Oncotarget

Research Papers:

Galectin-1 inhibits oral-intestinal allergy syndrome

Rui-Di Xie, Ling-Zhi Xu, Li-Tao Yang, Shuai Wang, Qi Liu, Zhi-Gang Liu and Ping-Chang Yang _

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Oncotarget. 2017; 8:13214-13222. https://doi.org/10.18632/oncotarget.14571

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Abstract

Rui-Di Xie1,2,*, Ling-Zhi Xu1,*, Li-Tao Yang3,4,*, Shuai Wang3, Qi Liu2, Zhi-Gang Liu1, Ping-Chang Yang1

1The Research Center of Allergy & Immunology, Shenzhen University School of Medicine, Shenzhen, China

2Periodontal Department, the Affiliated Hospital of Zunyi Medical College, Zunyi, China

3The ENT Hospital of Shenzhen University and Shenzhen ENT Institute, Shenzhen, China

4Brain Body Institute, McMaster University, Hamilton, ON, Canada

*These authors contributed equally to this work

Correspondence to:

Ping-Chang Yang, email: [email protected]

Zhi-Gang Liu, email: [email protected]

Qi Liu, email: [email protected]

Keywords: oral mucosa, oral allergy, peanut, micro RNA-98, galectin-1

Received: August 25, 2016     Accepted: December 27, 2016     Published: January 10, 2017

ABSTRACT

Background and aims: The pathogenesis of oral-intestinal allergy syndrome (OIAS) has not been well understood. Published data indicate that galectin (Gal) 1 has immune regulatory functions. This study tests a hypothesis that Gal1 inhibits oral-intestinal allergy syndrome.

Methods: Mice were sensitized to peanut extracts (PE) via the buccal mucosa with or without using Gal1 together.

Results: Upon re-exposure to specific antigen, the OIAS mice showed the systemic allergic response, the oral allergic reactions, and intestinal allergic inflammation, including increases in serum histamine, drop of the core temperature, higher levels of PE-specific IgE and interleukin (IL)-4. Increases in mast cell and eosinophil in the oral mucosa and intestinal mucosa were also observed. The OIAS was inhibited by co-administration with Gal1 via a mechanism of suppressing micro RNA (miR)-98 and reversing the expression of IL-10 in CD14+ cells in the intestine.

Conclusions: The OIAS can be induced by applying specific antigens to the oral mucosa, which can be inhibited by co-administration with Gal1.


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