Role of Common Irritants in Development of FA’s

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Can Chemical Agents and Pollens Induce Food Allergies?

Aude Lecrubier
June 13, 2024
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Can the increasingly present "irritants" in our environment, such as detergents or microplastics, alter the intestinal barrier and induce food allergies?

During a session at the French-speaking Allergy Congress, Virginie Doyen, MD, a pneumologist at University Hospital Namur in Namur, Belgium, reviewed the current knowledge on this subject, explaining that few studies have been conducted on the potential link between "irritants" and food allergies.

The mechanisms involved are progressive, and the multiple predisposing factors (eg, genetic, epigenetic, internal, and external environmental factors) make the study of this question particularly complex, said Doyen.

Poor Dietary Habits
Regarding changes in dietary habits, data indicate that the consumption of additives and preservatives, foods rich in sugars and fats, and foods low in short-chain fatty acids is associated with an increased risk for food allergies. In contrast, the Mediterranean diet during breastfeeding and pregnancy and a diet rich in fruits and vegetables during childhood are associated with a decreased risk for food allergies.

But by what mechanisms can poor dietary habits alter the protective systems at the intestinal level and allow food allergens, which are the origin of sensitization, to pass through? One hypothesis is that the lack of dietary fiber consumption could stimulate the degradation of intestinal mucus via the microbiome.

"Neglected by scientific work, mucus nonetheless plays an important role in the intestine by limiting exposure to antigens and maintaining immune tolerance. It is rich in glycoproteins, carbohydrates, antimicrobial peptides, and IgA [immunoglobulin A]," said Doyen. "It is also a niche for our commensal flora, which has immunomodulatory effects and can degrade this mucus if modified by our diet."

In addition, data from cellular models and experimental animal models show that ingesting large amounts of advanced glycation end products (eg, ultraprocessed food) seems to alter the intestinal barrier.

Researchers have shown that exposing epithelial cell cultures or peripheral blood mononuclear cells (PBMC) from children at risk for food allergy to advanced glycation end products leads to an alteration of tight junctions between epithelial cells, which ensure the cohesion of the intestinal barrier.

Contact with ultraprocessed foods reduces occludin, a component of these tight junctions, and the ZOT1 protein, which regulates these junctions. Allergens and other irritants, therefore, have the possibility of passing through the barrier.

Furthermore, following exposure to advanced glycation end products, researchers observed an increase in the production of T helper cells 2 (Th2)-type proinflammatory cytokines by PBMC and the alarm signals interleukin (IL)-25 and IL-33, which direct the Th2-type immune response.

Dysbiosis and a less diverse microbiome are observed in cases of food allergy. It seems that the initial alteration of the microbiome leads to a fragility of the intestinal barrier. However, a defective barrier due to a genetic mutation in filaggrin is also associated with an increased risk for peanut allergy. The relationship is bidirectional.

Detergents, Emulsifiers, Microplastics
Besides the effect of an unbalanced diet, chemical agents and pollens may have an indirect effect on the occurrence of food allergy symptoms in sensitized patients, said Doyen.

Studies have shown that emulsifiers (eg, lecithin, carboxymethylcellulose, sorbitol, monostearate, and polysorbate 80) that solubilize aqueous and oily phases affect the intestinal level. Contact with an emulsifier induces a thickening of the dense part of the intestinal mucus, which limits interactions between the epithelium and the intestinal flora.

The disruption of interactions between mucus and bacteria leads to a modification of the microbiota via a change in bacteria that express more proinflammatory molecules such as flagellins and lipopolysaccharides.

In mice, this activation of inflammatory processes has been associated with chronic inflammation in the digestive tract. In wild-type mice without predisposition, only metabolic disorders were observed. However, in predisposed mice, inflammatory colitis developed.

Regarding detergents (eg, residues from dishwasher detergents and rinse products on dishes), researchers have observed from explanted pseudo-organs that when tissues are not exposed to these detergents, the epithelial barrier is intact. However, if epithelial structures are exposed to detergents, the barrier shows alterations associated with an overexpression of genes involved in immune response and inflammatory processes.

Another experiment looked at the effect of the detergent sodium dodecyl sulfate, which is present in toothpaste, on the digestive epithelium. They found that it decreases the integrity of the epithelial barrier, promoting eosinophilia, CD4 lymphocyte–type inflammation, and remodeling of the intestinal epithelium. The altered barrier can promote the penetration of irritating substances, bacteria, or allergens.

As for microplastics (insoluble particles < 5 mm), data suggest that they penetrate tissues at the skin and respiratory levels. But what about the intestinal level?

Two studies in mice given food containing microplastics have shown that these microplastics penetrate the epithelium and induce dysbiosis. They reduce mucus production and alter the intestinal barrier function.

What About Pollen?
Pollution and climate change are responsible for increased protease activity in pollens. These pollens are responsible for an increasing number of respiratory allergies, but do they affect the intestinal barrier? An international study showed in a cellular culture model and in mice that actinidin (Act d 1), a kiwi allergen, causes a rupture of tight junctions and increased intestinal permeability.

In summary, food allergies are associated with an alteration of the digestive epithelial barrier, and experimental data suggest that certain irritants could contribute to this phenomenon, making us more susceptible to inflammatory reactions and inappropriate immune responses.

"It would be possible to consider joint actions in terms of prevention and therapy," said Doyen. "Therapeutic approaches could include antialarmin treatments, particularly anti-TSLP, which blocks the cascade of reactions at the starting point, at the epithelial level in severe asthma. We could also consider modifying the microbiota to act on mucus. Finally, there seems to be a dose factor. Limiting the quantity of all the toxic products we use, without completely abstaining from them, is probably a path to follow."

This story was translated from the Medscape French edition using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication.
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