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Bordetella pertussisInfection of Human Monocytes Inhibits Antigen‐Dependent CD4 T Cell Proliferation
Author(s) -
Jeffrey S. Boschwitz,
Janet West Batanghari,
Hassya Kedem,
David A. Relman
Publication year - 1997
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/514090
Subject(s) - bordetella pertussis , pertussis toxin , filamentous haemagglutinin adhesin , monocyte , biology , pertactin , microbiology and biotechnology , phagocytosis , immune system , antigen , bordetella , adenylate cyclase toxin , whooping cough , macrophage , immunology , in vitro , g protein , signal transduction , vaccination , bacteria , biochemistry , genetics
Human monocytes and macrophages bind Bordetella pertussis through multiple specific receptor-ligand interactions; however, the effect of these interactions on monocyte and macrophage function is not well understood. In an in vitro system, B. pertussis infection of human monocytes significantly impaired T cell proliferation to exogenous antigen at MOIs as low as 1.0. B. pertussis isogenic mutant strains deficient in filamentous hemagglutinin or adenylate cyclase toxin were incapable of proliferation inhibition, suggesting that these virulence-associated factors are essential for this activity. B. pertussis-induced monocyte death alone did not explain these results, nor did differences in intracellular survival. In addition, B. pertussis infection did not significantly alter monocyte phagocytosis of complement-opsonized latex particles, indicating that B. pertussis infection does not globally impair monocyte functions in this system. These results suggest that B. pertussis may be capable of subverting cellular immune defenses in an infected host.

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