# Unique RNA Gene Expression Profile Is Seen in Chronic Non-Specific Low Back Pain

## TL;DR

This study identifies a unique RNA gene expression profile in chronic non-specific low back pain, suggesting distinct inflammatory and neuroplastic changes compared to subacute cases.

## Contribution

The study reveals a distinct gene expression profile in chronic non-specific low back pain linked to neuroplastic and inflammatory changes.

## Key findings

- Chronic nsLBP is associated with 139 uniquely differentially expressed genes, distinct from subclinical and control groups.
- Minimal overlap in DEGs between chronic and subclinical nsLBP suggests a clear inflammatory distinction.
- Chronic nsLBP shows differences in axon guidance, indicating neuroplastic changes during progression.

## Abstract

Previous reports suggest that the progression from subacute to chronic non-specific low back pain (nsLBP) involves functional changes in both the nervous and immune systems. The purpose of the present study was to characterize the gene expression profiles of circulating immune cells that affect the interaction between these two systems when subacute nsLBP turns into chronic nsLBP. Participants aged 18–55 were included based on the presence or duration of LBP, with peripheral blood mononuclear cells collected for RNA sequencing from 20 healthy controls (no nsLBP), 20 subclinical patients (intermittent nsLBP), and 19 chronic patients (long-term nsLBP). The data revealed that chronic nsLBP is linked to a distinct gene expression profile, with 139 uniquely differentially expressed genes (DEGs), differing from those in the subclinical and control groups. Interestingly, comparing chronic and subclinical groups showed minimal overlap in DEGs, indicating a clear inflammatory distinction between subclinical nsLBP and chronic nsLBP. The findings also indicated that patients with chronic nsLBP were different from other individuals regarding axon guidance, indicating neuroplastic changes when intermittent nsLBP turns into chronic nsLBP. Hence, early recognition of the transition from subclinical to chronic nsLBP using RNA profiling may pave the way for more precise therapeutic strategies targeting neuroplastic changes and inflammatory processes.