Research Papers: Immunology:
IL-33-induced alternatively activated macrophage attenuates the development of TNBS-induced colitis
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Lei Tu1,*, Jie Chen2,*, Dandan Xu2, Zhongming Xie2, Bing Yu3, Ying Tao3, Guixiu Shi3 and Lihua Duan3
1 Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China
2 College of Medicine, Xiamen University, Fujian, China
3 Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China
* These authors have contributed equally to this work
Lihua Duan, email:
Guixiu Shi, email:
Keywords: IL-33, inflammatory bowel disease, macrophage, M2, Arginase-1, Immunology and Microbiology Section, Immune response, Immunity
Received: January 17, 2017 Accepted: February 28, 2017 Published: March 07, 2017
Accumulated data have shown that alternatively activated macrophage exerts a modulatory role in many diseases, including colitis. Interleukin-33 (IL-33), a critical modulator in adaptive and innate immune, has been implicated in autoimmunity and inflammation. Previously, we have reported that IL-33 functions as a protective modulator in TNBS-induced colitis, which is closely related to a Th1-to-Th2/Treg switch. Here, we present novel evidence suggesting that IL-33 primes macrophage into alternatively activated macrophages (AAM) in TNBS-induced colitis. The strong polarized effect of IL-33 was tightly associated with the markedly increased induction of Th2-type cytokines. To confirm the beneficial effects of AAM induced by IL-33, peritoneal AAMs isolated from IL-33-treated mice were transferred to recipient mice with TNBS colitis. The adoptive transfer resulted in prominent inhibition of disease activity and inflammatory cytokines in the TNBS-treated mice. In conclusion, our data provide clear evidence that IL-33 plays a protective role in TNBS-induced colitis, which is closely related to AAM polarization.
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