| Summary: | 碩士 === 國立陽明大學 === 腦科學研究所 === 103 === Acute stress will increase gut permeability. Increased gut permeability would facilitate an increased serum level of circulating endotoxin and promote systemic inflammation through Toll like receptor-4 (TLR4). TLR4 is a major mediator involved in the crosstalk between the innate immune system and the endocrine stress response. Probiotics provide beneficial effects for clinical symptoms in IBS patients. We aimed to investigate the impact of acute stress on intestinal barrier function and hypothalamus-pituitary-adrenal (HPA) response. Secondly, we hypothesized that stress-induced HPA response can be reversed by probiotic treatment through the modulations of circulating lipopolysaccharides (LPS) and TLR receptor on adrenal gland. Water avoidance stress (WAS) for 1.5 hours was used as the acute stress model. Intestinal permeability was measured 2, 4, 6 and 24 hours after the WAS. The TLR4 expression on adrenal cortex after acute stress was examined by Western blot. Single-dose administration of Lacidofil or Lactobacillus casei was given through oral gavage immediately after the acute stress. In our study, acute stress led to increased intestinal permeability evidenced at 6 hours after the stress (P<0.05). A single-dose treatment of Lacidofil, but not Lactobacillus casei, reversed the stress-induced elevated intestinal permeability. Lacidofil treatment would potentially inhibit the elevated stress-induced plasma corticosterone level (P=0.05). The TLR4 protein expression on adrenal cortex and LPS concentration showed no significant difference among the studied groups. In conclusion, single dose of probiotics would improve acute stress-induced dysfunction in intestinal permeability and associated enhanced responses in HPA axis. The beneficial effect of probiotics in stress-induced alteration is strain-specific. The mechanisms behind the Lacidofil treatment to reverse the stress-induced elevated plasma level seemed not go through the modulation between the interactions of adrenal TLR4 receptor and circulating LPS.
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