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A novel pathway by which the environmental toxin 4-Nonylphenol may promote an inflammatory response in inflammatory bowel disease Kim A; Jung BH; Cadet PMed Sci Monit Basic Res 2014[Apr]; 20 (ä): 47-54Background 4-Nonylphenol is a ubiquitous environmental toxin that is formed as a byproduct in the manufacturing and/or sewage treatment of regular household items. Previous work in our lab has implicated 4-NP in the progression of autoimmune diseases such as inflammatory bowel disease in which macrophages mistakenly attack the intestinal linings, causing chronic inflammation. Several key pro-and anti-inflammatory molecules have been shown to be involved in the manifestation of this disease, including IL-23A, COX-2, IL-8, TLR-4, and IL-10. Material and Methods 4-NP's effects on these known mediators of IBD were effectively analyzed using a novel model for IBD, by which 4-NP may promote an inflammatory response. Data were collected using DNA Microarray, RT-PCR, and ELISA, after 48 hour treatment of U937 histiocytic lymphocyte cells and COLO320DM human intestinal epithelial cells with 1 nM and 5 nM concentrations of 4-NP. Results Significant dysregulation of the expression of both pro- and anti-inflammatory genes was observed in U937 cells that would promote and prolong inflammation. However, TLR-4, IL-8, and COX-2 gene expressions showed unprecedented effects in COLO320DM cells suggesting that these genes mediate apoptotic processes within the gastrointestinal tract. Conclusions Overall, our results suggest that 4-NP administration engenders immune responses linked to apoptotic processes via dysregulation of macrophage signaling. In sum, 4-NP appears to increases the risk of developing inflammatory bowel disease by promoting or prolonging adverse progression of inflammation in the gastrointestinal tract.|Cell Line[MESH]|Cytokines/metabolism[MESH]|Environmental Pollutants/*toxicity[MESH]|Gene Expression Regulation/drug effects[MESH]|Humans[MESH]|Inflammation/genetics/*pathology[MESH]|Inflammatory Bowel Diseases/genetics/*pathology[MESH]|Oligonucleotide Array Sequence Analysis[MESH]|Phenols/*toxicity[MESH]|RNA, Messenger/genetics/metabolism[MESH]|Reference Standards[MESH]|Reverse Transcriptase Polymerase Chain Reaction[MESH]|Signal Transduction/*drug effects/genetics[MESH] |
