Atopy and the gastrointestinal tract – a review of a common association in unexplained gastrointestinal disease

Abstract

In addition to diseases conventionally associated with atopy there is increasing recognition that atopy is also linked to a spectrum of gastrointestinal (GI) manifestations, including food allergy, primary eosinophilic GI disease, functional gastrointestinal disorders, gluten interactions, gastroesophageal reflux disease and inflammatory bowel disease. These associations may be underpinned by shared genetic susceptibilities, initiation of related immune pathways and common patterns of exposure to environmental cues, including allergen/pathogen encounters and variations in the composition of the intestinal microbiota. Further scrutiny of GI diseases with prominent allergic-type immune responses may yet redefine treatment paradigms for these common and important atopy-associated diseases. Looking forward, interventions by manipulation of the microbiota or host immune responses hold promise, but there is still room for further exploration of this novel field of host susceptibility, host-microbe interactions and atopy-associated GI diseases.

Keywords::

• allergy
• atopy
• eosinophilic gastrointestinal disease
• food allergy
• gastrointestinal inflammation
• intestinal microbiota

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Atopic diseases are increasing in prevalence in parallel with numerous gastrointestinal (GI) diseases.

• Epidemiological evidence has highlighted links between atopy and various GI diseases, including functional GI disorders, eosinophilic GI diseases and inflammatory bowel disease.

• These associations may be underpinned by shared genetic susceptibilities, initiation of similar immune response networks and dysregulated host–microbe interactions.

• Patterns of immune pathway activation may be common to these diseases, including triggering of TH2 immunity and inappropriate mobilization of eosinophils and mast cells.

• The genetic architecture of these linked diseases overlap with some shared risk alleles and involvement of similar immune pathways, such as innate immune recognition molecules.

• The composition of the microbial communities colonizing the gut profoundly impacts host immunity and may be dysregulated in these diseases.

• Manipulation of the intestinal microbiota with probiotics, antibiotics, fecal microbiota transplantation and supplementation with bacteria, which selectively induce Treg cells hold therapeutic promise in this disease area.

• Selective targeting of key cytokines/mediators involved in these related pathologies will appear in the clinic in coming years.

Notes