Abstract
—Accumulating evidence supports that spinal cord injury (SCI) produces robust inflammatory plasticity. We previously showed that the pro-inflammatory cytokine tumor necrosis factor (TNF)α is increased in the spinal cord after SCI. SCI also induces a systemic inflammatory response that can impact peripheral organ functions. The kidney plays an important role in maintaining cardiovascular health. However, SCI-induced inflammatory response in the kidney and the subsequent effect on renal function have not been well characterized. This study investigated the impact of high and low thoracic (T) SCI on C-fos, TNFα, interleukin (IL)-1β, and IL-6 expression in the kidney at acute and sub-chronic timepoints. Adult C57BL/6 mice received a moderate contusion SCI or sham procedures at T4 or T10. Uninjured mice served as naïve controls. mRNA levels of the proinflammatory cytokines IL-1β, IL-6, TNFα, and C-fos, and TNFα and C-fos protein expression were assessed in the kidney and spinal cord 1 day and 14 days post-injury. The mRNA levels of all targets were robustly increased in the kidney and spinal cord, 1 day after both injuries. Whereas IL-6 and TNFα remained elevated in the spinal cord at 14 days after SCI, C-fos, IL-6, and TNFα levels were sustained in the kidney only after T10 SCI. TNFα protein was significantly upregulated in the kidney 1 day after both T4 and T10 SCI. Overall, these results clearly demonstrate that SCI induces robust systemic inflammation that extends to the kidney. Hence, the presence of renal inflammation can substantially impact renal pathophysiology and function after SCI.
Highlights
Spinal cord injury (SCI) causes many devastating health challenges during the acute and chronic stages post-injury
Because the kidney is a main regulator of blood pressure, compromised renal function after SCI can indirectly contribute to blood pressure dysregulation, and impaired cardiovascular health, a leading cause of morbidity and mortality for spinal cord injured patients [4,5,6]
This study investigated the effect of SCI on the expression profile of inflammatory markers in the kidney
Summary
Spinal cord injury (SCI) causes many devastating health challenges during the acute and chronic stages post-injury. Because the kidney is a main regulator of blood pressure, compromised renal function after SCI can indirectly contribute to blood pressure dysregulation, and impaired cardiovascular health, a leading cause of morbidity and mortality for spinal cord injured patients [4,5,6]. A hallmark feature of SCI is the initiation of an inflammatory response typically at or near the lesion epicenter [7]. These events can be expressed as increases in glial cell migration and proliferation response, release of inflammatory cytokines, and subsequent apoptotic cascades. We have previously shown an increase in the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) and several of its downstream signaling molecules in the lesioned spinal cord after SCI [8, 9]
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