Elevated levels of colonic interleukin-1beta and interleukin-8 in isolated REM sleep behavior disorder without associated changes in permeability.
Colonic biopsies from iRBD (prodromal PD) and PD patients show increased mRNA for IL-1β and IL-8 (with TNF-α up in PD) despite no detectable changes in gut permeability, tight-junction proteins, or fecal calprotectin.
What the AI sees
Colonic biopsies from iRBD (prodromal PD) and PD patients show increased mRNA for IL-1β and IL-8 (with TNF-α up in PD) despite no detectable changes in gut permeability, tight-junction proteins, or fecal calprotectin.
Research significance
Findings implicate low-level enteric inflammation early in PD and nominate IL-1β/IL-8 pathways as potential early biomarkers or anti-inflammatory therapeutic targets, without evidence that barrier dysfunction is required for this gut immune signature.
Source abstract
Gastrointestinal inflammation could contribute to the early development of Parkinson's disease (PD). This study investigated gut inflammation, intestinal barrier function, and integrity in patients with isolated REM sleep behavior disorder (iRBD), a prodromal stage of PD. Sigmoid colon biopsies from patients with iRBD (n = 20), PD (n = 34), and controls (n = 20) were analyzed by qPCR to measure the expression levels of proinflammatory cytokines and enteric glial markers, along with fecal calprotectin. Gut permeability was evaluated in biopsies mounted in Ussing chambers, and the integrity of the intestinal epithelial barrier was assessed by analyzing the expression of tight junction protein by Western blot. We found that the mRNA expression levels of interleukin-1β and interleukin-8 were increased in both patients with iRBD and PD relative to controls; the expression of TNF-α was also higher in PD but not in iRBD patients. We did not observe any differences in colonic permeability, tight junction proteins expression, and calprotectin levels groups. Our study is the first to characterize the inflammatory profile in the gut in iRBD. Our findings provide evidence that enteric inflammation is present at a moderate level in prodromal PD, not higher than in individuals with established PD, and without concurrent changes in intestinal permeability.