HMGB1 is upregulated in the airways in asthma and potentiates airway smooth muscle contraction via TLR4

Asthma is characterized by variable airflow obstruction, airway hyperresponsiveness, and inflammation. Airway smooth muscle (ASM) contributes to asthma pathophysiology via hypercontractility, increased mass, and inflammatory mediator release.1 Clinical studies and animal models demonstrate a role for high-mobility group box 1 (HMGB1) and its receptors in airway inflammation and asthma.2,3 HMGB1's activity and receptor interactions is determined by its redox state, with oxidation rendering HMGB1 inactive.

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