Exp Neurobiol 2019; 28(1): 74-84
Published online February 28, 2019
© The Korean Society for Brain and Neural Sciences
Jeongtae Kim1, Meejung Ahn1, Yuna Choi1, Poornima Ekanayake1, Chul Min Park2, Changjong Moon3, Kyungsook Jung4, Akane Tanaka5, Hiroshi Matsuda6, and Taekyun Shin1*
1Department of Veterinary Anatomy, College of Veterinary Medicine and Veterinary Medical Research Institute, Jeju National University, Jeju 63243, Korea.
2Department of Obstetrics and Gynecology, School of Medicine, Jeju National University, Jeju 63243, Korea.
3Department of Veterinary Anatomy, College of Veterinary Medicine and BK21 Plus Project Team, Chonnam National University, Gwangju 61186, Korea.
4Immunoregulatory Materials Research Center, Korea Research Institute of Bioscience and Biotechnology, Jeongeup 56212, Korea.
5Laboratory of Comparative Animal Medicine, Division of Animal Life Science, Institute of Agriculture, Tokyo University of Agriculture and Technology, Tokyo 183-8509, Japan.
6Laboratory of Veterinary Molecular Pathology and Therapeutics, Division of Animal Life Science, Graduate School, Institute of Agriculture, Tokyo University of Agriculture and Technology, Tokyo 183-8509, Japan.
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-64-754-3363, FAX: 82-64-756-3354
Olfactory dysfunction occurs in multiple sclerosis in humans, as well as in an animal model of experimental autoimmune encephalomyelitis (EAE). The aim of this study was to analyze differentially expressed genes (DEGs) in olfactory bulb of EAE-affected mice by next generation sequencing, with a particular focus on changes in olfaction-related signals. EAE was induced in C57BL/6 mice following immunization with myelin oligodendrocyte glycoprotein and adjuvant. Inflammatory lesions were identified in the olfactory bulbs as well as in the spinal cord of immunized mice. Analysis of DEGs in the olfactory bulb of EAE-affected mice revealed that 44 genes were upregulated (and which were primarily related to inflammatory mediators), while 519 genes were downregulated; among the latter, olfactory marker protein and stomatin-like 3, which have been linked to olfactory signal transduction, were significantly downregulated (log2 [fold change] >1 and p-value <0.05). These findings suggest that inflammation in the olfactory bulb of EAE-affected mice is associated with the downregulation of some olfactory signal transduction genes, particularly olfactory marker protein and stomatin-like 3, which may lead to olfactory dysfunction in an animal model of human multiple sclerosis.