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Molecular Medicine

, Volume 19, Issue 1, pp 36–42 | Cite as

IL-1β Inhibits Human Osteoblast Migration

  • Nina-Emily Hengartner
  • Jörg Fiedler
  • Anita Ignatius
  • Rolf E. Brenner
Research Article

Abstract

Bone has a high capacity for self-renewal and repair. Prolonged local secretion of interleukin 1β (IL-1β), however, is known to be associated with severe bone loss and delayed fracture healing. Since induction of bone resorption by IL-1β may not sufficiently explain these pathologic processes, we investigated, in vitro, if and how IL-1β affects migration of multipotent mesenchymal stromal cells (MSC) or osteoblasts. We found that homogenous exposure to IL-1 β significantly diminished both nondirectional migration and site-directed migration toward the chemotactic factors platelet-derived growth factor (PDGF)-BB and insulinlike growth factor 1 (IGF-1) in osteoblasts. Exposure to a concentration gradient of IL-1β induced an even stronger inhibition of migration and completely abolished the migratory response of osteoblasts toward PDGF-BB, IGF-1, vascular endothelial growth factor A (VEGF-A) and the complement factor C5a. IL-1β induced extracellular signal-regulated kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinases (JNK) activation and inhibition of these signaling pathways suggested an involvement in the IL-1β effects on osteoblast migration. In contrast, basal migration of MSC and their migratory activity toward PDGF-BB was found to be unaffected by IL-1β. These results indicate that the presence of IL-1β leads to impaired recruitment of osteoblasts which might influence early stages of fracture healing and could have pathological relevance for bone remodeling in inflammatory bone disease.

Notes

Acknowledgments

The excellent technical assistance of Giovanni Ravalli is gratefully acknowledged. The study was funded in part by the German Research Council (Deutsche Forschungsgemeinschaft; KFO 200).

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Authors and Affiliations

  • Nina-Emily Hengartner
    • 1
  • Jörg Fiedler
    • 1
  • Anita Ignatius
    • 2
  • Rolf E. Brenner
    • 1
  1. 1.Department of Orthopedics, Division for Biochemistry of Joint and Connective Tissue DiseasesUniversity of UlmUlmGermany
  2. 2.Institute of Orthopedic Research and Biomechanics, Center of Musculoskeletal Research UlmUniversity of UlmUlmGermany

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