Presentation Details
| Immune response dynamics in the anterior taste field after nerve injury Joshua I.Brown1, 2, Yonggang Bao2, Tagwa Ali2, Emma Heisey1, 2, Osarume Ogalala2, Taylor Hardeman2, Lynnette McCluskey2. 1Graduate Program in Neuroscience, Augusta, GA, USA.2Department of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, USA |
Abstract
Damage to the chorda tympani (CT) nerve through trauma or experimental nerve axotomy results in the degeneration of anterior taste buds and taste loss. IL-1R and ligands IL-1a and IL-1b are widely expressed in taste receptor cells and surrounding epithelium, gustatory neurons, and infiltrating immune cells. Our previous work demonstrated that IL-1 receptor (IL-1R) signaling is required for taste bud regeneration and the recovery of taste function. However, little is known about changes in immune cell populations in the anterior taste field after experimental axotomy in the absence of IL-1R signaling. To test this, we performed unilateral CT sectioning in Il1r KO or wild-type mice. We found that CD45+ immune cells, CD68+ and CD206+ M2-like macrophages are significantly increased near anterior taste buds at day two post-injury in WT mice but not in Il1r KO. By day 5 or later at day 56-60, these immune cell types were at baseline levels in both strains, indicating that immune responses to injury were suppressed rather than delayed in the absence of IL-1R signaling. However, taste buds degenerated at similar time points in both strains. These results suggest that delayed taste bud degeneration in Il1r KO mice is not the primary reason for later functional deficits, though other unidentified immune and mesenchymal cells may have roles that have yet to be elucidated in the injured peripheral taste system.
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No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.