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tat protein stimulates production of transforming growth factor-beta 1 by
marrow macrophages: a potential mechanism for human immunodeficiency
virus-1-induced hematopoietic suppression
G Zauli, BR Davis, MC Re, G Visani, G Furlini and M La Placa
Institute of Microbiology, University of Bologna, Italy.
In this study, we examined the potential role of the human immunodeficiency
virus (HIV) tat protein in causing the hematopoietic abnormalities
frequently observed in HIV-infected individuals. Recombinant tat (r-tat)
protein, at concentrations up to 10 micrograms/mL, did not display any
stimulatory or inhibitory effect on the survival/proliferative capacity of
CD34+ hematopoietic progenitor cells, purified from normal bone marrow
(BM). However, exposure of r- tat protein (at concentrations between 10
ng/mL and 10 micrograms/mL) to enriched normal BM macrophages induced the
production of a factor(s) in conditioned media that inhibited the in vitro
growth of CD34+ cells in liquid cultures and of immature hematopoietic
progenitors (day 14 colony-forming unit-granulocyte-macrophage,
burst-forming unit- erythroid, and colony-forming unit-megakaryocyte) in
semisolid assays. Pre-exposure of r-tat protein with a monoclonal
neutralizing anti-tat antibody completely abrogated the inhibitory activity
present in BM macrophage culture supernatants. The main factor responsible
for this suppressive activity was transforming growth factor-beta 1
(TGF-beta 1), as shown by the ability of a polyclonal anti-TGF-beta 1
neutralizing antibody to almost completely reverse the suppressive effect
of BM macrophage supernatants on CD34+ cells. TGF-beta 1 bioassays showed
that exposure of r-tat protein to BM macrophages significantly increased
the levels of both active and latent forms of TGF-beta 1. These results
indicate that the production of TGF-beta 1, one of the most potent negative
regulator of hematopoiesis, is increased by HIV tat protein and that such
increase could contribute to the derangement of the hematopoietic system in
HIV-infected individuals.
Volume 80,
Issue 12,
pp. 3036-3043,
12/15/1992
Copyright © 1992 by The American Society of Hematology
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