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Vol. 60, Issue 4, 646-655, October 2001
-Induced Interleukin-6 and RANTES in Human
Airway Smooth Muscle Cells: Role of p38 and p42/44 Mitogen-Activated
Protein Kinases
Department of Medicine, Pulmonary, Allergy, and Critical Care
Division, University of Pennsylvania Medical Center, Philadelphia,
Pennsylvania
Little information is available regarding the mechanisms involved in
cytokine-induced synthetic function of human airway smooth muscle (ASM)
cells. Here, we report that tumor necrosis factor receptor (TNFR)
1-induced p38 and p42/44 mitogen-activated protein kinase (MAPK)
activation modulates tumor necrosis factor-
(TNF)-mediated synthetic responses: expression of intercellular adhesion molecule-1 (ICAM-1) and secretion of interleukin (IL)-6 and the
regulated-on-activation, normal T-cell expressed and secreted (RANTES)
chemokine in human ASM cells. Pretreatment of ASM cells with SB203580,
a p38 MAPK inhibitor, slightly enhanced TNF-induced ICAM-1
expression in a dose-dependent manner but partially inhibited secretion
of RANTES and IL-6. In contrast, PD98059, a p42/44 inhibitor, reduced
ICAM-1 expression by 50% but had no effect on TNF-induced RANTES or IL-6 secretion. SB203580 and PD98059 had little effect on
TNF-induced nuclear factor-
B (NF-B) activation as determined
in cells transfected with a NF-B-luciferase reporter construct. We
also found that agonistic antibodies specific for either TNFR1 or TNFR2
stimulated IL-6 and RANTES secretion and activated p38 and p42/44
MAPKs. In addition, both antibodies induced NF-B-mediated gene
transcription. Using receptor-specific blocking antibodies, we found
that TNFR1 primarily regulates TNF-induced IL-6 and RANTES secretion
and activation of p38 and p42/44 MAPK pathways. Interestingly, we found
that TNFR1 and TNFR2 are expressed differently on the cell surface of
ASM cells. Our data suggest that despite the presence of functional
TNFR2, TNFR1 associated with MAPK-dependent and -independent pathways
is the primary signaling pathway involved in TNF-induced synthetic
functions in ASM cells.
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