Myeloid cell-specific HMGB1 deficiency exaggerates mucoinflammatory responses but promotes bacterial clearance in mucoinflammatory lung disease.

ABSTRACT: High mobility group box 1 (HMGB1), a highly conserved nuclear protein, is released into the extracellular milieu serving as a modulator of inflammatory responses. HMGB1 levels are elevated in the airspaces of CF patients and mice with cystic fibrosis (CF)--like lung disease. To reduce extracellular release of HMGB1 into the lung airspaces, we previously introduced airway epithelial cell-specific HMGB1 deficiency in Scnn1b-Tg+ (Tg+) mice, a model of human CF-like lung disease. While the deletion of airway epithelial cell-specific HMGB1 did not reduce bronchoalveolar lavage fluid (BALF) HMGB1 levels, the intracellular HMGB1 deficiency resulted in exaggerated inflammatory responses. In this study, because HMGB1 protein levels were found significantly elevated in Tg+ BALF cells, we hypothesize

SUBMITTER: Mao Y 

PROVIDER: S-EPMC12834952 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature