Typhimurium Infection Reduces the Ascorbic Acid Uptake in the Intestine.

Typhimurium infection of the gastrointestinal tract leads to damage that compromises the integrity of the intestinal epithelium and results in enterocolitis and inflammation. infection promotes the expression of inflammasome NLRP3, leading to activation and release of proinflammatory cytokines such as IL-1, and the infected host often displays altered nutrient levels. To date, the effect of infection and proinflammatory cytokine IL-1 on the intestinal uptake of ascorbic acid (AA) is unknown. Our results revealed a marked decrease in the rate of AA uptake in mouse jejunum infected with wild type (WT). However, the nonpathogenic mutant () strain did not affect AA uptake. The decrease in AA uptake due to WT infection is accompanied by significantly lower expression of mouse (m)SVCT1 protein, mRNA, and hnRNA levels. NLRP3 and IL-1 expression levels were markedly increased in -infected mouse jejunum. IL-1-exposed Caco-2 cells displayed marked inhibition in AA uptake and significantly decreased hSVCT1 expression at both protein and mRNA levels. Furthermore, the activity of the promoter was significantly inhibited by IL-1 exposure. In addition, GRHPR (a known SVCT1 interactor) protein and mRNA expression levels were significantly reduced in -infected mouse jejunum. These results indicate that infection inhibits AA absorption in mouse jejunum and IL-1-exposed Caco-2 cells. The observed inhibitory effect may partially be mediated through transcriptional mechanisms.