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Picogram doses of lipopolysaccharide exacerbate antibody‐mediated thrombocytopenia and reduce the therapeutic efficacy of intravenous immunoglobulin in mice
Author(s) -
Tremblay Tony,
Aubin Éric,
Lemieux Réal,
Bazin Renée
Publication year - 2007
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.2007.06777.x
Subject(s) - antibody , in vivo , immunology , lipopolysaccharide , medicine , exacerbation , platelet , immune thrombocytopenia , immune system , thrombocytopenic purpura , biology , microbiology and biotechnology
Summary Exacerbation of antibody‐mediated thrombocytopenia following infection with viruses has recently been demonstrated in a mouse model of the disease. The phenomenon was caused by an increased activation of phagocytes through gamma‐interferon secretion in response to infection. Endotoxins from Gram‐negative bacteria are also known to be potent activators of phagocytic cells. The objective of the present work was to determine whether lipopolysaccharide (LPS) could exacerbate antibody‐mediated thrombocytopenia in vivo and so alter the therapeutic efficacy of intravenous immunoglobulin (IVIg), using a mouse model of thrombocytopenia. Very low doses of LPS (picogram range) and of anti‐platelet antibodies (nanogram range), which did not induce thrombocytopenia individually, could synergize in vivo , resulting in significant decreases in platelet counts. The therapeutic efficacy of IVIg in antibody‐mediated thrombocytopenia was significantly reduced in presence of LPS. These in vivo observations further support a role for bacterial infections in the aetiology of immune thrombocytopenic purpura (ITP) and may contribute to better understand the recognized lack of efficacy of IVIg in a significant proportion of patients with ITP.