Oncotarget

Research Papers: Immunology:

Myelin oligodendrocyte glycoprotein (MOG35-55)-induced experimental autoimmune encephalomyelitis is ameliorated in interleukin-32 alpha transgenic mice

Jaesuk Yun, Sun Mi Gu, Hyung Mun Yun, Dong Ju Son, Mi Hee Park, Moon Soon Lee and Jin Tae Hong _

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Oncotarget. 2015; 6:40452-40463. https://doi.org/10.18632/oncotarget.6306

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Abstract

Jaesuk Yun1,*, Sun Mi Gu2,*, Hyung Mun Yun3, Dong Ju Son2, Mi Hee Park2, Moon Soon Lee4 and Jin Tae Hong2

1 Pharmacological Research Division, National Institute of Food and Drug Safety Evaluation (NIFDS), Ministry of Food and Drug Safety (MFDS), Osong-eup, Heungdeok-gu, Cheongju-si, Chungbuk, Republic of Korea

2 College of Pharmacy and Medical Research Center, Chungbuk National University, Osong-eup, Heungdeok-gu, Cheongju-si, Chungbuk, Republic of Korea

3 Department of Maxillofacial Tissue Regeneration, School of Dentistry and Research Center for Tooth and Periodontal Regeneration (MRC), Kyung Hee University, Dongdaemun-gu, Seoul, Republic of Korea

4 College of Agriculture, Life and Environmental Sciences, Chungbuk National University, Heungdeok-gu, Cheongju-si, Chungbuk, Republic of Korea

* These authors have contributed equally to this paper

Correspondence to:

Jin Tae Hong, email:

Moon Soon Lee, email:

Keywords: IL-32 alpha, experimental autoimmune encephalomyelitis, inflammation, multiple sclerosis, cytokines, Immunology and Microbiology Section, Immune response, Immunity

Received: August 14, 2015 Accepted: October 22, 2015 Published: November 11, 2015

Abstract

Multiple sclerosis (MS), also known as disseminated sclerosis or encephalomyelitis disseminate, is an inflammatory disease in which myelin in the spinal cord and brain are damaged. IL-32α is known as a critical molecule in the pathophysiology of immune-mediated chronic inflammatory disease such as rheumatoid arthritis, chronic pulmonary disease, and cancers. However, the role of IL-32α on spinal cord injuries and demyelination is poorly understood. Recently, we reported that the release of proinflammatory cytokines were reduced in IL-32α-overexpressing transgenic mice. In this study, we investigated whether IL-32α plays a role on MS using experimental autoimmune encephalomyelitis (EAE), an experimental mouse model of MS, in human IL-32α Tg mice. The Tg mice were immunized with MOG35-55 suspended in CFA emulsion followed by pertussis toxin, and then EAE paralysis of mice was scored. We observed that the paralytic severity and neuropathology of EAE in IL-32α Tg mice were significantly decreased compared with that of non-Tg mice. The immune cells infiltration, astrocytes/microglials activation, and pro-inflammatory cytokines (IL-1β and IL-6) levels in spinal cord were suppressed in IL-32α Tg mice. Furthermore, NG2 and O4 were decreased in IL-32α Tg mice, indicating that spinal cord damaging was suppressed. In addition, in vitro assay also revealed that IL-32α has a preventive role against Con A stimulation which is evidenced by decrease in T cell proliferation and inflammatory cytokine levels in IL-32α overexpressed Jurkat cell. Taken together, our findings suggested that IL-32α may play a protective role in EAE by suppressing neuroinflammation in spinal cord.


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