Date of Award

5-2017

Rights

© 2017 Scott A. Scarneo

Document Type

Thesis

Degree Name

Master of Science in Biological Sciences

Department

Biology

First Advisor

Katherine Hanlson

Second Advisor

Derek Molliver

Third Advisor

Geoffrey Ganter

Fourth Advisor

Wendy Roberts

Abstract

Persistent pain remains a significant burden on the US healthcare system with more than 100 million patients experiencing persistent pain annually. Complex etiology coupled with functional plasticity of cells involved often results in a chronic health concern with limited treatment modalities. To date, most work aimed at describing neuro-immune interactions in pain focuses on the site of injury, leaving the functional significance of resident tissue macrophages in the dorsal root ganglia largely unexplored in both uninjured and peripheral injury states. Here, we systematically evaluate the phenotype of naïve DRG resident tissue macrophages and compare to naïve spinal microglia and bone marrow derived monocytes. We report the upregulation of CD39 and MHC Class II by DRG macrophages 24 and 72 hours following distal insult in multiple models of inflammatory pain. Further, we demonstrate functional changes induced in DRG macrophages in response to peripheral injury by profiling the cytokine proteome: DRG expression of 111 cytokines were evaluated with and without injury. Taken together, these data suggest that resident tissue macrophages actively respond to distant injury stimuli with functional changes and may influence nociception via neuro-immune communication.

Comments

Master's thesis

This work was supported by NIH/NIGMS award 1P20GM103643-01A1 to I. Meng and the Rita Allen Foundation American Pain Society award to Katherine Hanlon.

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