The LPS-induced neutrophil recruitment into rat air pouches is mediated by TNFα: likely macrophage origin

• Main Authors: C-D. Arreto (Author), C. Dumarey (Author), M-A. Nahori (Author), B. B. Vargaftig (Author)
• Format: Book
• Published: Hindawi Limited, 1997-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

The role of resident cells during the lipopolysaccharide (LPS)-induced neutrophil recruitment into rat air pouches was investigated. In this model, LPS (Escherichia coli, O55: B5 strain; 2-2000 ng) induced a dose- and time-dependent neutrophil recruitment accompanied by the generation of a tumour necrosis factor-α (TNFα)-like activity. Dexamethasone (0.05-5 mug) and cycloheximide (6 ng), injected 2 h before LPS into the pouches, inhibited the neutrophil recruitment and the generation of the TNFα-like activity, while the H1-receptor antagonist mepyramine (1 and 4 mg/kg, i.p., 0.5 h before LPS) and the PAF-receptor antagonist WEB 2170 (0.05 and 1 mg/kg, i.p., 0.5 h before LPS) had no effect. Purified alveolar macrophages (AM) were used to replenish the pouches of cycloheximide-treated recipient rats. AM provided by PBS-treated animals led to the recovery of the LPS-induced neutrophil recruitment and of the TNFα-like formation contrasting with those from cycloheximide-treated animals (1 mg/kg, i.p.). When delivered in situ, liposome-encapsulated clodronate, a macrophage depletor, significantly impaired both the LPSinduced neutrophil recruitment and the TNFα-like activity. An anti-murine TNFα polyclonal antibody (0.5 h before LPS) was also effective. These results emphasize the pivotal role of macrophages for LPS-induced neutrophil recruitment via the formation of TNFα.

Item Description

0962-9351
1466-1861
10.1080/09629359791479