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Gene Expression in Activated Alveolar Macrophages: Decreased NF-
B Activation and IB Kinase Activity1
Department of Developmental Biochemistry, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY 10314
Taurine prevents tissue damage in a variety of models that involve
inflammation, including oxidant-induced lung damage. The mechanism of
protection is uncertain, but is postulated to involve the actions of
taurine chloramine (Tau-Cl) derived via halide-dependent
myeloperoxidase associated with neutrophils. Understanding the
influence of Tau-Cl on the production of inflammatory mediators by
alveolar macrophages provides an opportunity for determining the
mechanism of Tau-Cl action. The effects of Tau-Cl were evaluated on the
production of NO and TNF-
in NR8383, a cloned cell line derived from
rat alveolar macrophages (RAM), and in primary cultures of RAM.
Production of NO and TNF-, and expression of inducible NO synthase
was inhibited by Tau-Cl in activated NR8383 cells as well as in RAM.
Temporal (2, 4, 8, 24 h) expression of inducible NO synthase and
TNF- mRNAs was reduced by Tau-Cl in NR8383 cells. Tau-Cl depressed
NF-
B migration into the nucleus of activated NR8383 cells and caused
a more sustained presence of IB in the cytoplasm. Stabilization of
cytoplasmic IB- in Tau-Cl-treated cells resulted from decreased
phosphorylation of IB- serine-32 and a lower activity of IB
kinase (IKK). Additional experiments demonstrated that Tau-Cl does not
directly inhibit IKK activity. These results suggest that Tau-Cl exerts
its effects at some level upstream of IKK in the signaling pathway and
inhibits production of inflammatory mediators through a mechanism that,
at least in part, involves inhibition of NF-B
activation.
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