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and IL-13 Synergistically Increase Eotaxin-1 Production in Human Airway Fibroblasts1
National Jewish Medical and Research Center and University of Colorado Health Sciences Center, Denver, CO 80206
Chronic diseases may involve an "innate" response followed by
an adaptive immune response, of a Th1 or Th2 variety. Little is known
regarding the interactions of these responses. We hypothesized that
TGF-
1 (innate response factor associated with wound repair) in
combination with IL-13 (Th2 factor) might augment inflammatory
processes associated with asthma. Airway fibroblasts were cultured from
asthmatic subjects and normal controls. These fibroblasts were exposed
to TGF-1 and IL-13 alone or in combination, and eotaxin-1 expression
and production were evaluated. At 48 h, eotaxin-1 production was
markedly increased with the combination of TGF-1 and IL-13
(p < 0.0001) compared with either stimulus alone.
mRNA increased slightly at 1 h with IL-13 or TGF-1 plus IL13,
peaked, and became significantly increased over IL-13 alone at 24
h. Protein was measurable from 6 h with IL-13 and TGF-1 plus
IL-13, but greater levels were measured over time with the combination.
Actinomycin ablated the increase in mRNA and protein seen with IL-13
alone and with TGF-1 plus IL-13. Cycloheximide blocked the increase
in mRNA at 6 h in both conditions, but also blocked the increase
at 24 h with TGF-1 plus IL-13. STAT-6 was rapidly activated
with both IL-13 and the combination, without difference. Finally,
eotaxin-1-positive fibroblasts were identified in severe asthma
biopsies in greater numbers than in normals. These results support the
concept that interactions of innate and adaptive immune systems may be
important in promoting the tissue eosinophilia of asthma, particularly
in those with more severe disease.
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