Stress-induced decrease of the intestinal barrier function. The role of muscarinic receptor activation

Area of Science:

• Gastroenterology
• Neuroscience
• Physiology

Background:

• The intestinal epithelium acts as a crucial barrier against harmful substances.
• Stress is known to impact physiological functions, including gut health.

Purpose of the Study:

• To investigate the effects of psychological and physical stress on intestinal barrier function in rats.
• To identify the cellular and neural pathways involved in stress-induced intestinal permeability.

Main Methods:

• Application of an experimental stress protocol (psychological and physical) to rats.
• Assessment of intestinal permeability to small and large molecules.
• Analysis of the zonula occludens and endocytotic activity.
• Investigation of cellular signaling pathways (protein kinase C, muscarinic, histamine receptors).
• Examination of the role of the autonomic nervous system (parasympathetic branch).

Main Results:

• Stress significantly increased intestinal permeability, allowing passage of macromolecules like antigens and toxins.
• Increased permeability was linked to reduced tight junction integrity (zonula occludens) and enhanced transcytosis.
• Activation of protein kinase C pathways via muscarinic or histamine receptors may underlie these changes.
• The parasympathetic nervous system appears to mediate stress signals to the gut.
• Different rat strains exhibited varied responses, suggesting a role for coping style.

Conclusions:

• Experimental stress compromises intestinal barrier integrity, increasing permeability to harmful substances.
• Neural and cellular mechanisms, including the autonomic nervous system and specific signaling pathways, are involved in this stress response.
• Individual coping mechanisms can modulate the gut's susceptibility to stress-induced barrier dysfunction.