Glycan changes in the olfactory mucosa of rats with experimental autoimmune encephalomyelitis.

Glycans are components of glycoconjugates and function in odorant recognition and cell signaling in the olfactory mucosa. However, little is known about glycan expression in the olfactory mucosa in the presence of neuroinflammatory disorders, which can influence olfaction. We evaluated the changes in glycan in the olfactory mucosa of rats with experimental autoimmune encephalomyelitis (EAE) by histochemical analyses of 21 lectins. In the olfactory mucosa of normal control rats, 16 lectins bound to olfactory sensory neurons, supporting cells, basal cells, nerve and Bowman's glands, and their expression did not significantly change during the course of EAE. In rats with paralytic-stage EAE, five lectins showed different reactivities with the olfactory mucosa compared to those of normal control rats. Of them, Bandeiraea simplicifolia lectin (BSL)-II and BSL-I showed transiently downregulated binding to olfactory sensory neurons and supporting cells in rats with EAE. The reactivities of Lens culinaris agglutinin for the basement membrane, Vicia villosa agglutinin for Bowman's glands and Dolichos biflorus agglutinin for all nuclei were upregulated in the olfactory mucosa of EAE rats. These results suggest that BSL-II-binding N-acetyl-glucosamine and BSL-I-binding N-acetyl-galactose are involved in transient olfactory dysfunction in EAE, which may hamper odor perception and/or signal processing in olfactory sensory neurons.