Eosinophilic esophagitis causes

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Causes

• The causes of EoE are as follows:
• The food and pollen react with the lining of the esophagus, these allergens cause the multiplication of eosinophils in the layers of the esophagus and produce a protein that causes inflammation.
• The inflammation further cause scarring, excessive fibrous tissue deposition over the lining of the esophagus eventually leading to dysphagia.
• The dysphagia can sometimes worsen to cause food impaction and additional symptoms such as chest pain.

EoE contributes to or causes GERD

• Various hypotheses have been proposed that EoE contributes to the development of GERD.
• Mucosal barrier- Eosinophils secrete inflammatory mediators such as VIP (Vasoactive intestinal peptide), PAF (platelet-activating factor), IL-6 which damages the integrity of the mucosal barrier and the smooth muscles of the esophagus.
• Peristalsis- VIP and PAF predisposes a patient to reflux by inducing relaxation of the LES, whereas the IL-6 affects the peristalsis and clearance of the acid, the alterations in oesophageal function contribute to increased acid exposure due to impaired clearance of refluxed contents
• Cytotoxic effect- Eosinophil cationic protein, Major basic protein, and Eosinophil peroxidase secreted by eosinophils have a direct cytotoxic effect on the mucosa, rendering the oesophageal epithelium more susceptible to caustic injury by refluxed gastric contents.
• Epithelial cells and Nerves- the above-mentioned events exposes the epithelial cells and nerves to further acid injury.
• Remodeling- fibrosis and increased thickness of the esophageal wall, eventually leads to an increase in esophageal mural stiffness causing esophageal remodeling.

GERD contributes to or causes EoE

Counter to the hypothesis of the previous section, it is possible that GERD could cause EoE. The pathognomic histological feature of the GERD is dilatation of inter-cellular spaces of the esophageal squamous epithelium. Increased mucosal permeability in GERD due to a breach of the mucosal integrity of the esophagus leading to the penetration of allergens that were swallowed into the subepithelial space, which can then be accessed by antigen-presenting cells. The initial step of allergic sensitization involves antigen presentation by dendritic cells to naive T cells which are transformed to antigen-specific type 2 T helper (TH2) cells. The thymic stromal lymphopoietin (TSLP) production from the oesophageal epithelium primes oesophageal mucosal basophils to secrete IL-4, which promotes the allergic sensitization process.

References

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