Staphylococcus aureus regulates secretion of interleukin-6 and monocyte chemoattractant protein-1 through activation of nuclear factor kappaB signaling pathway in human osteoblasts

OBJECTIVE: Activation of nuclear factor kappaB by diverse bacteria regulates the secretion of chemokines and cytokines. Staphylococcus aureus (S. aureus)-infected osteoblasts can significantly increase the secretion of interleukin-6 and monocyte chemoattractant protein-1. The aim of this study was to investigate whether S. aureus can activate nuclear factor kappaB in human osteoblasts, and whether the activation of nuclear factor kappaB by S. aureus regulates the secretion of interleukin-6 and monocyte chemoattractant protein-1. METHODS: Immunoblot and electrophoretic mobility shift assay were used to detect the degradation of IκBa and activation of nuclear factor kappaB in human osteoblasts in response to S. aureus, respectively. Enzyme-linked immunosorbent assay was used to measure the secretion of interleukin-6 and monocyte chemoattractant protein-1 in the supernatants. Lastly, carbobenzoxyl-l-leucinyl-l-leucinyl-l-leucinal, an inhibitor of the nuclear factor kappaB, was used to determine if activation of nuclear factor kappaB by S. aureus in human osteoblasts regulates the secretions of interleukin-6 and monocyte chemoattractant protein-1. RESULTS: Our results for the first time demonstrated that S. aureus can induce the degradation of IκBa and activation of nuclear factor kappaB in human osteoblasts in a time and dose-dependent manner. In addition, inhibition of nuclear factor kappaB by carbobenzoxyl-l-leucinyl-l-leucinyl-l-leucinal suppressed the secretion of interleukin-6 and monocyte chemoattractant protein-1 in the supernatants of S. aureus-infected human osteoblasts in a dose-dependent manner. CONCLUSION: These findings suggest that S. aureus can activate nuclear factor kappaB in human osteoblasts, and subsequently regulate the secretion of interleukin-6 and monocyte chemoattractant protein-1. The nuclear factor kappaB transcription factor regulates a number of genes involved in a wide variety of biological processes. Further study of the effects of nuclear factor kappaB activation on S. aureus-infected human osteoblast may provide us new insights into discovery of the immune mechanisms in osteomyelitis

Staphylococcus aureus regulates secretion of interleukin-6 and monocyte chemoattractant protein-1 through activation of nuclear factor kappaB signaling pathway in human osteoblasts

OBJECTIVE: Activation of nuclear factor kappaB by diverse bacteria regulates the secretion of chemokines and cytokines. Staphylococcus aureus (S. aureus)-infected osteoblasts can significantly increase the secretion of interleukin-6 and monocyte chemoattractant protein-1. The aim of this study was to investigate whether S. aureus can activate nuclear factor kappaB in human osteoblasts, and whether the activation of nuclear factor kappaB by S. aureus regulates the secretion of interleukin-6 and monocyte chemoattractant protein-1. METHODS: Immunoblot and electrophoretic mobility shift assay were used to detect the degradation of IκBa and activation of nuclear factor kappaB in human osteoblasts in response to S. aureus, respectively. Enzyme-linked immunosorbent assay was used to measure the secretion of interleukin-6 and monocyte chemoattractant protein-1 in the supernatants. Lastly, carbobenzoxyl-l-leucinyl-l-leucinyl-l-leucinal, an inhibitor of the nuclear factor kappaB, was used to determine if activation of nuclear factor kappaB by S. aureus in human osteoblasts regulates the secretions of interleukin-6 and monocyte chemoattractant protein-1. RESULTS: Our results for the first time demonstrated that S. aureus can induce the degradation of IκBa and activation of nuclear factor kappaB in human osteoblasts in a time and dose-dependent manner. In addition, inhibition of nuclear factor kappaB by carbobenzoxyl-l-leucinyl-l-leucinyl-l-leucinal suppressed the secretion of interleukin-6 and monocyte chemoattractant protein-1 in the supernatants of S. aureus-infected human osteoblasts in a dose-dependent manner. CONCLUSION: These findings suggest that S. aureus can activate nuclear factor kappaB in human osteoblasts, and subsequently regulate the secretion of interleukin-6 and monocyte chemoattractant protein-1. The nuclear factor kappaB transcription factor regulates a number of genes involved in a wide variety of biological processes. Further study of the effects of nuclear factor kappaB activation on S. aureus-infected human osteoblast may provide us new insights into discovery of the immune mechanisms in osteomyelitis

Correlation of preoperative CT imaging shift parameters of the lateral plateau with lateral meniscal injury in Schatzker IV-C tibial plateau fractures

Abstract Background Schatzker IV-C is a high-energy tibial plateau fracture often accompanied by lateral meniscus injuries. While imaging examinations are routine preoperative measurements, the correlation between CT imaging shift parameters of the lateral plateau and lateral meniscal injury in Schatzker IV-C fractures remains uncovered. Methods This retrospective study enrolled a total of 60 patients with Schatzker IV-C tibial plateau fractures at the First People’s Hospital of Hefei. Prior to surgery, CT imaging was used to measure the numerical values of lateral plateau depression (LPD) and lateral plateau widening (LPW). The degree of lateral meniscus injury was confirmed based on intraoperative direct vision, with patients being classified into meniscus injury and non-meniscus injury groups. Dichotomous logistic regression was employed to evaluate the correlation between LPD, LPW, and lateral meniscus injury, while the optimal cut-off points for predicting lateral meniscal injury with LPD and LPW were determined using receiver operator characteristic (ROC) curves. Results The meniscus injury group exhibited a mean LPD of 15.3 ± 3.5 mm, which was significantly higher than the non-meniscus injury group’s mean LPD of 8.4 ± 3.4 mm (P < 0.05). Similarly, the meniscus injury group had a larger mean LPW of 9.4 ± 1.8 mm compared to the non-meniscus injury group’s mean LPW of 6.9 ± 0.9 mm (P < 0.05). The optimal cut-off points for predicting lateral meniscal injury were determined to be 8.40 mm for LPD (with a sensitivity of 95%, specificity of 85%, and AUC of 0.898) and 7.90 mm for LPW (with a sensitivity of 75%, specificity of 90%, and AUC of 0.897). Conclusions Patients with Schatzker IV-C tibial plateau fractures are at a significantly higher risk of lateral meniscal injury when the LPD exceeds 8.40 mm and/or the LPW exceeds 7.90 mm. Our results may provide novel reference metrics for the early diagnosis of lateral meniscal injury in Schatzker IV-C tibial plateau fracture patients when the MRI examination is not available