Background: Many food components influence intestinal epithelial barrier properties and might therefore also affect susceptibility to the development of food allergies. Such allergies are triggered by increased antibody production initiated in Peyer’s patches (PP). Usually, the presentation of antigens in the lumen of the gut to the immune cells of the PP is strongly regulated by the follicle-associated epithelium (FAE) that covers the PP. As the food component caprate has been shown to impede barrier properties in villous epithelium, we hypothesized that caprate also affects the barrier function of the PP FAE, thereby possibly contributing a risk factor for the development of food allergies. Methods: In this study, we have focused on the effects of caprate on the barrier function of PP, employing in vitro and ex vivo experimental setups to investigate functional and molecular barrier properties. Incubation with caprate induced an increase of transepithelial resistance, and a marked increase of permeability for the paracellular marker fluorescein in porcine PP to 180% of control values. These effects are in accordance with changes in the expression levels of the barrier-forming tight junction proteins tricellulin and claudin-5. Conclusions: This barrier-affecting mechanism could be involved in the initial steps of a food allergy, since it might trigger unregulated contact of the gut lumen with antigens.

Dysbiosis and impaired gastrointestinal barrier function have emerged as potential chronic kidney disease (CKD) modulators. Accumulation of gut-derived uremic toxins, a subsequent shift in the gut microbiome, and modified expression levels of intestinal tight junction proteins are all contributing factors to hyperpermeability and endotoxemia in CKD. Experimental studies in animals provide evidence that renal decline is linked to gastrointestinal health and that pharmacological or dietary intervention might attenuate this process. In this review, we will highlight the current knowledge on CKD-induced changes in the gut microbiome and the resulting consequences regarding gastrointestinal health with a focus on animal studies. Furthermore, we will explore possible disease management options linking to evidence in humans, if available.

Loss of bone mass has a devastating effect on quality of life. Higher potassium (K ⁺ ) intake is positively correlated with bone health. Here, we investigated whether kidney calcium (Ca ²⁺ ) and phosphate (Pi) handling mechanisms mediate dietary K ⁺ effects. Kidney Ca ²⁺ and Pi handling proteins were altered in abundance in mice fed a 0% K ⁺ diet for 2 weeks. In mice fed a 0.1% K ⁺ diet for 4 or 8 weeks, urinary Ca ²⁺ excretion increased, plasma Ca ²⁺ levels were lower and plasma parathyroid hormone (PTH) levels were higher relative to control 1% K ⁺ fed mice. The 0.1% K ⁺ fed mice had greater excretion of the bone resorption marker deoxypyridinoline, increased osteoclast number, and decreased total femoral bone mineral density. During chronic low K ⁺ intake, major changes in renal Ca ²⁺ and Pi transport pathways were absent, except higher abundances of the sodium-potassium-chloride cotransporter (NKCC2) and the sodium-chloride cotransporter (NCC), in line with their role in kidney Ca ²⁺ handling. Low dietary K ⁺ induced hypocalcemia and changes in PTH were absent in mice with constitutively active NCC, supporting its role in mediating low K ⁺ effects on Ca ²⁺ homeostasis. Our study provides insights into the management of bone disorders in conditions of chronic electrolyte imbalance.