Cortical Inflammation is Increased in a DSS-Induced Colitis Mouse Model

Abstract

While inflammatory bowel disease (IBD) might be a risk factor in the development of brain dysfunctions, the underlying mechanisms are largely unknown. Here, mice were treated with 5% dextran sodium sulfate (DSS) in drinking water and sacrificed on day 7. The serum level of IL-6 increased, accompanied by elevation of the IL-6 and TNF-α levels in cortical tissue. However, the endotoxin concentration in plasma and brain of mice with DSS-induced colitis showed a rising trend, but with no significant difference. We also found significant activation of microglial cells and reduction in occludin and claudin-5 expression in the brain tissue after DSS-induced colitis. These results suggested that DSS-induced colitis increases systemic inflammation which then results in cortical inflammation via up-regulation of serum cytokines. Here, we provide new information on the impact of colitis on the outcomes of cortical inflammation.

Effect of N‐palmitoylethanolamine‐oxazoline on comorbid neuropsychiatric disturbance associated with inflammatory bowel disease

“…The expression of cleaved caspase3 in the cortex was also upregulated, suggesting the occurrence of apoptosis in the brain after DSS treatment. 8 In that regard, in our study we demonstrated, for the first time, that oral treatment with PEAOXA at the dose of 10 mg/kg can restore intestinal permeability and TJ expression not only in the colon but also in the brain, particularly in the subventricular zone. In that regard, apoptosis induced by DSS was also attenuated by oral treatment of PEA-OXA in colon as well as brain tissues.…”

“…In addition, it has been reported that peripheral inflammation can induce neuroinflammation in the CNS via disruption of the BBB . The unique characteristics of this barrier include tight intercellular junctions.…”

“…58 In addition, it has been reported that peripheral inflammation can induce neuroinflammation in the CNS via disruption of the BBB. 8 The unique characteristics of this barrier include tight intercellular junctions. A recent study showed that the expression of occludin and claudin-5 was markedly downregulated in the cortex and hippocampus of the group treated with DSS.…”

“…Recent studies using an animal model of IBD induced by dextran sulfate sodium (DSS) administration have demonstrated not only activation of the inflammatory pathway, oxidative stress, and the alteration in serotonin (5‐hydroxytryptamine [5‐HT])‐producing enterochromaffin cells (EC), as are well known, but also anxiety‐like and depressive‐like behavior, cognitive impairment and decreased social interactions . One of the most supported ideas linked IBD with central nervous system (CNS) neuroinflammation . As is well known, neuroinflammation is driven by the activation of astrocytes and microglia, which leads to a series of events, such as the increase in pro‐inflammatory cytokine release .…”

“…[2][3][4][5][6] One of the most supported ideas linked IBD with central nervous system (CNS) neuroinflammation. 7,8 As is well known, neuroinflammation is driven by the activation of astrocytes and microglia, which leads to a series of events, such as the increase in pro-inflammatory cytokine release. 9 Additionally, neuroinflammation alters blood-brain barrier (BBB) functions 10 and, as a consequence, tight junction expression.…”