Presentation Details
| TNF/TNFR1 signaling mediates inflammation-induced remodeling of gustatory innervation Emily Holder, Ryan Wood, Lindsey Macpherson. University of Texas at San Antonio, San Antonio, TX, USA |
Abstract
A number of inflammatory conditions, including infections and injury, are associated with taste alterations that diminish quality of life and contribute to depression and malnutrition. Despite this clinical significance, effective treatments for taste disorders remain limited due to an incomplete understanding of the relationship between inflammation and gustatory dysfunction. Current literature emphasizes changes in taste receptor cell turnover and function. However, the effects of inflammation on gustatory innervation are less understood. Here, we investigated how inflammation, modeled by lipopolysaccharide (LPS), alters gustatory innervation through tumor necrosis factor (TNF) signaling. Using immunohistochemistry, we quantified nerve fiber volume, TNF expression, and taste bud volume in fungiform papillae at 1 and 4 days following LPS treatment. LPS significantly increased gustatory nerve fiber volume from 1800 μm³ per bud to 2500 μm³ per taste bud by day 4. TNF expression, assessed by fluorescent intensity, was also significantly upregulated in the taste bud at day 4 post-treatment. To determine whether TNF mediates this increased innervation pattern, TNF-knockout and TNFR1-knockout mice were treated with LPS and assessed for alterations in nerve fiber volume using immunohistochemistry. Preliminary findings indicate that mice lacking TNF or TNFR1 failed to exhibit the LPS-induced increase in gustatory innervation observed in wild-type controls. Together, these results suggest that TNF/TNFR1 signaling is required for inflammation-induced remodeling of taste nerve fibers. These findings establish a mechanistic link between inflammatory signaling and gustatory innervation and identify TNF/TNFR1 as a potential mediator of inflammation-driven taste alterations.
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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.
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