Inter-α inhibitor protein and its associated glycosaminoglycans protect against histone-induced injury

Blood. 2015 Apr 2;125(14):2286-96. doi: 10.1182/blood-2014-06-582759. Epub 2015 Jan 28.

Abstract

Extracellular histones are mediators of tissue injury and organ dysfunction; therefore they constitute potential therapeutic targets in sepsis, inflammation, and thrombosis. Histone cytotoxicity in vitro decreases in the presence of plasma. Here, we demonstrate that plasma inter-α inhibitor protein (IAIP) neutralizes the cytotoxic effects of histones and decreases histone-induced platelet aggregation. These effects are mediated through the negatively charged glycosaminoglycans (GAGs) chondroitin sulfate and high-molecular-weight hyaluronan (HMW-HA) associated with IAIP. Cell surface anionic glycosaminoglycans heparan sulfate and HA protect the cells against histone-mediated damage in vitro. Surface plasmon resonance showed that both IAIP and HMW-HA directly bind to recombinant histone H4. In vivo neutralization of histones with IAIP and HMW-HA prevented histone-induced thrombocytopenia, bleeding, and lung microvascular thrombosis, decreased neutrophil activation, and averted histone-induced production of inflammatory cytokines and chemokines. IAIP and HMW-HA colocalized with histones in necrotic tissues and areas that displayed neutrophil extracellular traps. Increasing amounts of IAIP-histone complexes detected in the plasma of septic baboons correlated with increase in histones and/or nucleosomes and consumption of plasma IAIP. Our data suggest that IAIP, chondroitin sulfate, and HMW-HA are potential therapeutic agents to protect against histone-induced cytotoxicity, coagulopathy, systemic inflammation, and organ damage during inflammatory conditions such as sepsis and trauma.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alpha-Globulins / metabolism*
  • Animals
  • Apoptosis
  • Blood Coagulation
  • Blotting, Western
  • Cells, Cultured
  • Cytokines / metabolism
  • Flow Cytometry
  • Glycocalyx / metabolism
  • Glycosaminoglycans / metabolism*
  • HL-60 Cells
  • Hemorrhage / etiology
  • Hemorrhage / metabolism
  • Hemorrhage / prevention & control*
  • Histones / toxicity*
  • Humans
  • Inflammation / etiology
  • Inflammation / metabolism
  • Inflammation / prevention & control*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Nucleosomes / metabolism
  • Papio
  • Platelet Aggregation
  • Sepsis / etiology
  • Sepsis / metabolism
  • Sepsis / prevention & control*
  • Thrombocytopenia / etiology
  • Thrombocytopenia / metabolism
  • Thrombocytopenia / prevention & control*
  • Thrombosis / etiology
  • Thrombosis / metabolism
  • Thrombosis / prevention & control*

Substances

  • Alpha-Globulins
  • Cytokines
  • Glycosaminoglycans
  • Histones
  • Nucleosomes
  • inter-alpha-inhibitor