Presentation Details
| Cyclophosphamide Chemotherapy Produces a Transient Loss of Taste Bud Innervation in Mice. Ryan M Wood, Emily Holder, Ireland Little, Victoria Valtr, Erin L Vasquez, Krystal A Goyins, Eduardo G Kuri, Kevin Connelly, Saima Humayun, Lindsey Macpherson. Univeristy of San Antonio, San Antonio, TX, USA |
Abstract
Taste dysfunction affects more than 17% of adults in the United States and is especially common among chemotherapy patients, with 50–80% reporting partial or complete taste loss. These changes are often persistent and underrecognized, contributing to malnutrition, delayed recovery, and reduced quality of life. Despite this significant clinical burden, effective treatments remain limited due to an incomplete understanding of the underlying mechanisms. Cyclophosphamide (CYP), a widely used alkylating chemotherapeutic, disrupts taste by damaging mature taste receptor cells (TRCs) and their progenitors. However, proper taste perception also depends on intact gustatory nerve fibers that innervate TRCs, and the effects of CYP on these peripheral nerves remain poorly defined. Here, we examine how CYP alters gustatory innervation and neural integrity using immunohistology to quantify structural changes in taste buds and two-photon microscopy to assess morphological alterations in peripheral gustatory fibers. Emerging evidence suggests TNF/TNFR1 signaling regulates neural development and axonal growth through canonical and reverse signaling pathways. Preliminary data demonstrate TNF/TNFR1 expression in taste tissues, leading us to hypothesize that this pathway contributes to chemotherapy- or inflammation-induced taste dysfunction. Defining these mechanisms may identify novel therapeutic targets to restore taste function.
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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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