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Endogenous Tumor Necrosis Factor (TNF) α Mediates Neutrophil Accumulation at the Mid‐Phase of a Murine Model of Pseudomonas aeruginosa Pneumonia
Author(s) -
Sonoda Fuminari,
Oishi Kazunori,
Iwagaki Akitaka,
Matsumoto Keizo
Publication year - 1997
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1997.tb01898.x
Subject(s) - tumor necrosis factor alpha , bronchoalveolar lavage , antiserum , immunology , biology , neutrophil extracellular traps , pneumonia , endogeny , immune system , lung , inflammation , medicine , endocrinology , antibody
To determine the role of endogenous tumor necrosis factor (TNF) α on neutrophil influx into the lungs in acute Pseudomonas aeruginosa pneumonia, we evaluated TNF α activity, inflammatory cell response and neutrophil chemotactic activity in the bronchoalveolar lavage fluids (BALFs) of P. aeruginosa‐ infected mice. In the case of fatal pneumonia, the TNF α activity in the BALFs appeared within 3 hr, peaked at 6–12 hr and attenuated within 24 hr after intratracheal challenging, while no TNF α activity was detected in the plasma. The elevation of TNF α activity in the BALFs was closely associated with neutrophil accumulation. Mirroring the TNF α activity response and the influx of neutrophils into the murine airway, the number of neutrophils in the BALFs increased within 3 hr, peaked at 6–12 hr and remained elevated up to 24 hr after challenging. Neutralization of the TNF α activity in the BALFs with anti‐murine TNF antiserum decreased the level of neutrophil migration by BALF 45.0–49.7% at 6 hr and 49.3–54.2% at 12 hr, while the neutralizing antiserum had no effect on the level of neutrophil migration by BALFs at 3 and 24 hr. Furthermore, the intravenous administration of anti‐murine TNF antiserum 2 hr before challenging significantly inhibited neutrophil migration into the lungs of mice with sublethal pneumonia ( P < 0.05; compared with mice receiving pre‐immune serum). These data suggest that intra‐alveolar TNF α plays an important role in causing lung neutrophil accumulation at the mid‐phase of murine P. aeruginosa pneumonia.