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Prepublished online as a Blood First Edition Paper on April 17, 2002; DOI 10.1182/blood-2002-01-0136. This Article Full Text (PDF) All Versions of this Article: 2002-01-0136v1 100/2/474    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Papadaki, H. A Articles by Eliopoulos, G. D Search for Related Content PubMed PubMed Citation Articles by Papadaki, H. A Articles by Eliopoulos, G. D Social Bookmarking                   What's this? Submitted January 16, 2002 Accepted March 12, 2002 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 Helen A Papadaki*, Heraklis D Kritikos, Vasilis Valatas, Dimitrios T Boumpas, and George D Eliopoulos Hematology, University of Crete School of Medicine, Heraklion, Crete, Greece Rheumatology, Clinical Immunology and Allergiology, University of Crete School of Medicine, Heraklion, Crete, Greece * Corresponding author; email: epapadak{at}med.uoc.gr. Circumstantial evidence has implicated tumor necrosis factor (TNF)in the pathogenesis of anemia of chronic disease (ACD) in rheumatoid arthritis (RA). We have investigated the role of TNF in erythropoiesis of patients with active RA (n=40) and the effect of anti-TNF antibody administration (cA2). RA patients had lower number of CD34+/CD71+ and CD36-/GlycoA+ bone marrow (BM) cells and increased proportion of apoptotic cells within the CD34+/CD71+ and CD36+/GlycoA+ cell compartments, compared to normal controls (n=24). Erythroid-burst forming units (BFU-E) obtained by BM mononuclear or purified CD34+ cells were significantly lower in RA patients compared to controls. These abnormalities were more pronounced among patients with ACD. Increased TNF levels in patient long-term BM culture supernatants inversely correlated with BFU-E and hemoglobin and positively with the percentage of apoptotic CD34+/CD71+ and CD36+/GlycoA+ cells. Following cA2 therapy, a normalization was documented in the number of CD34+/CD71+ and CD36-/GlycoA+ cells, the number of BFU-E, and the proportion of apoptotic CD34+/CD71+ and CD36+/GlycoA+ cells, that was associated with a significant increase in hemoglobin levels compared to baseline. Recovery from anemia was more prominent in patients with ACD. The exogenous addition of an anti-TNF antibody in the cultures increased BFU-E number in patients prior to cA2 treatment but not after treatment, further substantiating the inhibitory role of TNF on patients erythropoiesis. We conclude that TNF-mediated apoptotic depletion of BM erythroid cells may account for ACD in RA, and that cA2 administration may ameliorate ACD in these patients by down-regulating the apoptotic mechanisms involved in erythropoiesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. C. MacNamara, R. Racine, M. Chatterjee, D. Borjesson, and G. M. Winslow Diminished Hematopoietic Activity Associated with Alterations in Innate and Adaptive Immunity in a Mouse Model of Human Monocytic Ehrlichiosis Infect. Immun., September 1, 2009; 77(9): 4061 - 4069. [Abstract] [Full Text] [PDF] P. Brendt, A. Horwat, S. T. Schafer, S. C. Dreyer, J. Gothert, and J. Peters Lipopolysaccharide Evokes Resistance to Erythropoiesis Induced by the Long-Acting Erythropoietin Analogue Darbepoetin Alfa in Rats Anesth. Analg., September 1, 2009; 109(3): 705 - 711. 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