Household detergent exposure may be linked to eosinophilic esophagitis

Sodium dodecyl sulfate, a common household detergent, decreased the integrity of the esophageal barrier, stimulated IL-33 production and promoted epithelial hyperplasia and tissue eosinophilia, according to a study published in Allergy.

As a result, the detergent may contribute to eosinophilic esophagitis, Alfred D. Doyle, PhD, assistant professor in the division of allergy, asthma and clinical immunology at Mayo Clinic in Arizona, Scottsdale, and colleagues wrote in the study.

Although the etiology of EoE remains unknown, the researchers wrote, there has been a 20-fold increase in its incidence over recent decades. EoE primarily happens in industrialized nations, the researchers continued, presenting in the third and fourth decades of life and suggesting a role for environmental factors such as detergents in its development.

In the study, researchers exposed normal human esophageal epithelial cells and 3D organoids to serial dilutions of sodium dodecyl sulfate (SDS) — a detergent occurring as an ingredient in common products such as dish soap and toothpaste — ranging from 10 ng/mL to 10,000 ng/mL. By comparison, SDS may be used in toothpaste at concentrations up to 3%, or 30 mg/mL.

Transepithelial electrical resistance temporarily increased by 24 hours with the 5,000 ng/mL dilution and then declined through 96 hours (P = .03), which the researchers said suggested increased epithelial permeability with SDS.

Also, fluorescein isothiocyanate-dextran 4kDa passage through air liquid interface cultures increased in a manner that depended on SDS concentration, with significant increases in permeability at 5,000 ng/mL (P = .0002).

Expression of desmoglein-1, an epithelial junction molecule that is downregulated in patients who have active EoE, appeared significantly suppressed when cells were exposed to 5,000 ng/mL or 10,000 ng/mL of SDS for 72 hours (P < .0001).

After 6 hours, the researchers also found increases in IL-33 expression in cells treated with 5,000 ng/mL and 10,000 ng/mL of SDS (P < .05).

The researchers also exposed mice to SDS via 0.5% concentrations in their drinking water for 14 days, with mice kept on untreated drinking water used as controls.

Those exposed to SDS had enlarged and thickened esophagi and patchy eosinophilic esophageal inflammation throughout their esophagi, with esophageal inflammation commonly observed in 50% to 100% of the mice, in addition to eosinophilic abscesses and spongiosis, basal zone hyperplasia and infiltration of inflammatory cells including eosinophils in the submucosa.

Further, the researchers noted increased IL-33 expression in the mucosal layer, CD4⁺ lymphocyte infiltration in the submucosa, and elevated chemotactic factors for eosinophils and T cells in homogenates from whole esophagi of mice exposed to SDS.

RNA analysis showed upregulation of genes involved in activating acute inflammatory and remodeling pathways and downregulation of molecules associated with tissue development and muscle contraction, overall indicating that exposure to SDS triggers inflammatory immune responses and dysregulates esophageal tissue homeostasis.

Very low concentrations of SDS triggered biological effects, the researchers concluded, by altering esophageal integrity, inducing barrier permeability, and eliciting type 2 inflammatory signals and eosinophilic inflammation, potentially contributing to the pathogenesis of EoE.

However, the researchers cautioned, whether SDS promotes an allergic sensitization to food or environmental allergens alone or in combination with other environmental factors remains unknown, although sensitization is possible.

Further research should replicate human exposure conditions, the researchers continued. Studies also should investigate the role of genetic susceptibility in influencing responses and how SDS influences the esophageal and the entire gastrointestinal microbiomes, they added.