Neuropathic Pain: Characterization and Modulation of the M1/M2 Monocyte Spectrum


Name: Ann Ketz

Rank: MAJ

Organization: Henry M. Jackson Foundation for the Advancement of Military Medicine

Performance Site: Uniformed Services University of Health Sciences, Bethesda, MD

Year Published: 2013

Abstract Status: Project Completed


Understanding the mechanisms involved in neuropathic pain is essential for the development of novel therapies to ensure the preservation of a fit and ready force. Inflammation plays a central role in many diseases of the nervous system, and contributes to the initiation and maintenance of neuropathic pain. Our long-term goal is to understand the contribution of inflammation to neuropathic pain and explore the therapeutic potential of modulating this inflammatory response.

Microglia are tissue macrphages that exhibit a sectrum of responses to injury, ranging from resting to pro-inflammatory (M1 phenotype) to anti-inflammatory (M2 phenotype). Macrophages and microglia are increased at the site peripheral nerve injury and along the ascending somatosensory pathways in CNS. This increased inflammation correlates with neuropathic pain behavior, however, the temporal-spatial activation of the M1/M2 phenotypes along the pathway following peripheral nerve injury is unknown. Photobiomodulation (PBM) (low-level light therapy) is an effective treatment for injuries in the CNS and PNS in part by causing an anti-inflmmatory effect. Therefore, we hypothesize that alterations of macrohage/microglial activation following peripheral nerve injury are implicated in the initiation and maintenance of chronic neuropathic pain and that modulating the sustained inflammatory response using PBM will decrease chronic pain behavior.

Aim 1: Characterize the temporal-spatial activation of M1/M2 macrophages/microglia along the ascending somatosensory pathways related to pain behavior.

Aim 2: Modulate the temporal-spatial activation of the inflammatory response using PBN to alter establishment and maintenance of chronic neuropathic pain. 

For both aims, the spared nerve injury (SNI) model of neuropathic pain will be used since it has characteristics of multiple peripheral neuropathies. Mechanical allodynia will be used to characterize pain behavior alterations. Immuncohistochemistry and gene expression will be used to investigate M1/M2 plarization at multiple time points after SNI.


Final report is available on NTRL: