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B and IL-8 in human bronchial
epithelial cells
Pulmonary and Critical Care Medicine, Stanford University Medical Center, Stanford, California 94305-5236
In 16HBE transformed human bronchial
epithelial cells, histamine stimulated interleukin (IL)-8 mRNA and
protein secretion, and this histamine stimulation was inhibited by the
H1-receptor antagonist diphenhydramine (DPH), by the
inhibitor of 5-lipoxygenase-activating protein (FLAP) MK-886, by the
5-lipoxygenase inhibitor Zileuton, and by dexamethasone. Histamine
stimulated bronchial epithelial cell production of leukotriene
B4
(LTB4), and this production was
inhibited by FLAP inhibitors MK-886 and L-655,238 and Zileuton. Histamine stimulated IL-8 luciferase reporter gene activity that was
inhibited with DPH, dexamethasone, MK-886 and L-655,238, and Zileuton.
The inhibition of IL-8 transcription and protein secretion by FLAP
inhibitors and Zileuton was reversed with exogenous
LTB4. There was increased IL-8
nuclear factor-
B (NF-B) DNA-binding activity after histamine
stimulation, and this was inhibited by DPH and MK-886. Cytoplasmic
phospholipase A2 mRNA levels were also potently induced by histamine. Thus histamine stimulation of
bronchial epithelial cells involves binding at H1
receptors, production of LTB4,
activation of NF-B and increased expression of IL-8.
inflammation; cytokine; transcription; Zileuton; phospholipase
A2; nuclear factor-B; interleukin-8
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