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P030. Prolactin mediates psychological stress-induced dysfunction of regulatory T cells to facilitate intestinal inflammation

W. Wu1, C. Liu1, P.-C. Yang2, Z. Liu1, 1Shanghai Tenth People's Hospital, Tongji University, Department of Gastroenterology, Shanghai, China, 2Shenzhen University School of Medicine, Shenzhen Key Laboratory of Allergy & Immunology, Shenzhen, China

Background

The dysfunction of immune regulation plays a critical role in the pathogenesis of a number of chronic inflammation in the body. A close relation between psychological stress and intestinal inflammation has been noted, the underlying mechanism remains to be further elucidated. This study aims to elucidate a pathological pathway between psychological stress and the dysfunction of regulatory T cells (Treg), and its effect on facilitating intestinal inflammation.

Methods

A restraint stress model was employed to induce psychological stress in mice. The functions of Tregs were determined by assessing the immune suppressor effects in the intestine. A mouse model of intestinal inflammation was developed with a half dose of trinitrobenzene sulfonic acid (TNBS) together with treatment with chronic stress.

Results

After treating mice with restraint stress, the suppressor function of intestinal Treg was compromised although the frequency of Treg was not changed in the intestine. Further observation revealed that stress induced intestinal Tregs to differentiate into Foxp3+ IL-17+ TNF-α+ T cells. We also observed that exposure to stress-derived prolactin induced dendritic cells to produce IL-6 and IL-23 in the culture, which played a critical role in altering Treg's phenotypes. Treating mice with chronic stress facilitated the initiation of intestinal inflammation by a half dose of TNBS that was abolished by pretreatment with blockers of prolactin.

Conclusion

Psychological stress-derived prolactin alters Tregs' properties to contribute to the intestinal inflammation.