Molecular and cellular determinants associated with clinical parameters of eosinophilic gastritis

Eosinophilic gastritis (EoG) is characterized by gastric eosinophil accumulation. Additionally, mastocytosis has been observed in EoG. We hypothesized that molecular markers of eosinophils and mast cells correlate with clinical parameters in patients with active EoG. Baseline data were obtained from active EoG patients (≥30 eosinophils per high-power field [HPF] in at least 5 fields) in a study conducted at the Cincinnati Center for Eosinophilic Disorders (NCT03473977). Pain, non-pain, and satisfaction scores were determined from the severity of dyspepsia assessment (SODA) instrument. Normalized expression of the eosinophil-specific gene Charcot-Leyden crystal galectin (CLC) and the mast cell-specific gene carboxypeptidase 3 (CPA3) were measured in gastric biopsies by quantitative real-time PCR. Correlations between these surrogate genetic markers and EoG disease parameters were calculated. Gastric CLC and CPA3 gene expression significantly correlated (r = 0.53, p = 0.02). Whereas the correlation was non-significant, we observed a positive trend between CLC gene expression and pain (r = 0.38, p = 0.13), CPA3 gene expression and pain (r = 0.19, p = 0.45), as well as CLC gene expression and non-pain (r = 0.15, p = 0.56). We also observed a non-significant, negative trend between CPA3 gene expression and satisfaction scores (r = -0.15, p = 0.55). There was a positive correlation between gastric CLC and CPA3 gene expression. Although non-significant, there were positive trends between gastric CLC and CPA3 gene expression and pain. The results suggest that eosinophils and mast cells may be involved in the pain response in EoG.