Table 1.

Possible mechanisms involved in eosinophilic esophagitis pathogenesis

Mechanism	Evidence	Ref.
Atopy	Reactivity 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
Food	Disease activity is responsive to elemental diets	[55]
Aeroallergens	Severity of disease affected by seasonal variations which correlate with pollen counts	[56]
Chemo attractants	Increased 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 cells	Increased number of mast cells in the esophageal epithelium	[70,71]
	Mast cells linked to IgE
TGF-β	Obstructive 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 C4	Leukotriene C4 is metabolized to LTD4 and LTE4 both of which stimulate smooth muscle contraction	[74]

EoE: Eosinophilic esophagitis; IL-3: Interleukin-3; TGF-β: Transforming growth factor-β.