Background:
Basophils are an
active participant
in the pathogenesis
of local
inflammation in
allergic diseases
such as asthma, but
it is not fully
known how basophil
activation is
regulated in
inflamed tissue.
Objective: In
order to clarify the
control mechanisms
of basophil
activation in
chronic inflammation
and at remodeling
sites, we analyzed
the effects of fi
broblast-derived
cytokines, stem cell
factor (SCF), and
insulinlike growth
factor-I (IGF-I) on
basophils.
Methods: The effects
of SCF and IGF-I on
degranulation and
surface activation
marker expression by
basophils were
assessed and
compared.
Results: SCF
enhanced human
basophil histamine
release elicited by
some, but not all,
secretagogues;
degranulation in
response to IgE- or
FcεRI-mediated
stimulation and
12-o-tetradecanoyl-phorbol-13-acetate
(TPA) was enhanced
by SCF. SCF slightly
enhanced ionophore
A23187-induced
histamine release by
basophils from some
donors, but it
failed to affect the
release elicited by
monocyte
chemoattractant
protein-1 (MCP-1),
formylmethionyl-leucyl-phenylalanine
(FMLP) or C5a. The
repertoire of
secretagogues
responsive to SCF
was similar to that
of IGF-I. Expression
levels of both CD11b
and CD69 markers
were significantly
enhanced by the
combination of SCF
and IGF-I.
Conclusions:
These results
suggest that SCF and
IGF-I may modify the
activation of
basophils in a
similar and/or
synergistic fashion.
Interaction of
basophils with these
cytokines might be
involved in the
pathogenesis of
local inflammation
and the remodeling
process in asthma.
Key words:
Basophils.
Insulin-like growth
factor. Stem cell
factor.
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