## 4 Discussion
This finding supports the concept that intestinal epithelial barrier dysfunction is a common pathophysiological mechanism in functional gastrointestinal disorders, including patients with gastrointestinal symptoms not directly linked to specific foods but responsive to antigenic stimulation. Not only were mucosal alterations observed; for example, the group led by [PERSON] reported an increase in eosinophil activity in the duodenum and the secretion of eosinophil cationic protein (ECP) in duodenal fluids following exposure to specific foods [39]. These findings suggest that eosinophils may play a role in mucosal reactions triggered by food antigens, unfortunately, the lack of data on ECP levels pre- and post-reaction limits conclusions about whether this activity was triggered acutely. An increase in eosinophil activity has been observed in functional dyspepsia [53; 54] and even in eosinophil esophagitis [55; 56]. This reaction also occurs in the absence of IgE or positive skin tests for allergens, suggesting a different mode of immunologic response, likely in the context of mild intestinal mucosal inflammation. The authors observed an increase in intraepithelial lymphocytes (IEL) on confocal laser endomicroscopy (CLE) in patients experiencing acute reactions, both initially and after the reaction. However, this finding was not corroborated by CD3 immunohistochemistry. Moreover, the reported lack of correlation between IEL identified through CLE and immunohistochemistry raises doubts about the reliability of using CLE to quantify lymphocytes [38]. In the larger follow-up study, patients with reactions showed increased IEL at baseline, but no changes were observedfollowing acute reactions [39]. Recent research revealed normal lymphocyte levels and no variations in mast cell counts in biopsies taken after acute alterations [40; 41]. However, no baseline comparison analyses were conducted. Low-grade inflammation is well-known to contribute to the disruption of gastrointestinal reflexes and the activation of the visceral sensory system, leading to symptoms associated with IBS, such as visceral hypersensitivity [57]. Some studies have shown that ion channels and their receptors are critical for gastrointestinal sensitivity [58; 59; 60]. Specifically, TRPV channels have been linked to heightened intestinal sensitivity in IBS patients [61; 62; 63; 64]. These channels, part of the broader TRP family (Transient Receptor Potential), play essential physiological roles, including pain perception, thermoregulation, chemosensitivity, and epithelial barrier maintenance [65]. [PERSON] and colleagues observed mucosal structural changes via CLE following lipid infusion rather than direct antigenic stimulation. This study represents an important step in correlating intestinal mucosal stimulation by food mixtures with increased TRPV channel expression, heightened intestinal symptoms, and CLE-detected permeability changes. These findings provide insights into the relationship between mucosal alterations and sensory perception in IBS patients [42]. Although this technique shows promise, its application in clinical practice remains unproven, and prescribing a diet based on these findings requires further thorough evaluation. A literature search in the PubMed database shows no connection between Food Protein Induced Enterocolitis Syndrome (FPIES), and the use of advanced endoscopic techniques. FPIES is the most well-known type of non-IgE-mediated food allergy [66], is a delayed inflammatory reaction to specific food proteins that primarily affects the gastrointestinal tract. It is characterized by inflammatory lymphocyte and neutrophil infiltrates, edema and vascular congestion, villous atrophy, crypt structural changes, and, in a more advanced stage, tissue necrosis.