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Decreased concentrations of tumor necrosis factor-alpha in supernatants of
monocytes from homozygotes for hereditary hemochromatosis
VR Gordeuk, S Ballou, G Lozanski and GM Brittenham
Department of Medicine, MetroHealth Medical Center, Case Western Reserve
University School of Medicine, Cleveland, OH 44109.
To determine whether release of tumor necrosis factor-alpha (TNF- alpha), a
cytokine that affects iron homeostasis, may be selectively altered in
hereditary hemochromatosis, we measured concentrations of TNF-alpha and
interleukin-1 beta (IL-1 beta) in supernatants of cultured peripheral blood
monocytes from 11 homozygotes for hereditary hemochromatosis, 11 healthy
individuals, and five patients with iron- loading anemia. The gene for
hereditary hemochromatosis is tightly linked to the HLA locus on chromosome
6, but its exact site and product are not known. The gene for TNF-alpha
also is located within the HLA region. Monocytes were incubated from 4 to
36 hours in medium alone or with added lipopolysaccharide. Mean
concentrations of immunoreactive TNF-alpha in supernatants were
significantly lower for subjects with hereditary hemochromatosis as
compared to healthy controls (P less than .037) and patients with
iron-loading anemia (P less than .005); differences between homozygotes for
hemochromatosis and healthy controls were up to 4.5-fold at 4 hours (P =
.008), 1.9-fold at 12 hours (P = .036), and 7.0-fold at 36 hours (P =
.001). Importantly, concentrations of IL-1 beta in supernatants were not
significantly different among the three groups. We conclude that release of
TNF-alpha by monocytes may be selectively impaired in hereditary
hemochromatosis. Deficient activity of TNF-alpha may contribute to the
disordered iron metabolism of this disease.
Volume 79,
Issue 7,
pp. 1855-1860,
04/01/1992
Copyright © 1992 by The American Society of Hematology
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