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

Abstract

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.

Emerging and legacy PFAS and cytokine homeostasis in women of childbearing age

“…For example, 10 mg/kg PFOS exposure was positively associated with the expression levels of IL-1β and TNF-α in rats after 14-day exposure 36 . PFAS can also induce a markable upregulation of proinflammatory cytokines TNF-α expression in the jejunum of the PFOS 1 mg/kg and 10 mg/kg groups compared with the control in rats 37 . Collectively, these results indicated that PFOS exposure induces an upregulated pro-inflammatory infiltration.…”

“…Many in vivo and in vitro experiments have demonstrated that dysregulation of cytokine caused by environmental pollutants induces the inflammatory response 11 , 36 , 37 . For example, 10 mg/kg PFOS exposure was positively associated with the expression levels of IL-1β and TNF-α in rats after 14-day exposure 36 .…”

Emerging And Legacy PFAS And Cytokine Homeostasis In Women of Childbearing Age

“…For example, 10 mg/kg PFOS exposure was positively associated with the expression levels of IL-1β and TNF-α in rats after 14-day exposure 33 . PFAS can also induce a markable upregulation of proin ammatory cytokines TNF-α expression in the jejunum of the PFOS 1 mg/kg and 10 mg/kg groups compared with the control in rats 34 . Collectively, these results indicated that PFOS exposure induces an upregulated proin ammatory in ltration.…”

Hippocampal Proteomics Reveals the Role of Glutamatergic Synapse Activation in the Depression Induced by Perfluorooctane Sulfonate

“…It is noteworthy that when regulating macrophage activation, we also found response to interferon-gamma in the BP of GO enrichment analysis. In fact, macrophage accumulation and inflammatory cytokine infiltration were remarkably increased in rats exposed to PFOS . Furthermore, PFOS exposure may induce distinct tumor necrosis factor-alpha through the upregulation of phosphorylated nuclear factor kappa B p65 expression .…”

“…In fact, macrophage accumulation and inflammatory cytokine infiltration were remarkably increased in rats exposed to PFOS. 51 Furthermore, PFOS exposure may induce distinct tumor necrosis factor-alpha through the upregulation of phosphorylated nuclear factor kappa B p65 expression. 52 These findings suggest that M1 polarization of microglia should be studied further.…”