Journal
BLOOD
Volume 108, Issue 10, Pages 3397-3405Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-04-014779
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Funding
- NCI NIH HHS [CA098852, CA16056] Funding Source: Medline
- NIAID NIH HHS [AI056082] Funding Source: Medline
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Elevation of serum sialic acid and the ST6Gal-1 sialyltransferase is part of the hepatic system inflammatory response, but the contribution of ST6Gal-1 has remained unclear. Hepatic ST6Gal-1 elevation is mediated by P1, 1 of 6 promoters regulating the ST6Gal1 gene. We report that the P1-ablated mouse, Siat1 Delta P1, and a globally ST6Gal-1-deficient mouse had significantly increased peritoneal leukocytosis after intraperitoneal challenge with thioglycollate. Exaggerated peritonitis was accompanied by only a modest in-crease in neutrophil viability, and transferred bone marrow-derived neutrophils from Slat1 Delta P1 mice migrated to the peritonea of recipients with normal efficiency after thioglycollate challenge. Slat1 Delta P1 mice exhibited 3-fold greater neutrophilia by thioglycollate, greater pools of epinephrine-releasable marginated neutrophils, greater sensitivity to G-CSF, elevated bone marrow CFU-G and proliferative-stage myeloid cells, and a more robust recovery from cyclophosphamide-induced myelosuppression. Bone marrow leukocytes from Siat1 Delta P1 are indistinguishable from those of wild-type mice in alpha 2,6-sialylation, as revealed by the Sambucus nigra lectin, and in the expression of total ST6Gal-1 mRNA. Together, our study demonstrated a role for ST6Gal-1, possibly from extramedullary sources (eg, produced in liver) in regulating inflammation, circulating neutrophil homeostasis, and replenishing granulocyte numbers.
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