Journal
CELLS
Volume 10, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/cells10102791
Keywords
high mobility group box 1; TRPV1; nociception; cytokine; inflammation; nerve injury; arthritis
Categories
Ask authors/readers for more resources
Neuronal HMGB1 plays a crucial role in the development of neuroinflammation, with knock out or neutralization ameliorating nerve injury and arthritis. Furthermore, the active release of HMGB1 during neuronal depolarization suggests a key etiologic role in the initiation and amplification of neuroinflammation, making direct targeting of HMGB1 a promising approach for novel anti-inflammatory therapy.
Recent data show that activation of nociceptive (sensory) nerves turns on localized inflammation within the innervated area in a retrograde manner (antidromically), even in the absence of tissue injury or molecular markers of foreign invaders. This neuroinflammatory process is activated and sustained by the release of neuronal products, such as neuropeptides, with the subsequent amplification via recruitment of immunocompetent cells, including macrophages and lymphocytes. High mobility group box 1 protein (HMGB1) is a highly conserved, well characterized damage-associated molecular pattern molecule expressed by many cells, including nociceptors and is a marker of inflammatory diseases. In this review, we summarize recent evidence showing that neuronal HMGB1 is required for the development of neuroinflammation, as knock out limited to neurons or its neutralization via antibodies ameliorate injury in models of nerve injury and of arthritis. Further, the results of study show that HMGB1 is actively released during neuronal depolarization and thus plays a previously unrecognized key etiologic role in the initiation and amplification of neuroinflammation. Direct targeting of HMGB1 is a promising approach for novel anti-inflammatory therapy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available