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*
Immunopharmacology, Departamento de Bioquímica e Imunologia, Instituto Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil;
Departmento de Fisiologia e Farmacodinâmica, Instituto Oswaldo Cruz, Fundaçao Oswaldo Cruz, Rio de Janeiro, Brazil;
Serono Pharmaceuticals, Geneva, Switzerland; and
Department of Pathology, University of Michigan, Ann Arbor, MI 48109
The understanding of the mechanisms underlying eosinophil
recruitment in vivo may aid in the development of novel strategies for
the treatment of allergic disorders. In this study, we investigated the
role of chemokines in the cascade of events leading to eosinophil
recruitment in a stem cell factor (SCF)- and leukotriene B4
(LTB4)-dependent allergic pleurisy model in mice. The
intrapleural administration of the eosinophil-active chemokines
eotaxin, RANTES, and macrophage-inflammatory protein 1
(MIP-1) induced a time- and dose-dependent eosinophil recruitment.
Pretreatment with anti-eotaxin, but not anti-RANTES or
anti-MIP-1, blocked the recruitment of eosinophils following Ag
challenge of sensitized animals, and significant eotaxin
immunoreactivity was detected in the pleural cavity of these animals.
Similarly, only the anti-eotaxin inhibited the eosinophil
recruitment induced by injection of SCF in naive animals. However,
blockade of SCF did not inhibit the release of eotaxin after Ag
challenge of sensitized mice. Akin to its effects on SCF and in the
allergic reaction, eotaxin-induced eosinophil recruitment was blocked
by the LTB4 receptor antagonist CP105696. Nevertheless,
SCF, but not eotaxin, appeared to regulate the endogenous release of
LTB4 after Ag challenge. Finally, we show that low doses of
eotaxin synergized with LTB4 to induce eosinophil
recruitment in the pleural cavity. Overall, the present results show
that eotaxin and SCF-induced LTB4 cooperate to induce
eosinophil recruitment into sites of allergic inflammation. Cooperation
between inflammatory mediators must be an important phenomenon in vivo,
explaining both the ability of lower concentrations of mediators to
induce a full-blown functional response and the effectiveness of
different strategies at inhibiting these
responses.
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