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Laboratoire d’endocrinologie de la reproduction and
Unité de recherche en genétique humaine et moléculaire, Centre de recherche de St-Françoise d’Assise, Centre Hospitalier Universitaire de Québec, Pavillon Saint-Françoise d’Assise, Québec, Canada; and
Centre de recherche en rhumatologie et immunologie, Centre Hospitalier Universitaire de Québec, Pavillon Centre Hospitalier de l’Université Laval, and Department of Medicine, Laval University, Sainte-Foy, Québec, Canada
Haptoglobin (Hp), TNF-
, and neutrophils are parts of a
highly interactive ensemble participating in inflammatory processes. Hp
is taken up by neutrophils, stored within a cytoplasmic granular
compartment, and is secreted during phagocytosis by those cells. In the
present study, the effects of TNF- on the release of Hp from human
neutrophils were investigated. Incubation of neutrophils with TNF-
induced the release of Hp from cells in a time- and
concentration-dependent manner as revealed by Western blot analysis and
immunofluorescence. The release of Hp induced by TNF- was not due to
nonspecific lysis of the cells. TNF- is a highly pleiotropic
cytokine that mediates its effects by binding to two distinct receptors
(p55 and p75). Administration of TNF- mutants binding specifically
either to the p55 or to the p75 TNF receptors showed that there is a
preference of TNF- for the p55 receptor in the mediation of Hp
release by neutrophils. A stimulated release of Hp was also induced by
the chemotactic tripeptide fMLP. The TNF--induced release of Hp from
neutrophils was inhibited by erbstatin, a tyrosine kinase inhibitor.
These findings suggest that TNF- may promptly increase the level of
Hp at sites of infection or injury, leading to the modulation of the
acute inflammatory response.
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