induces intervertebral discs degeneration by increasing MMP-1 and inhibiting TIMP-1 expression via the NF-κB pathway.

Emerging evidence suggests that () may be a new pathogen implicated in intervertebral disc degeneration (IVDD), although the underlying mechanisms are unclear. Since the most significant biochemical change of IVDD is inability of the extracellular matrix (ECM) synthesis by nucleus pulposus cells, we first analyzed the expression of aggrecan and collagen II in nucleus pulposus tissues of IVDD patients with or without infection. Compared with the -negative controls, the expression levels of aggrecan and collagen II were significantly dampened in nucleus pulposus tissues with infection. Interestingly, we found that infection strongly increased matrix-degrading metalloproteinase-1 (MMP-1) expression but decreased that of tissue inhibitor of metalloproteinase-1 (TIMP1). Furthermore, the dampened aggrecan and collagen II synthesis concomitant with the increased MMP-1 and decreased TIMP-1 expression seen in -induced IVDD were confirmed by a rat model. Mechanistically, infection increased MMP-1 levels, while decreasing TIMP-1 expression via the NF-κB pathway. Overall, these findings reveal that infection dampens aggrecan and collagen II synthesis in nucleus pulposus cells by increasing MMP-1 and inhibiting TIMP-1 expression via the NF-κB pathway, which may ultimately lead to IVDD.