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Originally published online as doi:10.1189/jlb.0108009 on February 2, 2009

Published online before print February 2, 2009
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(Journal of Leukocyte Biology. 2009;85:855-861.)
© 2009 Society for Leukocyte Biology

Migration inhibitory factor (MIF) released by macrophages upon recognition of immune complexes is critical to inflammation in Arthus reaction

Claudia N. Paiva*,1, Rosa H. Arras*,1, Elisabeth S. Magalhães*, Letícia S. Alves*, Luiz Paulo Lessa*, Maria Helena Silva*, Regina Ejzemberg*, Cláudio Canetti{dagger} and Marcelo T. Bozza*,2

* Departamento de Imunologia, Instituto de Microbiologia Prof. Paulo de Góes, and
{dagger} Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro-UFRJ, Rio de Janeiro, Brazil

2 Correspondence: Departamento de Imunologia, Instituto de Microbiologia, CCS Bloco I, UFRJ. Avenida Carlos Chagas Filho, 373 Cidade, Universitária, Rio de Janeiro, RJ, 21941-902 Brazil. E-mail: mbozza{at}micro.ufrj.br or mtbozza{at}gmail.com

ABSTRACT

Deposition of immune complexes (IC) triggers Fc{gamma}R-dependent inflammation, leading to tissue damage in rheumatoid arthritis, systemic lupus erythematous, immune glomerulonephritis, and several immune vasculitides. Evidences support a role for macrophage migration inhibitory factor (MIF) in a number of inflammatory diseases, but the triggering of its secretion and its physiopathological role upon IC deposition remain elusive. Herein, we show that human macrophages secreted MIF after IC recognition, which in turn controlled the secretion of TNF. Macrophages from Mif–/– mice produced smaller amounts of TNF when stimulated with IgG-opsonized erythrocytes than wild-type (WT) cells. Using passive reverse Arthus reaction in the peritoneum and lungs as a model for IC-induced inflammation, we demonstrated that Mif–/– mice had a milder response, observed by reduced neutrophil recruitment, vascular leakage, and secretion of TNF, MIP-2, and keratinocyte-derived chemokine compared with WT controls. Adoptive transfer of alveolar macrophages from WT to Mif–/– mice rescued pulmonary neutrophil recruitment and TNF production upon passive reverse Arthus reaction. Our study indicates that Arthus inflammatory reaction is largely dependent on MIF and poses macrophages as a source of the MIF released upon IC recognition. These results give experimental support to the proposition that blockade of MIF might constitute an adjunctive, therapeutic approach to IC disease.

Key Words: monocytes • cytokines • Fc receptors




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