Migração de neutrofilos induzida por enterotoxinas estafilococicas para a cavidade peritoneal de camundongos : participação de macrofagos

AUTOR(ES)
DATA DE PUBLICAÇÃO

1999

RESUMO

In this study, the role role of macrophages in the neutrophil migration induced by staphylococcal enterotoxins A (SEA) and B (SEB) into the mouse peritoneal cavity was investigated. SEA and SEB induced dose- and timedependent neutrophil migration into the mouse peritoneal cavity. This migration was potentiated when the macrophage population was increased by pre-treating the mice with thioglycolate, and was reduced when the peritoneal cavities were washed with sterile saline. These results indicated that the neutrophil recruitment induced by these toxins was dependent on the number of resident macrophages. Dexamethasone inhibited the neutrophil migration induced by SEA and SEB. A similar response was observed with the P AF receptor antagonist (BN52021), the histamine H2 receptor (cimetidine), the lipoxygenase inhibitor (BW A4C) and a sensory C-fiber neuropeptide depletor (capsaicin). In contrast, indomethacin had no effect on the neutrophil chemotaxis. Thus, lipoxygenase metabolites, P AF, histamine and neuropeptides from sensory neurons play an important role in the neutrophil migration induced by SEA and SEB. When stimulated with SEA or SEB in vitro, mouse peritoneal macrophages secreted thermolabile proteins which induced neutrophil migration into the peritoneal cavities of naive mice. The release of these proteins was dose- and time-dependent and was inhibited by dexamethasone but not by indomethacin or BW755C The molecular mass of the neutrophil chemotactic protein secreted by SEB-stimulated macrophages was 1-3 kDa while that of the protein secreted by SEA was >100 kDa. The neutrophil migration induced by supematants from SEB-stimulated macrophages involved inflammatory mediators such as lipoxygenase metabolites, P AF and histamine. In contrast, these same mediators had no role in the neutrophil migration induced by supematants from SEA-stimulated macrophages, suggesting that the neutrophil chemotactic proteins described above, induce neutrophil accumulation by different mechanisms. Capsaicin and neurokinin1 (NKl) receptor antagonist SR140333 reduced the neutrophil recruitment induced by supematants from macrophage monolayers stimulated with SEA or SEB. In contrast, the neurokinin2 (NK2) receptor antagonist SR48968 had no effect on the neutrophil migratory response of the supematants. These results suggest that the neutrophil migration induced by these chemotactic proteins may involve the release of neuropeptides such as SP from sensory neurons. lu conc1usion, macrophage products may play an important role in the neurogenic inflammation .induced by SEA and SEB by releasing specific chemotactic proteins

ASSUNTO(S)

enterotoxinas macrofagos

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