Presentation Details
Defining CD11b-dependent Glial Phagocytosis and Gene Expression Changes After Olfactory Injury

David O.Poore, Diego J.Rodriguez-Gil.

East Tennessee State University, Johnson CIty, TN, USA

Abstract


Integrin CD11b, or complement receptor 3, is utilized by myeloid cells to govern phagocytosis and cellular movement to sites of infection or injury. Recognizing over 40 ligands, this integrin plays various immune roles throughout the body. In the olfactory system, CD11b is primarily expressed by microglia. Our lab uses a methimazole-induced olfactory injury model to ablate all olfactory sensory neurons and observe the glial response in both wild-type and global CD11b-deficient mouse models. Previously, our lab saw significant delays in functional recovery and changes in Iba1 expression in CD11b-deficient mice following methimazole injection. To further explore changes in this system, we injected methimazole at post-natal day 7 and collected olfactory bulbs at 3, 7, 14, and 21 days post-injection to quantify phagocytic and gene expression changes by flow cytometry and qPCR, respectively. We implemented a newly developed fluorescent cell sorting method based on marker proteins and the presence of internalized axonal debris and quantified the phagocytic activity of microglia and OECs in wild-type and CD11b-deficient mice. Expression changes in phagocytic markers, inflammatory mediators, and neuroprotective intermediates were quantified by qPCR to elucidate pathway alterations in the olfactory bulb that may contribute to the delays in functional olfactory recovery seen previously in this model.

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.
Content Locked. Log into a registered attendee account to access this presentation.