Perfluorooctane sulfonate exerts inflammatory bowel disease-like intestinal injury in rats

BACKGROUND: Perfluorooctane sulfonate (PFOS), a type of perfluorinated compounds (PFCs), can induce various organ toxicity, including hepatomegaly, immunotoxicity, and gut microbiota disorder. PFCs have been associated with inflammatory bowel disease (IBD). Yet, whether PFOS exposure causes IBD-like disorder and the underlying mechanism remains undefined. Here, we investigated the influence of PFOS exposure on the development of IBD-like disorder in rats. METHODS: Sprague-Dawley rats were intraperitoneally injected with PFOS (1 or 10 mg/kg) or normal saline (NS) every other day for 15 days. Body weight, serum concentrations of serum amyloid A (SAA) and high sensitivity C reactive protein (hsCRP) were measured. Pathological assessments of villi height and crypt depth in the proximal duodenum and jejunum were performed using H&E staining. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was used to assay cell apoptosis in the jejunum. The infiltration of inflammatory cells and cytokines in the jejunum were detected by immunohistochemistry analysis. RESULTS: PFOS (10 mg/kg) significantly increased the body weight, SAA and hsCRP, whereas no significant differences were observed in PFOS 1 mg/kg group of rats. The villi height and crypt depth in the proximal duodenum and jejunum were significantly reduced upon PFOS exposure. PFOS induced higher histopathological score in intestinal tissues compared to NS. Notably, TUNEL-positive cells were significantly higher in the jejunum upon PFOS exposure. Further, neutrophil and macrophage accumulated, and inflammatory cytokines infiltration were also remarkably increased in rats exposed to PFOS. CONCLUSION: PFOS induces IBD-like phenotypes in rats, with associated inflammatory infiltration to intestinal.