Inflammatory Effects of Severe Burn Injury in Rat Intervertebral Disc

IMPORTANCE: Severe burn injury leads to a myriad of clinical effects, some of which are mediated by systemic inflammatory cytokines. Although inflammation has been shown to increase skeletal muscle catabolism, little is known about the effects this inflammation has on the intervertebral disc tissue and whether or not it predisposes to spinal pathology. OBJECTIVE: To investigate the gene expression changes after severe burn injury in rat intervertebral disc tissue and explore the possible role of inflammatory cytokines in tissue remodeling imbalance. METHODS: Rats were given severe burn injury according to protocol, then harvested at multiple time points: 6h, 1d, 3d, 7d, and 14d post-burn. Unburned rats used for control. Rat intervertebral discs were dissected and removed, then used for measurement of gene expression using qPCR. RESULTS: Differences in gene expression of structural matrix proteins between time points were not statistically significant, however, TNF-alpha showed statistically significant (p<.05) decreased expression at 1d, after increased expression at 6h that approached significance (p=.055); this pattern of gene expression is consistent with previous results. In addition, there was a statistically significant (p<.05) increase in expression of the TRPV4 channel, which helps regulates osmolarity of the tissue in the nucleus pulposis. This could explain how osmotic dysregulation induced by pro-inflammatory cytokines leads to loss of water content from nucleus pulposis cells, thus triggering disc degeneration. CONCLUSIONS: These results indicate that in the post-burn state pro-inflammatory cytokines, such as TNF-alpha, likely have an effect on intervertebral disc tissue and the subsequent up-regulation of TRPV4 could have long-term effects that hasten the onset of disc degeneration related to loss of water content.