Salmonella Typhimurium Infection Reduces the Ascorbic Acid Uptake in the Intestine

Salmonella Typhimurium infection of the gastrointestinal tract leads to damage that compromises the integrity of the intestinal epithelium and results in enterocolitis and inflammation. Salmonella infection promotes the expression of inflammasome NLRP3, leading to activation and release of proinflam...

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Main Authors: Trevor Teafatiller, Sandeep B. Subramanya, Nils Lambrecht, Veedamali S. Subramanian
Format: Article
Language:English
Published: Hindawi Limited 2023-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2023/2629262
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author Trevor Teafatiller
Sandeep B. Subramanya
Nils Lambrecht
Veedamali S. Subramanian
author_facet Trevor Teafatiller
Sandeep B. Subramanya
Nils Lambrecht
Veedamali S. Subramanian
author_sort Trevor Teafatiller
collection DOAJ
description Salmonella Typhimurium infection of the gastrointestinal tract leads to damage that compromises the integrity of the intestinal epithelium and results in enterocolitis and inflammation. Salmonella infection promotes the expression of inflammasome NLRP3, leading to activation and release of proinflammatory cytokines such as IL-1β, and the infected host often displays altered nutrient levels. To date, the effect of Salmonella infection and proinflammatory cytokine IL-1β 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 Salmonella wild type (WT). However, the nonpathogenic mutant (Δ invA Δ spiB) strain did not affect AA uptake. The decrease in AA uptake due to Salmonella WT infection is accompanied by significantly lower expression of mouse (m)SVCT1 protein, mRNA, and hnRNA levels. NLRP3 and IL-1β expression levels were markedly increased in Salmonella-infected mouse jejunum. IL-1β-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 SLC23A1 promoter was significantly inhibited by IL-1β exposure. In addition, GRHPR (a known SVCT1 interactor) protein and mRNA expression levels were significantly reduced in Salmonella-infected mouse jejunum. These results indicate that Salmonella infection inhibits AA absorption in mouse jejunum and IL-1β-exposed Caco-2 cells. The observed inhibitory effect may partially be mediated through transcriptional mechanisms.
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spelling doaj.art-e11c8150514541bd9ac5badb4508ec2b2024-11-02T23:56:15ZengHindawi LimitedMediators of Inflammation1466-18612023-01-01202310.1155/2023/2629262Salmonella Typhimurium Infection Reduces the Ascorbic Acid Uptake in the IntestineTrevor Teafatiller0Sandeep B. Subramanya1Nils Lambrecht2Veedamali S. Subramanian3Department of MedicineDepartment of PhysiologyDepartment of Veteran Affairs Medical CenterDepartment of MedicineSalmonella Typhimurium infection of the gastrointestinal tract leads to damage that compromises the integrity of the intestinal epithelium and results in enterocolitis and inflammation. Salmonella infection promotes the expression of inflammasome NLRP3, leading to activation and release of proinflammatory cytokines such as IL-1β, and the infected host often displays altered nutrient levels. To date, the effect of Salmonella infection and proinflammatory cytokine IL-1β 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 Salmonella wild type (WT). However, the nonpathogenic mutant (Δ invA Δ spiB) strain did not affect AA uptake. The decrease in AA uptake due to Salmonella WT infection is accompanied by significantly lower expression of mouse (m)SVCT1 protein, mRNA, and hnRNA levels. NLRP3 and IL-1β expression levels were markedly increased in Salmonella-infected mouse jejunum. IL-1β-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 SLC23A1 promoter was significantly inhibited by IL-1β exposure. In addition, GRHPR (a known SVCT1 interactor) protein and mRNA expression levels were significantly reduced in Salmonella-infected mouse jejunum. These results indicate that Salmonella infection inhibits AA absorption in mouse jejunum and IL-1β-exposed Caco-2 cells. The observed inhibitory effect may partially be mediated through transcriptional mechanisms.http://dx.doi.org/10.1155/2023/2629262
spellingShingle Trevor Teafatiller
Sandeep B. Subramanya
Nils Lambrecht
Veedamali S. Subramanian
Salmonella Typhimurium Infection Reduces the Ascorbic Acid Uptake in the Intestine
Mediators of Inflammation
title Salmonella Typhimurium Infection Reduces the Ascorbic Acid Uptake in the Intestine
title_full Salmonella Typhimurium Infection Reduces the Ascorbic Acid Uptake in the Intestine
title_fullStr Salmonella Typhimurium Infection Reduces the Ascorbic Acid Uptake in the Intestine
title_full_unstemmed Salmonella Typhimurium Infection Reduces the Ascorbic Acid Uptake in the Intestine
title_short Salmonella Typhimurium Infection Reduces the Ascorbic Acid Uptake in the Intestine
title_sort salmonella typhimurium infection reduces the ascorbic acid uptake in the intestine
url http://dx.doi.org/10.1155/2023/2629262
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