Document Detail


Qualitative functional deficiency of affinity-purified lactoferrin from neutrophils of patients with chronic myelogenous leukemia, and lactoferrin/H-ferritin-cell interactions in a patient with lactoferrin-deficiency with normal numbers of circulating leukocytes.
MedLine Citation:
PMID:  2043267     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The iron-binding proteins lactoferrin (LF) and H-ferritin have been implicated in the negative regulation of myelopoiesis in vitro and in vivo. The present studies evaluated the functional activity of affinity-purified LF from polymorphonuclear neutrophils (PMN) of patients with chronic myelogenous leukemia (CML) and LF/H-ferritin-cell interactions in a nonleukemic patient with LF deficiency with normal levels of circulating blood leukocytes. Affinity-purified CML-PMN-LF was found to be qualitatively deficient as a suppressor of the release of colony-stimulating factors from mononuclear blood cells, adding to previous information from our group documenting defective LF-cell interactions in CML. LF was detected by immunoradiometric assay in PMN of the patient with LF deficiency, but at a much lower level than normal. This LF was found, however, to be active as a suppressor molecular against the patient's cells and normal donor cells. Patient cells were as responsive as normal cells to effects of purified milk LF. Decreased LF levels in this patient were associated with increased levels of monocyte H-ferritin inhibitory activity, consistent with the known suppressive effects in vitro of LF on H-ferritin release from monocytes. Patient marrow hematopoietic progenitor cells were as responsive as progenitors from normal donors to suppression by purified H-ferritin and prostaglandin E1. These results are consistent with a role of LF and H-ferritin in the control of myelopoiesis in this patient.
Authors:
H E Broxmeyer; D C Bicknell; S Cooper; G Sledge; D E Williams; W A McGuire; T D Coates
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Pathobiology : journal of immunopathology, molecular and cellular biology     Volume:  59     ISSN:  1015-2008     ISO Abbreviation:  Pathobiology     Publication Date:  1991  
Date Detail:
Created Date:  1991-07-17     Completed Date:  1991-07-17     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9007504     Medline TA:  Pathobiology     Country:  SWITZERLAND    
Other Details:
Languages:  eng     Pagination:  26-35     Citation Subset:  IM    
Affiliation:
Department of Medicine (Hematology/Oncology), Indiana University School of Medicine, Indianapolis.
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MeSH Terms
Descriptor/Qualifier:
Alprostadil / pharmacology
Chromatography, Affinity
Colony-Forming Units Assay
Colony-Stimulating Factors / secretion*
Depression, Chemical
Dinoprostone / pharmacology
Ferritins / pharmacology*
Hematopoietic Stem Cells / drug effects
Humans
Lactoferrin / blood,  deficiency*,  isolation & purification,  pharmacology
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology*
Leukocyte Count
Leukocytes, Mononuclear / drug effects*,  secretion
Neutrophils / chemistry*
Secretory Rate / drug effects
Grant Support
ID/Acronym/Agency:
CA36464/CA/NCI NIH HHS; CA36740/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Colony-Stimulating Factors; 0/Lactoferrin; 363-24-6/Dinoprostone; 745-65-3/Alprostadil; 9007-73-2/Ferritins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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