Eosinophilic Gastroenteritis

An Update

Alfredo J Lucendo; Angel Arias


Expert Rev Gastroenterol Hepatol. 2012;6(5):591-601. 

In This Article

Fibrous Remodeling in EGID and EGE

Eosinophilic inflammation of the airways leads to structural changes known as remodeling. The most clinically relevant components of this phenomenon are smooth muscle hypertrophy and collagen subepithelial deposition because they can lead to narrowing of the bronchial diameter and impairment of respiratory function. Fibrous remodeling has also been demonstrated in pediatric[41] and adult EoE patients;[42,43] it is a reversible phenomenon in the former,[44] but tends to persist in the latter.[42,43] In addition to digestive motor disturbances,[45] fibrous remodeling also explains strictures commonly associated with EoE and obstructive symptoms found in many reported cases of EGE affecting the pylorus and small bowel.[46] These often require resection of the affected area.[47]

Fibrosis in EGID is directly related to eosinophil activation, as evaluated through immunohistochemistry against major basic protein.[48] Eosinophil-released major basic protein increases gene expression of FGF-9, a cytokine implicated in the proliferative response after tissue damage.[49] Eosinophils also produce and secrete high amounts of CCL18, a type-2 chemokine implied in fibrous remodeling of the lungs through fibroblast proliferation and collagen deposition, whose expression levels have been shown to be increased in EoE.[42] However, the most widely studied cytokine in promoting fibrous remodeling in EGID is TGF-β1,the expression of which has been found to be upregulated in both children[41] and adults[42,50] with EoE, but which can be reduced with the aid of steroid treatment.[42,44,50,51]