INTRODUCTION: Chronic stress is a well-known modulator of inflammatory responses in the gastrointestinal tract, leading to increased intestinal permeability and dysregulation of the gut-brain axis. However, the mechanisms underlying the disruption of intestinal barrier integrity remain poorly understood.

AIM(S): The aim of this study was to assess the effect of 14-day overcrowding stress on the mRNA levels of pro-inflammatory (IL-1β, TNF, IL-6, MIF, PTGS2, NOS2, IFN-γ, CD163) and anti-inflammatory factors (IL-10, Tgfbr2, ARG2, IL-4) in the rat colon.

METHOD(S): Male Wistar HAN rats were divided into a control (CON) and a crowding stress (CS) group. To assess long-term effects, subsets of CS rats underwent recovery periods of 7, 14, or 21 days. On the final experimental day, distal colon segments were collected for RNA isolation, reverse transcription, and TaqMan probe-based qPCR.

RESULTS: Exposure to CS resulted in increased mRNA levels of TNF, Tgfbr2, NOS2, MIF, CD163, and ARG2. Except for TNF, the elevated levels of these molecules persisted for at least 7 days after cessation of CS exposure; in the case of NOS2 and ARG2, the increase was augmented.

CONCLUSIONS: Our results demonstrate the long-lasting impact of psychosocial stress on intestinal homeostasis. These findings provide new evidence for the link between psychological stress and immunological disturbances in the gut, supporting the brain-gut axis as a key mediator of these interactions.

FINANCIAL SUPPORT: This work was supported by statutory funding from the Department of Brain Biochemistry, Institute of Pharmacology, Polish Academy of Sciences.