Inhaled carbon monoxide reduces leukocytosis in a murine model of sickle cell disease

Joan D Beckman, John D Belcher, Julie V. Vineyard, Chunsheng Chen, Julia Nguyen, M. Osita Nwaneri, Gerard O'Sullivan, Evin Gulbahce, Robert P Hebbel, Gregory M Vercellotti

Research output: Contribution to journalArticlepeer-review

38 Scopus citations


Carbon monoxide (CO) has anti-inflammatory properties. We previously reported that acute treatments with inhaled CO inhibit vascular inflammation and hypoxia-induced vasoocclusion in sickle cell disease mouse models. Therefore, we hypothesized that chronic CO inhalation would decrease vascular inflammation and organ pathology in a sickle cell disease mouse model. The treatment of sickle cell disease mice with 25 or 250 parts/million inhaled CO for 1 h/day, 3 days/wk for 8-10 wk significantly decreased the total mean white blood cell, neutrophil, and lymphocyte counts in peripheral blood. Eight weeks of 250 parts/million CO treatments reduced staining for myeloid and lymphoid markers in the bone marrow of sickle mice. Bone marrow from treated sickle mice exhibited a significant decrease in colony-forming unit granulocyte-macrophage during colony-forming cell assays. Anti-inflammatory signaling pathways phospho-Akt and phospho-p38 MAPK were markedly increased in CO-treated sickle livers. Importantly, CO-treated sickle mice had a significant reduction in liver parenchymal necrosis, reflecting the anti-inflammatory benefits of CO. We conclude that inhaled CO may be a beneficial anti-inflammatory therapy for sickle cell disease.

Original languageEnglish (US)
Pages (from-to)H1243-H1253
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number4
StatePublished - Oct 2009


  • Heme oxygenase
  • Inflammation


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