2022
DOI: 10.1016/j.scitotenv.2022.158017
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Gene/environment interaction in the susceptibility of Crohn's disease patients to aluminum

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Cited by 7 publications
(3 citation statements)
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“…NHE3 is highly expressed in the apical membrane of the proximal tubules of the small intestine and colon, colon, and kidney, and is mainly responsible for neutral electrical uptake of Na + . NHE3 usually interacts with Cl − /HCO 3− , NaCl exchanger downregulated in adenomas (Dra; SLC26A3) [ 23 ] or possibly anion transporter 1 (PAT1; SLC26A6) [ 24 ] were conjugated to function. Previous studies have shown that NHE3 −/− mice have defects in intestinal and renal ion absorption, resulting in acid-base imbalance and deranged sodium levels [ 25 ].…”
Section: Discussionmentioning
confidence: 99%
“…NHE3 is highly expressed in the apical membrane of the proximal tubules of the small intestine and colon, colon, and kidney, and is mainly responsible for neutral electrical uptake of Na + . NHE3 usually interacts with Cl − /HCO 3− , NaCl exchanger downregulated in adenomas (Dra; SLC26A3) [ 23 ] or possibly anion transporter 1 (PAT1; SLC26A6) [ 24 ] were conjugated to function. Previous studies have shown that NHE3 −/− mice have defects in intestinal and renal ion absorption, resulting in acid-base imbalance and deranged sodium levels [ 25 ].…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, when bacterial antigens induce abnormal activation of adaptive immune cells, the irrepressible immune response forces further aggravation of CD damage [ 19 ]. Admittedly, although genetic and environmental differences in CD patients remain elusive, strong evidence for a dysregulated immune response may be attributed to a T cell-mediated inflammatory cascade [ 20 , 21 , 22 ].…”
Section: Discussionmentioning
confidence: 99%
“…In addition, TL1A helps balance promotion and inhibition of the inflammatory response in the intestinal mucosa in CD. At the initial stage of inflammation, when T cells are recruited to the inflammatory site of intestinal mucosa, TL1A interacts with DR3 to enhance inflammatory cytokine secretion, and these cytokines cause the recruitment and activation of macrophages and neutrophils, stimulating further inflammation[ 51 ].…”
Section: Susceptibility Genesmentioning
confidence: 99%