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Tumor necrosis factor α plus interleukin 1β treatment protects granulocytopenic mice from Pseudomonas aeruginosa lung infection: Role of an unusual inflammatory response
Author(s) -
Amura CLAUDIA R.,
Fontan PATRICIA A.,
Sanjuan NORBERTO,
Nociari MARCELO M.,
Buzzola FERNANDA R.,
Sordelli DANIEL O.
Publication year - 1995
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1995.tb01131.x
Subject(s) - tumor necrosis factor alpha , pseudomonas aeruginosa , myeloperoxidase , bronchoalveolar lavage , immunology , cytokine , inflammation , interleukin , proinflammatory cytokine , lung , parenchyma , microbiology and biotechnology , biology , medicine , pathology , bacteria , genetics
We have recently demonstrated that treatment with interleukin 1β (IL‐1β) plus tumor necrosis factor a (TNFα) protects granulocytopenic hosts from Pseudomonas aeruginosa aerosol challenge. In this study we characterized the inflammatory response induced by P. aeruginosa in granulocytopenic mice treated with 2,000 U IL‐1β plus 2,000 U TNFα. Treatment with the nonsteroidal anti‐inflammatory agent piroxicam abolished both the protective effect of cytokine treatment and the increase in myeloperoxidase (MPO) pulmonary activity. Histopathological studies revealed that, after aerosol challenge with P. aeruginosa , treatment with these cytokines induced migration and extravasation of mononuclear cells of immature appearance into the lung parenchyma. These cells contained MPO in their cytoplasm and displayed phagocytic capacity. Resident alveolar macrophages exhibited signs of activation and appeared in reduced numbers in bronchoalveolar lavage fluid. We suggest that the inflammatory response promoted by low TNFα plus IL‐1β doses may be one mechanism responsible for protection of granulocytopenic hosts from P. aeruginosa aerosol challenge.