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Figure 1 | Allergy, Asthma & Clinical Immunology

Figure 1

From: Eotaxin and FGF enhance signaling through an Extracellular signal-related kinase (ERK)-dependent pathway in the pathogenesis of Eosinophilic Esophagitis

Figure 1

a-f The fold expression of immune indicators bFGF, FGF-R, Eotaxin-3, CCR3, IL-5, IL-13, ERK, JNK, Bcl-2, Capase 8, and Fas. a) EoE subjects statistically significant increases in levels of bFG and FGFR2 (p < 0.001) There was an 8-fold increase in the bFGF levels in EoE subjects as compared to HC subjects and a 4-fold increase compared to GERD; b)There was a 6-fold increase in eotaxin-3 comparing EoE subjects to HC and a 2-fold increased when compared to GERD subjects. However, this was not statistically significant. CCR3 levels were consistent among all subject groups; c) There was a statistically significant increase in the amount of IL-5 in subjects with EoE as compared to GERD (p < 0.01). Increase in IL-13 in EoE was statistically significant compared to all other subject groups (p < 0.001); d) ERK was high increased compared to other subjects groups (p < 0.001) while JNK levels remained consistent; e) EoE subjects had a 3-fold increase of Bcl-2 and a 3-fold decrease in caspase 8 expression compared to treated EoE subjects (p < 0.05); f) Fas expression was down-regulated by 3-fold in EoE subjects as compared to treated EoE subjects (p < 0.05). EoE: Eosinophilic Esophagitis; GERD: gastroesophageal reflux disease; HC: healthy control; UC: ulcerative colitis; CD: Crohn's disease.

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