Inflammatory responses to acute elevations of carbon dioxide in mice.

Health risks are described from elevated indoor air carbon dioxide (CO₂), which often ranges from 1000 to 4000 parts per million (ppm), but mechanisms are unknown. Here, we demonstrate that mice exposed for 2 hours to 2000 or 4000 ppm CO₂ exhibit, respectively, 3.4 + 0.9 (SE, n=6) and 4.1 + 0.7 (n=10)-fold elevations in circulating microparticles (MPs); neutrophil and platelet activation and vascular leak in brain, muscle and distal colon. Interleukin (IL)-1β content of MPs also increases after 2000 ppm by 3.8 + 0.6 (n=6) and after 4000 ppm CO₂ by 9.3 + 1.1 (n=10)-fold greater than control. CO₂-induced vascular damage is abrogated by treating mice with an antibody to IL-1β or an IL-1β receptor inhibitor. Injecting naïve mice with CO₂-induced MPs expressing a protein found on mature neutrophils recapitulates vascular damage as seen with elevated CO₂, and destruction of MPs in CO₂-exposed mice abrogates vascular injuries without altering neutrophil or platelet activation. We conclude that environmentally relevant elevations of CO₂ trigger neutrophils to generate MPs containing high concentrations of IL-1β that cause diffuse inflammatory vascular injury.

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