Aluminum internalization was correlated with inflammatory status in Caco-2 cells.
New research indicates aluminum exposure induces cytokine secretion in the colons of patients with Crohn’s disease, but does not do so in a healthy control group.
A team, led by Madjid Djouina, Univ. Lille, Inserm, CHU Lille, U1286- INFINITE - Institute for translational research in inflammation, examined the role aluminum transport and subcellular localization on human colon susceptibility to aluminum-induced inflammation.
Environmental factors are known to play a role in the pathogenesis of IBD. However, while aluminum exposure is suspected to be an IBD risk factor, the mechanisms linking aluminum exposure to disease development are not known.
“We hypothesize that alteration in detoxifying response would lead to a deregulation of intestinal homeostasis and to the expression of IBD,” the authors wrote.
In the study, the investigators isolated human colon biopsies from patients with Crohn’s disease and control patients. They also induced Caco-2 cells with aluminum and evaluated the effects of aluminum on cytokine secretion and transporter expression.
The investigators also studied the role of aluminum kinetics parameters in Caco-2 using transport inhibitors and in human colon biopsies by assessing genetic polymorphisms of transporters.
The results show aluminum exposure induces cytokine secretion in the colons of patients with Crohn’s disease. However, this was not found in the healthy control group.
They also found aluminum internalization was correlated with inflammatory status in Caco-2 cells.
In the human colon, the analysis of genetic polymorphisms and the expression of decreased activity of ABCB1 and SLC26A3 transporters was involved in aluminum induced inflammation.
“Our study emphasizes the complexity of gene/environment interaction for aluminum adverse health effect, highlighting at risk populations or subtypes of patients,” the authors wrote. “A better understanding of correlations between gene expression or SNP and xenobiotic kinetics parameters would shift the medical paradigm to more personalized disease management and treatment.”
Diet is another risk factor for developing IBD.
Recently, a team, led by Farnaz Farsi, PhD, Minimally Invasive Surgery Research Center, Iran University of Medical Sciences, evaluated whether any relationship between nutrients and IBD exists.
In the case-control study, the investigators examined 145 participants newly diagnosed with IBD between 2017-2019. They also matched these patients with 145 health control participants by body mass index (BMI), sex, and age.
Each participant completed a 168-item food frequency questionnaire and the investigators conducted anthropometric measurements and physical activity levels. The participants also gave information on age, past drug history, socioeconomic and education status, alcohol consumption, smoking history, and IBD subtypes through a general information questionnaire.
Overall, higher amounts of seafood consumed and cholesterol were related to an increased risk of IBD, specifically ulcerative colitis.
On the other hand, individuals with a higher intake of calcium were less likely to have Crohn’s disease compared to the healthy group.
The investigators also found a positive relation between honey and jam, seafood, organ meats, salt, fruits on trees, fruit juice, olives, and nuts and the probability of IBD. However, there was a negative association between refined grains, potatoes, salty snacks, legumes, dairy, and cruciferous and the probability of IBD.
The study, “Gene/environment interaction in the susceptibility of Crohn's disease patients to aluminum,” was published online in the Science of The Total Environment.