Micro RNA-155 plays a critical role in the initiation of food allergen-related inflammation in the intestine
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Ri-Tian Lin1, Jiang-Qi Liu2, Hui-Ying Lu1, Ya-Mei Chen1, Li Guan3, Zhi-Gang Liu2, Zhan-Ju Liu1 and Ping-Chang Yang2
1Department of Gastroenterology, The Shanghai Tenth People’s Hospital of Tongji University, Shanghai 200072, China
2The Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen 518060, China
3Department of Physical Examination, Affiliated Luohu Hospital, Shenzhen University, Shenzhen 518001, China
Zhan-Ju Liu, email: [email protected]
Ping-Chang Yang, email: [email protected]
Keywords: food allergy, regulatory B cells, intestine, micro RNA, interleukin 13
Received: April 05, 2017 Accepted: May 23, 2017 Published: June 28, 2017
The pathogenesis of food allergy (FA) is to be further investigated. Regulatory B cells (B10 cell) play a critical in the maintenance of the homeostasis in the intestine. Deregulation of B10 cell is associated with immune inflammation. Micro RNA (miR) 155 is involved in affecting immune cell function. This study tests a hypothesis that miR-155 affects the B10 cell function to facilitate the initiation of FA. In this study, BALB/c mice were sensitized to ovalbumin (OVA) to induce FA-like inflammation in the intestine. B cells were isolated from the intestine by magnetic cell sorting. The expression of miR-155 and IL-10 in B cells was assessed by real time RT-PCR. The results showed that mice sensitized to OVA showed FA-like inflammation and lower frequency of B10 cell in the intestine. B cells isolated from the intestine of FA mice showed higher levels of miR-155 and lower levels of IL-10. Although all the three T helper (Th)2 cytokines, including interleukin (IL)-4, IL-5 and IL-13, were higher in the serum, only IL-13 was positively correlated with the levels of miR-155 in the intestinal B cells. Exposure to IL-13 in the culture markedly increased the expression of miR-155 and suppressed the expression of IL-10 in B cells. Blocking miR-155 abolished the IL-13-induced IL-10 suppression in B cells and inhibited FA response in mice. In conclusion, miR-155 plays a critical role in the initiation of FA in mice. Blocking miR-155 has therapeutic potential in the treatment of FA.
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