Bacterial infection of osteoblasts induces interleukin-1beta and interleukin-18 transcription but not protein synthesis.

Journal Article (Journal Article)

A growing body of evidence has shown that bacterially challenged bone-forming osteoblasts are a significant source of an array of cytokines and chemokines that can support immune responses during bone disease. In the present study, Staphylococcus aureus and Salmonella, two common pathogens of bone, were investigated for their ability to induce production of two related inflammatory cytokines, interleukin-1beta (IL-1beta) and IL18, in osteoblasts. Cultured mouse osteoblasts were found to respond rapidly to either bacterial challenge by upregulation in the levels of mRNA encoding both IL-1beta and IL-18. Surprisingly, this mRNA expression did not translate into intracellular accumulation of IL-1beta or IL-18 precursor proteins or secretion of mature cytokines, despite the presence of detectable caspase-1 activity in these cells. These studies demonstrate that although osteoblasts can secrete a number of key proinflammatory mediators in response to bacterial pathogens, IL-1beta and IL-18 are not among this number. We suggest that osteoblasts are an unlikely source of these cytokines during the progression of bacterial infection of bone.

Full Text

Duke Authors

Cited Authors

  • Marriott, I; Hughes, FM; Bost, KL

Published Date

  • October 2002

Published In

Volume / Issue

  • 22 / 10

Start / End Page

  • 1049 - 1055

PubMed ID

  • 12433285

International Standard Serial Number (ISSN)

  • 1079-9907

Digital Object Identifier (DOI)

  • 10.1089/107999002760624288


  • eng

Conference Location

  • United States