Interferon‐γ‐Induced Activation of Indoleamine 2,3‐Dioxygenase in Cord Blood Monocyte‐Derived Macrophages Inhibits the Growth of Group B Streptococci
Author(s) -
Colin R. MacKenzie,
U. Hadding,
Walter Däubener
Publication year - 1998
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 - 10.1086/515347
Subject(s) - indoleamine 2,3 dioxygenase , immune system , monocyte , tumor necrosis factor alpha , extracellular , neonatal sepsis , effector , microbiology and biotechnology , biology , intracellular , streptococcus agalactiae , interferon gamma , immunology , cytokine , interferon , sepsis , streptococcus , tryptophan , bacteria , biochemistry , amino acid , genetics
Neonatal sepsis is most often caused by group B streptococci (GBS) and is a major cause of death in the neonatal period. The response of the immune system in the newborn child has received much attention and is thought to be deficient in a number of ways. The effector response of neonatal monocyte-derived macrophages (MDM) was investigated. Interferon-gamma induced the activation of indoleamine 2,3-dioxygenase in MDM and inhibited the growth of GBS. Both effects were enhanced by the addition of tumor necrosis factor-alpha to the culture conditions. The coincident supplementation of L-tryptophan with the bacteria abrogated the bacterial growth inhibition, thus confirming the causative role of L-tryptophan depletion. Control of the extracellular as well as intracellular L-tryptophan levels may thus be one of the effector mechanisms with which the immune system defends the host against GBS dissemination and disease.
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