite: Animals / Humans Idioma: En Revista: J Infect Dis Año: 1999 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos