4.5 Article

High mobility group box-1 serves a pathogenic role in spinal cord injury via the promotion of pro-inflammatory cytokines

Journal

JOURNAL OF LEUKOCYTE BIOLOGY
Volume 110, Issue 6, Pages 1131-1142

Publisher

OXFORD UNIV PRESS
DOI: 10.1002/JLB.3MA0721-007R

Keywords

cytokine; high mobility group box-1; inflammation; microglia; spinal cord injury

Funding

  1. National Natural Science Foundation of China [81201434, 82072513]
  2. Department of Science and Technology of Guangdong Province [S2012040007947]
  3. Science and Technology Program of Guangzhou [202102080182]

Ask authors/readers for more resources

The study demonstrated the important role of HMGB1 in inflammation after spinal cord injury, with neutralizing HMGB1 significantly reducing SCI pathogenesis and hind limb paralysis. Additionally, blocking HMGB1 also led to a decrease in various pro-inflammatory cytokines levels at the SCI lesion site.
Traumatic spinal cord injury (SCI) is a devastating condition marked by permanent motor, sensory, and autonomic dysfunction, in which the inflammatory response serves an important and preventable role. High mobility group box-1 (HMGB1) is a potent regulator of inflammation in numerous acute and chronic inflammatory conditions.; however, the role of HMGB1 in SCI remains unclear. The present study aimed to characterize the temporal dynamics of HMGB1 release after SCI, to investigate the role of spinal microglia activation in mediating the effects of HMGB1 on SCI, and to explore the therapeutic potential of intrathecal anti-HMGB1 polyclonal antibody on alleviating SCI. The present study demonstrated that HMGB1 expression was increased immediately after traumatic injury of a primary spinal neuron culture. It was found that neutralizing HMGB1 significantly ameliorated SCI pathogenesis and hind limb paralysis. Moreover, the levels of a number of pro-inflammatory cytokines in the SCI lesion were reduced when local HMGB1 was blocked by anti-HMGB1 antibody. In addition, the injured neuron-derived conditioned medium increased TNF-alpha secretion and the NF-kappa B pathway in the BV2 microglia cell line via HMGB1. Collectively, these results indicated that HMGB1 served an important role in SCI inflammation and suggested the therapeutic potential of an anti-HMGB1 antibody for SCI.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.5
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available