A groundbreaking study published in Gastroenterology reveals that psychological stress can prompt immune reactions to food, leading to symptoms upon subsequent ingestion of the same food. This discovery sheds light on the potential role of stress in irritable bowel syndrome (IBS). Cecilia Berin, PhD, a co-author of the study, highlights the significance of this research, which goes beyond traditional food allergies to explore how food can act as a trigger for pain associated with IBS. The findings suggest that localized immune responses could contribute to gastrointestinal discomfort without inducing systemic allergic reactions.

In prior studies, it was established that bacterial infections in mice could lead to immune responses and allergic reactions to food antigens, resulting in food-induced abdominal pain—a hallmark symptom of IBS. However, these cases only account for a fraction of IBS diagnoses. To delve deeper, researchers investigated whether psychological stress might similarly induce immune reactions contributing to food-triggered pain.

The team exposed mice to ovalbumin, a protein found in egg whites, during a stressful test known as water avoidance stress. Following a five-week interval, the mice were re-exposed to ovalbumin. Through visceromotor response measurements and nerve recordings of intestinal distension, scientists evaluated the mice's nociception—the nervous system’s reaction to harmful stimuli. They also measured IgE-antibody responses and type 2 immunity using pharmacological and genetic methods.

Results showed that mice exposed to ovalbumin under stress experienced heightened pain signaling in their colon and small intestine upon re-exposure. These responses depended on mast cells, local IgE antibodies, and STAT6 signaling. When treated with pyrilamine, a drug used for allergic symptoms, sensory neuron activity decreased, reducing nerve firing and mitigating intestinal distension.

Berin noted the unexpected finding that allergic reactions could alter normal gastrointestinal function, causing pain without triggering systemic reactions like anaphylaxis. She emphasized the intriguing possibility that localized immune responses could still be functional despite their restricted nature.

Moving forward, Berin aims to examine gastrointestinal immune cells from IBS patients to determine if similar localized food-specific immune responses occur in humans. Targeting pathways involved in food allergies effectively reduced pain signaling in mice, suggesting promising therapeutic avenues for IBS treatment. By leveraging existing tools targeting these factors, new approaches to managing IBS may emerge.

This research opens doors to understanding the complex interplay between stress, immune responses, and gastrointestinal health. It underscores the importance of exploring localized immune mechanisms in addressing conditions like IBS, offering hope for more effective treatments in the future.