Review
Copyright ©The Author(s) 2016.
World J Gastrointest Pharmacol Ther. Feb 6, 2016; 7(1): 66-77
Published online Feb 6, 2016. doi: 10.4292/wjgpt.v7.i1.66
Table 1 Possible mechanisms involved in eosinophilic esophagitis pathogenesis
MechanismEvidenceRef.
AtopyReactivity to allergens by skin-prick testing[46,47,49,50,52,54]
Presence of specific serum IgE
Experimental evidence in animals undergone nasal inoculation with allergens
Strong association with other allergic diseases
High association with food-induced allergen-specific IgE
Abundant IgG4-containing plasma cells
FoodDisease activity is responsive to elemental diets[55]
AeroallergensSeverity of disease affected by seasonal variations which correlate with pollen counts[56]
Chemo attractantsIncreased IL-13 supports eosinophil migration by stimulating the chemo attractants production[43,63,64,66,67,68,69]
Increased levels of eotaxin-3
Gene-encoding eotaxin-3 the most highly induced gene in EoE patients
Single-nucleotide polymorphism in the eotaxin-3 gene associated with disease susceptibility
Mice deficient in the eotaxin receptor (CCR3) protected from experimental EoE
Mast cellsIncreased number of mast cells in the esophageal epithelium[70,71]
Mast cells linked to IgE
TGF-βObstructive symptoms seem to occur secondary to epithelial cell proliferation and extracellular matrix remodeling, processes linked to eosinophil-derived TGF-β[61]
TGF-β is known to increase smooth muscle cell hyperplasia
Leukotriene C4Leukotriene C4 is metabolized to LTD4 and LTE4 both of which stimulate smooth muscle contraction[74]