Official websites use .gov

A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS

A lock ( 🔒 ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

Need Help

Role of Macrophages in Inflammation and Degeneration of the Intervertebral Disc

Award Number: R01AR085957
ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 05/01/2026
PERIOD OF PERFORMANCE END DATE: 01/31/2031

Group Awards By:

View Award Description

Role of Macrophages in Inflammation and Degeneration of the Intervertebral Disc - Abstract Discogenic back pain, is a leading cause of disability, and involves degenerative changes of the intervertebral disc (IVD), including extracellular matrix (ECM) degradation, macrophage (Mɸ) infiltration, inflammation, and pathological nerve ingrowth. Since only a small subset of patients responds favorably to conventional treatments which address the symptoms but not the disease, there is a need for new therapies to treat disc degeneration (DD). Despite the extensive association between disc inflammation and DD, the mechanisms by which inflammatory factors drive DD in the disc are unclear. The goal of this proposal is to identify the role of monocyte- derived Mɸ on the cascade of painful DD, and to determine the contributions of CCL2/CCR2 signaling on Mɸ migration into the IVD. We hypothesize that inflammatory DD promotes increases in IVD levels of the chemokine CCL2/MCP1 that acts as a chemoattractant to CCR2+ monocyte-derived Mɸ, which degrade the ECM and promote a chronic inflammatory milieu over time. In Aim 1, we will identify the dynamics in which monocyte- derived Mɸ promote a chronic inflammatory, painful degenerate IVD. We have developed an in vivo mouse model of disc inflammation using inducible activation of NF-κB in the disc, which will be used. In Aim 2, we will determine the role of CCL2 in Mɸ migration into the IVD. In Aim 3, we will investigate the efficacy of sustained intradiscal delivery of a CCL2 neutralizing antibody during disease progression in a rat IVD injury model. Successful completion of this proposal will demonstrate that CCL2 secretion by IVD cells promotes recruitment of Mɸ, loss of IVD ECM leading to discogenic pain. Depletion of circulating Mɸ and deficiency in CCL2 signaling at the ‘right time’ will identify novel therapeutic mechanisms for painful DD.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $636,479 )
2026	2026	THE TRUSTEES OF COLUMBIA UNIVERSITY IN THE CITY OF NEW YORK	630 W 168TH ST FL 4	NEW YORK	NY	10032	NEW YORK	USA	Arthritis, Musculoskeletal and Skin Diseases Research	000	1	4/21/2026	NEW	$636,479
														Subtotal = $636,479

Grand Total All Awards = $636,479

Top

All Categories

About

Search

Reports

Data Submission

Award Information

Role of Macrophages in Inflammation and Degeneration of the Intervertebral Disc

Award Number: R01AR085957

ORGANIZATION: NATIONAL INSTITUTE OF ARTHRITIS & MUSCULOSKELETAL & SKIN DISEASES

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 05/01/2026

PERIOD OF PERFORMANCE END DATE: 01/31/2031

Federal Websites

Department of Health & Human Services

HHS Operating Divisions

HHS Staff Divisions

Download A Document Viewer