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Published online before print April 14, 2005
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[CCL3] acting on the CCR1 receptor mediates neutrophil migration in immune inflammation via sequential release of TNF- and LTB4
,
* Departments of Pharmacology and
Biochemistry and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil;
Department of Microbiology and Parasitology, Federal University of Rio Grande do Norte, Natal, RN, Brazil; and
Division of Pulmonary & Critical Care Medicine and
¶ Department of Pathology, University of Michigan, Ann Arbor
1 Correspondence: Departamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, USP, Avenida Bandeirantes, 3900 Ribeirão Preto, São Paulo, 14049-900 (Brazil). E-mail: fdqcunha{at}fmrp.usp.br
In the present study, we investigated the involvement of macrophage-inflammatory protein-1
(MIP-1)[CC chemokine ligand 3 (CCL3)], MIP-1ß[CCL4], regulated on activation, normal T expressed and secreted (RANTES)[CCL5], and CC chemokine receptors (CCRs) on neutrophil migration in murine immune inflammation. Previously, we showed that ovalbumin (OVA)-triggered neutrophil migration in immunized mice depends on the sequential release of tumor necrosis factor (TNF-) and leukotriene B4(LTB4). Herein, we show increased mRNA expression for MIP-1[CCL3], MIP-1ß[CCL4], RANTES[CCL5], and CCR1 in peritoneal cells harvested from OVA-challenged, immunized mice, as well as MIP-1[CCL3] and RANTES[CCL5] but not MIP-1ß[CCL4] proteins in the peritoneal exudates. OVA-induced neutrophil migration response was muted in immunized MIP-1[CCL3]–/– mice, but it was not inhibited by treatment with antibodies against RANTES[CCL5] or MIP-1ß[CCL4]. MIP-1[CCL3] mediated neutrophil migration in immunized mice through induction of TNF- and LTB4 synthesis, as these mediators were detected in the exudates harvested from OVA-challenged immunized wild-type but not MIP-1[CCL3]–/– mice; administration of MIP-1[CCL3] induced a dose-dependent neutrophil migration, which was inhibited by treatment with an anti-TNF- antibody in TNF receptor 1 (p55–/–)-deficient mice or by MK 886 (a 5-lipoxygenase inhibitor); and MIP-1[CCL3] failed to induce LTB4 production in p55–/– mice. MIP-1[CCL3] used CCR1 to promote neutrophil recruitment, as OVA or MIP-1[CCL3] failed to induce neutrophil migration in CCR1–/– mice, in contrast to CCR5–/– mice. In summary, we have demonstrated that neutrophil migration observed in this model of immune inflammation is mediated by MIP-1[CCL3], which via CCR1, induces the sequential release of TNF- and LTB4. Therefore, whether a similar pathway mediates neutrophil migration in human immune-inflammatory diseases, the development of specific CCR1 antagonists might have a therapeutic potential.
Key Words: chemokines • chemokine receptors • chemotaxis
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