Inflammatory cytokine expression in swine experimentally infected with Actinobacillus pleuropneumoniae
1995
Baarsch, M.J. | Scamurra, R.W. | Burger, K. | Foss, D.L. | Maheswaran, S.K. | Murtaugh, M.P.
An Actinobacillus pleuropneumoniae infection model in swine was established to study the expression of inflammatory cytokines during acute respiratory disease. Lavage fluid, ravage cells consisting primarily of alveolar macrophages, and lung tissue were analyzed for the presence of various cytokines at 2, 4, 8, and 24 h following endotracheal inoculation of A. pleuropneumoniae. Interleukin-1 beta (IL-1) and 1L-8 mRNA levels were elevated within 2 h in ravage cells of animals inoculated with A. pleuropneumoniae but not in cells from controls treated with saline-bovine serum albumin, based on Northern (RNA blot) analysis. Tumor necrosis factor (TNF) mRNA was present at low levels in all animals, and the level was not increased at any time point. In situ hybridization was more sensitive than Northern blotting and revealed elevations of all three cytokines in ravage cells within 2 to 4 h of A. pleuropneumoniae inoculation. IL-6 was detected in ravage cells by in situ hybridization but not by Northern blotting. In lung tissue obtained 18 to 24 h after A. pleuropneumoniae instillation, all cytokine mRNAs, including that of 1L-6, were detected by Northern blot analysis. The levels of bioactive IL-1 and 1L-6 in ravage fluids increased approximately 1,000-fold following A. pleuropneumoniae inoculation, but TNF bioactivity was not detected. Morphological localization of cytokine mRNAs by in situ hybridization indicated markedly increased levels of TNF, IL-1, and IL-8 mRNAs at the periphery of focal lung lesions. These findings indicate that inflammatory cytokines, particularly 1L-1 and IL-8, are associated with the development of pleuropneumonia and may contribute to disease severity.
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