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The mechanism for neurological deficits from carbon monoxide (CO) poisoning is unclear. In a series of 150 patients with CO poisoning, we found marked elevations of blood-borne inflammatory filamentous (F-) actin-coated microparticles (MPs), neutrophil activation, and a 90% reduction in the normal level of plasma gelsolin (pGSN), a protein capable of lysing F-actin-coated MPs. This led to studies in a murine model where the same events occur and cause neuroinflammation with cognitive dysfunction. All events are recapitulated when F-actin MPs are injected intravenously, which establishes a blood-to-brain-to-blood inflammatory cycle that persists for weeks. All changes, including cognitive dysfunction, can be abrogated by an injection of human recombinant pGSN within 2 weeks after CO poisoning. These findings demonstrate that CO-induced neurological injury has an inflammatory etiology. Because of MP-mediated communications between the brain and systemic circulation, CO-induced cognitive deficits may be reversible with a pharmaceutical intervention.
Arya et al. (Fri,) studied this question.