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

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 ne...

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Main Authors: C-D. Arreto, C. Dumarey, M-A. Nahori, B. B. Vargaftig
Format: Article
Language:English
Published: Wiley 1997-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1080/09629359791479
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author C-D. Arreto
C. Dumarey
M-A. Nahori
B. B. Vargaftig
author_facet C-D. Arreto
C. Dumarey
M-A. Nahori
B. B. Vargaftig
author_sort C-D. Arreto
collection DOAJ
description 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.
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spelling doaj-art-00a00e24333c44f789ae2f2cb725d8e52025-02-03T07:24:44ZengWileyMediators of Inflammation0962-93511466-18611997-01-0165-633534310.1080/09629359791479The LPS-induced neutrophil recruitment into rat air pouches is mediated by TNFα: likely macrophage originC-D. Arreto0C. Dumarey1M-A. Nahori2B. B. Vargaftig3Unité de Pharmacologie Cellulaire, Institut Pasteur, 25, rue du Dr Roux, Paris Cedex 15 75724, USAUnité de Pharmacologie Cellulaire, Institut Pasteur, 25, rue du Dr Roux, Paris Cedex 15 75724, USAUnité de Pharmacologie Cellulaire, Institut Pasteur, 25, rue du Dr Roux, Paris Cedex 15 75724, USAUnité de Pharmacologie Cellulaire, Institut Pasteur, 25, rue du Dr Roux, Paris Cedex 15 75724, USAThe 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.http://dx.doi.org/10.1080/09629359791479
spellingShingle C-D. Arreto
C. Dumarey
M-A. Nahori
B. B. Vargaftig
The LPS-induced neutrophil recruitment into rat air pouches is mediated by TNFα: likely macrophage origin
Mediators of Inflammation
title The LPS-induced neutrophil recruitment into rat air pouches is mediated by TNFα: likely macrophage origin
title_full The LPS-induced neutrophil recruitment into rat air pouches is mediated by TNFα: likely macrophage origin
title_fullStr The LPS-induced neutrophil recruitment into rat air pouches is mediated by TNFα: likely macrophage origin
title_full_unstemmed The LPS-induced neutrophil recruitment into rat air pouches is mediated by TNFα: likely macrophage origin
title_short The LPS-induced neutrophil recruitment into rat air pouches is mediated by TNFα: likely macrophage origin
title_sort lps induced neutrophil recruitment into rat air pouches is mediated by tnfα likely macrophage origin
url http://dx.doi.org/10.1080/09629359791479
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