Mechanisms of erythroid suppression in the anemia of chronic disease

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

The mechanism underlying the hypoproliferative anemia in patients with chronic diseases has not been clearly defined. We have examined the effects of marrow macrophages from anemic patients with chronic diseases and normals to determine if they suppress erythroid progenitors in vitro. We found that marrow macrophages from patients with the anemia of chronic disease (ACD) significantly suppressed erythroid progenitor cell growth, whereas marrow macrophages from normals did not. Since ACD is seen in conditions that activate macrophages, we then determined if activated macrophages could suppress erythroid progenitor cell growth. Peritoneal macrophages activated by chronic Cryptococcus neoformans infection significantly suppressed erythroid progenitor cell growth, although resting macrophages did not. We then examined the effects of a product of activated macrophages, tumor necrosis factor (TNF), for its effects on CFU-E and BFU-E. TNF significantly suppressed CFU-E and BFU-E growth in concentrations as low as 10-11-10-12 M. Preincubation of marrow samples with TNF for as little as 15 minutes was sufficient to suppress CFU-E and BFU-E growth. Addition of TNF, after the onset of culture could only suppress CFU-E and BFU-E if added within the first 48 hours. TNF (10-10-10-11 M) also inhibited the growth of hematopoietic cell lines K562, HL60, and HEL cells. These cell lines expressed low numbers of high affinity TNF receptors, with 80%-90% of the cells expressing TNF receptors.

Original languageEnglish (US)
Pages (from-to)171-184
Number of pages14
JournalBlood Cells
Volume13
Issue number1-2
StatePublished - 1987
Externally publishedYes

Fingerprint

Erythroid Precursor Cells
Anemia
Chronic Disease
Macrophages
Tumor Necrosis Factor-alpha
Growth
Bone Marrow
Tumor Necrosis Factor Receptors
Cell Line
Cryptococcus neoformans
HL-60 Cells
Peritoneal Macrophages

ASJC Scopus subject areas

  • Hematology

Cite this

Mechanisms of erythroid suppression in the anemia of chronic disease. / Roodman, G. David.

In: Blood Cells, Vol. 13, No. 1-2, 1987, p. 171-184.

Research output: Contribution to journalArticle

@article{04ea442114f04705a9e1b943eda56816,
title = "Mechanisms of erythroid suppression in the anemia of chronic disease",
abstract = "The mechanism underlying the hypoproliferative anemia in patients with chronic diseases has not been clearly defined. We have examined the effects of marrow macrophages from anemic patients with chronic diseases and normals to determine if they suppress erythroid progenitors in vitro. We found that marrow macrophages from patients with the anemia of chronic disease (ACD) significantly suppressed erythroid progenitor cell growth, whereas marrow macrophages from normals did not. Since ACD is seen in conditions that activate macrophages, we then determined if activated macrophages could suppress erythroid progenitor cell growth. Peritoneal macrophages activated by chronic Cryptococcus neoformans infection significantly suppressed erythroid progenitor cell growth, although resting macrophages did not. We then examined the effects of a product of activated macrophages, tumor necrosis factor (TNF), for its effects on CFU-E and BFU-E. TNF significantly suppressed CFU-E and BFU-E growth in concentrations as low as 10-11-10-12 M. Preincubation of marrow samples with TNF for as little as 15 minutes was sufficient to suppress CFU-E and BFU-E growth. Addition of TNF, after the onset of culture could only suppress CFU-E and BFU-E if added within the first 48 hours. TNF (10-10-10-11 M) also inhibited the growth of hematopoietic cell lines K562, HL60, and HEL cells. These cell lines expressed low numbers of high affinity TNF receptors, with 80{\%}-90{\%} of the cells expressing TNF receptors.",
author = "Roodman, {G. David}",
year = "1987",
language = "English (US)",
volume = "13",
pages = "171--184",
journal = "Blood Cells, Molecules, and Diseases",
issn = "1079-9796",
publisher = "Academic Press Inc.",
number = "1-2",

}

TY - JOUR

T1 - Mechanisms of erythroid suppression in the anemia of chronic disease

AU - Roodman, G. David

PY - 1987

Y1 - 1987

N2 - The mechanism underlying the hypoproliferative anemia in patients with chronic diseases has not been clearly defined. We have examined the effects of marrow macrophages from anemic patients with chronic diseases and normals to determine if they suppress erythroid progenitors in vitro. We found that marrow macrophages from patients with the anemia of chronic disease (ACD) significantly suppressed erythroid progenitor cell growth, whereas marrow macrophages from normals did not. Since ACD is seen in conditions that activate macrophages, we then determined if activated macrophages could suppress erythroid progenitor cell growth. Peritoneal macrophages activated by chronic Cryptococcus neoformans infection significantly suppressed erythroid progenitor cell growth, although resting macrophages did not. We then examined the effects of a product of activated macrophages, tumor necrosis factor (TNF), for its effects on CFU-E and BFU-E. TNF significantly suppressed CFU-E and BFU-E growth in concentrations as low as 10-11-10-12 M. Preincubation of marrow samples with TNF for as little as 15 minutes was sufficient to suppress CFU-E and BFU-E growth. Addition of TNF, after the onset of culture could only suppress CFU-E and BFU-E if added within the first 48 hours. TNF (10-10-10-11 M) also inhibited the growth of hematopoietic cell lines K562, HL60, and HEL cells. These cell lines expressed low numbers of high affinity TNF receptors, with 80%-90% of the cells expressing TNF receptors.

AB - The mechanism underlying the hypoproliferative anemia in patients with chronic diseases has not been clearly defined. We have examined the effects of marrow macrophages from anemic patients with chronic diseases and normals to determine if they suppress erythroid progenitors in vitro. We found that marrow macrophages from patients with the anemia of chronic disease (ACD) significantly suppressed erythroid progenitor cell growth, whereas marrow macrophages from normals did not. Since ACD is seen in conditions that activate macrophages, we then determined if activated macrophages could suppress erythroid progenitor cell growth. Peritoneal macrophages activated by chronic Cryptococcus neoformans infection significantly suppressed erythroid progenitor cell growth, although resting macrophages did not. We then examined the effects of a product of activated macrophages, tumor necrosis factor (TNF), for its effects on CFU-E and BFU-E. TNF significantly suppressed CFU-E and BFU-E growth in concentrations as low as 10-11-10-12 M. Preincubation of marrow samples with TNF for as little as 15 minutes was sufficient to suppress CFU-E and BFU-E growth. Addition of TNF, after the onset of culture could only suppress CFU-E and BFU-E if added within the first 48 hours. TNF (10-10-10-11 M) also inhibited the growth of hematopoietic cell lines K562, HL60, and HEL cells. These cell lines expressed low numbers of high affinity TNF receptors, with 80%-90% of the cells expressing TNF receptors.

UR - http://www.scopus.com/inward/record.url?scp=0023194376&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023194376&partnerID=8YFLogxK

M3 - Article

C2 - 2822178

AN - SCOPUS:0023194376

VL - 13

SP - 171

EP - 184

JO - Blood Cells, Molecules, and Diseases

JF - Blood Cells, Molecules, and Diseases

SN - 1079-9796

IS - 1-2

ER -