I've been doing some research on this since my endoscopy yesterday. Looks like I was right, mast cell problems could definitely be involved in eosinophilic esophagitis.
You can read the complete paper here:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902643/?tool=pubmedInvolvement of mast cells in eosinophilic esophagitis
IntroductionEosinophilic esophagitis (EE) is an emerging worldwide disease, as documented by case series from all continents except Africa, which appears to be a growing health problem with an annual incidence of at least 1:10,000 children. The primary symptoms of EE (chest and abdominal pain, dysphagia, heartburn, vomiting, and food impaction) are also observed in patients with chronic esophagitis (CE) including those patients with gastroesophageal reflux disease (GERD). However, in contrast to GERD, EE occurs more frequently in males (80%), appears to have a common familial form, has a high rate of associated atopic disease (70%), and is typically associated with a normal pH probe recording of the esophagus;. EE patients respond inadequately to anti-GERD therapy alone, but may respond to anti-inflammatory therapy and/or allergen elimination as determined by allergen testing, or empiric dietary elimination.
Abstract
BackgroundEosinophilic esophagitis (EE) is an emerging disorder with poorly understood pathogenesis.
ObjectiveWhereas prior studies have primarily focused on the role of eosinophils in disease diagnosis and pathogenesis, this study investigates the involvement of mast cells.
MethodsTotal and degranulated mast cell counts were correlated to microarray and RT-PCR data to generate transcriptome expression profiles related to mast cell number and degranulation in EE patients and normal controls.
ResultsEsophageal mastocytosis and mast cell degranulation was readily apparent in EE patients compared with controls (p < 0.01) as assessed by staining for total mast cells and the presence of extracellular mast cell tryptase (p < 0.01). Microarray analysis revealed that mast cell levels correlated with the dysregulation of 0.8% (301 genes) of the genome which were partially distinct from the genes that correlated with tissue eosinophilia. The expression of transcripts for the mast cell proteases carboxypeptidase A3 (CPA3) and tryptase, but not chymase, correlated with mast cell levels and distinguished EE patients from controls. Suprabasilar mast cell counts (p < 0.01) and degranulation (p < 0.01) were proportional with KIT ligand mRNA expression. Treatment of EE patients with swallowed fluticasone propionate (FP) normalized levels of mast cells and the mast cell related transcriptome in responder patients.
ConclusionHerein we have identified local mastocytosis and mast cell degranulation in the esophagus of EE patients; identified an esophageal mast cell associated transcriptome that is significantly divergent from the eosinophil-associated transcriptome with CPA3 mRNA levels serving as the best mast cell surrogate marker; and provide evidence for the involvement of KIT ligand in the pathogenesis of EE.
Keywords: Mast Cells/Basophils, Eosinophils, Human