Targeting Inflammation Driven by HMGB1

Huan Yang, Haichao Wang, Ulf Andersson, Huan Yang, Haichao Wang, Ulf Andersson

Abstract

High mobility group box 1 (HMGB1) is a highly conserved, nuclear protein present in all cell types. It is a multi-facet protein exerting functions both inside and outside of cells. Extracellular HMGB1 has been extensively studied for its prototypical alarmin functions activating innate immunity, after being actively released from cells or passively released upon cell death. TLR4 and RAGE operate as the main HMGB1 receptors. Disulfide HMGB1 activates the TLR4 complex by binding to MD-2. The binding site is separate from that of LPS and it is now feasible to specifically interrupt HMGB1/TLR4 activation without compromising protective LPS/TLR4-dependent functions. Another important therapeutic strategy is established on the administration of HMGB1 antagonists precluding RAGE-mediated endocytosis of HMGB1 and HMGB1-bound molecules capable of activating intracellular cognate receptors. Here we summarize the role of HMGB1 in inflammation, with a focus on recent findings on its mission as a damage-associated molecular pattern molecule and as a therapeutic target in inflammatory diseases. Recently generated HMGB1-specific inhibitors for treatment of inflammatory conditions are discussed.

Keywords: HMGB1; RAGE; TLR4; danger signal; drug target; inflammation.

Copyright © 2020 Yang, Wang and Andersson.

Figures

Figure 1
Figure 1
Inhibiting TLR4- or RAGE-mediated effects induced by HMGB1 or LPS-HMGB1 complexes. During endotoxemia, LPS and extracellular HMGB1 forms complexes that are endocytosed via the RAGE-dependent pathway. LPS and HMGB1 activate TLR4 system. The unique contribution by HMGB1 is disruption of the lysosomal membrane enabling LPS to reach and activate its cytosolic receptor caspase-11, which cleaves gasdermin D to form an active oligomer. Activated gasdermin D will subsequently start coagulation and cause cellular pyroptosis in murine macrophages. The HMGB1-specific inhibitors recombinant HMGB1 box A, anti-HMGB1 m2G7, and acetylcholine each inhibits the cellular internalization of LPS-HMGB1 complexes and resultant immune activation. Anti-HMGB1 m2G7 and acetylcholine also inhibit HMGB1/TLR4-mediated inflammation, whereas P5779 and resveratrol selectively block the HMGB1/TLR4 pathway only.

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