# The Impact of the Oral and Esophageal Microbiota in EoE and Achalasia

## TL;DR

This paper reviews how changes in the oral and esophageal microbiota may contribute to Eosinophilic Esophagitis and Achalasia, suggesting potential for new biomarkers and therapies.

## Contribution

The paper provides a comparative overview of microbial and immune alterations in EoE and Achalasia, highlighting distinct microbial signatures and their therapeutic implications.

## Key findings

- EoE is associated with increased bacterial diversity and a shift toward Prevotella, linked to inflammation and barrier dysfunction.
- Achalasia features reduced microbial diversity and a shift to Gram-negative bacteria that activate pro-inflammatory pathways.
- Both conditions show dysbiosis but differ in immune profiles (Th2 vs. Th17), suggesting microbiota-based diagnostic and therapeutic opportunities.

## Abstract

Background/Objectives: Eosinophilic esophagitis (EoE) and achalasia are two chronic esophageal disorders, characterized by inflammatory and neuromotor dysfunction, respectively, that share overlapping immune-inflammatory features. Emerging evidence suggests that dysbiosis of the oral and esophageal microbiota may represent a common determinant in their pathophysiology. This review aims to provide a comparative and integrated overview of microbial and immune alterations in EoE and Achalasia, with potential diagnostic and therapeutic implications. Methods: A bibliographic search was conducted on PubMed and Scopus including clinical studies, experimental research, and review articles published between 2015 and 2025. The keywords Eosinophilic Esophagitis, Achalasia, Microbiota, and Dysbiosis were used for article selection. Results: In EoE, several studies demonstrated increased bacterial diversity with predominance of Prevotella and reduction of Streptococcus, findings associated with greater inflammatory severity and epithelial barrier dysfunction. Conversely, Achalasia is characterized by reduced microbial diversity and a shift from Gram-positive commensals to Gram-negative taxa capable of activating pro-inflammatory pathways (TLR4-MYD88-NF-κB), leading to neuronal loss and impaired peristalsis. Conclusions: Both EoE and Achalasia share the hallmark of dysbiosis, although with distinct immune profiles (Th2 vs. Th17). The identification of specific microbial “signatures” suggests promising perspectives for non-invasive biomarkers and microbiota-targeted therapies, including probiotics and glycan-modulating strategies. Further prospective studies are needed to clarify causal mechanisms and validate microbiota manipulation as a complementary therapeutic approach in esophageal diseases.