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Shawn J. Skerrett, Gregory J. Bagby, Rodney A. Schmidt, Steve Nelson, Antibody-Mediated Depletion of Tumor Necrosis Factor-α Impairs Pulmonary Host Defenses to Legionella pneumophila, The Journal of Infectious Diseases, Volume 176, Issue 4, October 1997, Pages 1019–1028, https://doi.org/10.1086/516530
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Abstract
Tumor necrosis factor-α (TNF-α) has been shown to stimulate the resistance of alveolar macrophages and neutrophils to Legionella pneumophila in vitro. To determine whether endogenous TNF-α is necessary for host defense against legionellosis in vivo, anti-TNF-α IgG or control IgG was administered to rats exposed to aerosolized L. pneumophila. Treatment with anti-TNF-a neutralized >90% of the intrapulmonary TNF-α response to infection, resulting in persistent pneumonitis and failure to clear L. pneumophila from the lungs. Depletion of TNF-α limited the recruitment of mononuclear cells to the lungs and resulted in a progressive increase in the proportion of alveolar macrophages that were infected; neutrophil recruitment and phagocytosis were not impaired. Both systemic and intrapulmonary IFN-γ levels were significantly higher in rats depleted of TNF-α. These observations indicate that TNF-α is required for the prompt resolution of pneumonic legionellosis and point to a direct role for TNF-α in the activation of phagocytes.
