| First Author | Wang Y | Year | 2020 |
| Journal | J Orthop Res | Volume | 38 |
| Issue | 8 | Pages | 1800-1809 |
| PubMed ID | 31975434 | Mgi Jnum | J:321679 |
| Mgi Id | MGI:6879087 | Doi | 10.1002/jor.24608 |
| Citation | Wang Y, et al. (2020) Interleukin-1beta and tumor necrosis factor are essential in controlling an experimental orthopedic implant-associated infection. J Orthop Res 38(8):1800-1809 |
| abstractText | 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-1alpha (IL-1alpha), IL-1beta, 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-1alpha, IL-1beta, or TNF. Mice deficient in IL-1beta or TNF (to a lesser extent) but not IL-1alpha had increased bacterial burden at the site of the OIAI throughout the 28-day experiment. IL-1beta 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-1alpha- and IL-1beta-deficient mice had impaired neutrophil recruitment whereas IL-1beta-, TNF-, and IL-1R/TNF-deficient mice all had impaired recruitment of both neutrophils and monocytes. Therefore, IL-1beta and TNF contributed to host defense against S. aureus OIAI and neutrophil recruitment was primarily mediated by IL-1beta and monocyte recruitment was mediated by both IL-1beta and TNF. |
