|
|
 Previous Article | Table of Contents | Next Article 
Chronic exposure to tumor necrosis factor in vivo preferentially inhibits
erythropoiesis in nude mice
RA Johnson, TA Waddelow, J Caro, A Oliff and GD Roodman
VA Hospital, Wilford Hall US Air Force Medical Center, San Antonio, TX.
The anemia of chronic disease (ACD) is associated with conditions in which
macrophage activation occurs. Activated marrow macrophages suppress
erythropoiesis in vitro and produce tumor necrosis factor (TNF). Therefore,
we tested the effects of chronic in vivo exposure to TNF to determine if it
was a candidate for a mediator of ACD. Nude mice were inoculated with
Chinese hamster ovary (CHO) cells expressing the human TNF gene or with
control cells containing the transfection vector alone. The TNF mice
promptly became reticulocytopenic, and after 3 weeks their corrected
reticulocytes were 2.6% +/- 0.7% as compared with 7.3% +/- 4% in control
mice. The hematocrit at 3 weeks was 28.4% +/- 1.7% in TNF mice as compared
with 46% +/- 0.8% in control mice. This anemia was also associated with low
serum iron and normal iron stores and increased erythropoietin (Epo)
levels. The TNF mice showed an absolute monocytosis with twice the number
of circulating monocytes as control mice and had M-colony-stimulating
factor (CSF) activity in their serum. The TNF mice also became mildly
thrombocytopenic. Marrow CFU-E and BFU-E were profoundly decreased (1.2 +/-
0.2 x 10(3) v 8.6 +/- 0.2 x 10(4) CFU-E per femur, and 6.5 +/- 1 x 10(2) v
8.5 +/- 0.2 x 10(4) BFU-E per femur). Splenic CFU-E and BFU-E were
similarly depressed. In contrast, marrow CFU-GM and CFU-GEMM were not
affected. The residual BFU-E in TNF mice were relatively resistant to TNF
as compared with control mice. These data demonstrate that TNF
preferentially inhibits erythropoiesis in vivo and may be important in the
pathogenesis of ACD.
Volume 74,
Issue 1,
pp. 130-138,
07/01/1989
Copyright © 1989 by The American Society of Hematology
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
J. W. Adamson
The Anemia of Inflammation/Malignancy: Mechanisms and Management
Hematology,
January 1, 2008;
2008(1):
159 - 165.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Furuta, T. Kikuchi, Y. Iwakura, and N. Watanabe
Protective Roles of Mast Cells and Mast Cell-Derived TNF in Murine Malaria.
J. Immunol.,
September 1, 2006;
177(5):
3294 - 3302.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. Tsantes, S. Tassiopoulos, S. I. Papadhimitriou, S. Bonovas, L. Kavalierou, G. Vaiopoulos, and I. Meletis
Suboptimal Erythropoietic Response to Hypoxemia in Idiopathic Pulmonary Fibrosis
Chest,
August 1, 2003;
124(2):
548 - 553.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. A. Papadaki, H. D. Kritikos, V. Valatas, D. T. Boumpas, and G. D. Eliopoulos
Anemia of chronic disease in rheumatoid arthritis is associated with increased apoptosis of bone marrow erythroid cells: improvement following anti-tumor necrosis factor-alpha antibody therapy
Blood,
June 28, 2002;
100(2):
474 - 482.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. Silvestris, P. Cafforio, M. Tucci, and F. Dammacco
Negative regulation of erythroblast maturation by Fas-L+/TRAIL+ highly malignant plasma cells: a major pathogenetic mechanism of anemia in multiple myeloma
Blood,
February 15, 2002;
99(4):
1305 - 1313.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. Silvestris, M. Tucci, P. Cafforio, and F. Dammacco
Fas-L up-regulation by highly malignant myeloma plasma cells: role in the pathogenesis of anemia and disease progression
Blood,
March 1, 2001;
97(5):
1155 - 1164.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. L. Greenberg, V. Gordeuk, S. Issaragrisil, N. Siritanaratkul, S. Fucharoen, and R. C. Ribeiro
Major Hematologic Diseases in the Developing World-- New Aspects of Diagnosis and Management of Thalassemia, Malarial Anemia, and Acute Leukemia
Hematology,
January 1, 2001;
2001(1):
479 - 498.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. S. Postma, R. C. Hermsen, D. J. A. Crommelin, W. M. C. Eling, and J. Zuidema
Thiolated Recombinant Human Tumor Necrosis Factor-Alpha Protects against Plasmodium berghei K173-Induced Experimental Cerebral Malaria in Mice
Antimicrob. Agents Chemother.,
May 1, 1999;
43(5):
1027 - 1033.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
N. S. Postma, D. J. A. Crommelin, W. M. C. Eling, and J. Zuidema
Treatment with Liposome-Bound Recombinant Human Tumor Necrosis Factor-alpha Suppresses Parasitemia and Protects against Plasmodium berghei k173-Induced Experimental Cerebral Malaria in Mice
J. Pharmacol. Exp. Ther.,
January 1, 1999;
288(1):
114 - 120.
[Abstract]
[Full Text]
|
|
|
|
|
|
|
S. J. Tornquist and T. B. Crawford
Suppression of Megakaryocyte Colony Growth by Plasma From Foals Infected With Equine Infectious Anemia Virus
Blood,
September 15, 1997;
90(6):
2357 - 2363.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
