Abstract
BackgroundThe objective of this study was to elucidate the pathogenic mechanisms of how Mycoplasma hyopneumoniae enhances secondary Pasteurella multocida type A infection which leads to porcine enzootic pneumonia in infected pigs. Sixteen pigs were experimentally infected with M. hyopneumoniae and then euthanized at 7, 14, 21 and 28 days post inoculation. In situ hybridization for M. hyopneumoniae DNA and Ulex europaeus agglutinin-I (UEA-I) lectin histochemistry for fucosyl glycoconjugate, was performed in serial lung sections to determine alteration of fucosyl glycoconjugate in M. hyopneumoniae-infected bronchial and bronchiolar epithelium. Bacterial overlay assay was performed to determine the affinity of P. multocida type A with L-fucose.ResultsThe luminal surface of bronchial and bronchiolar epithelial cells that were stained with UEA-I always showed hybridization signals for M. hyopneumoniae but it was negative in the unaffected parts of the lung from M. hyopneumoniae-infected pigs and in lung from negative control pigs. Colocalization of M. hyopneumoniae and UEA-I was especially prominent in the luminal surface of bronchial and bronchiolar epithelial cells in serial section of lung. The mean number of M. hyopneumoniae-positive cells correlated with the mean number of UEA-I-positive cells in lungs from infected pigs throughout the experiment. All eight P. multocida type A isolates from naturally occurring enzootic pneumonia, bound strongly at levels of 2 μg and 5 μg of L-fucose.ConclusionsThe results of the present study demonstrate that M. hyopneumoniae increases the L-fucose composition to enhance adherence of P. multocida type A to the bronchial and bronchiolar epithelial cells.
Highlights
The objective of this study was to elucidate the pathogenic mechanisms of how Mycoplasma hyopneumoniae enhances secondary Pasteurella multocida type A infection which leads to porcine enzootic pneumonia in infected pigs
M. hyopneumoniae DNA was detected at the luminal surface of bronchial and bronchiolar epithelial cells (Fig. 1a), alveolar (Fig. 2a) and interstitial macrophages, and type I pneumocytes (Fig. 2b) in the lung from all infected pigs at 7, 14, 21, and 28 dpi
A positive hybridization signal was especially intense at the luminal surface of bronchial and bronchiolar epithelial cells, whereas the hybridization was sparse in alveolar and interstitial macrophages, and type I pneumocytes
Summary
The objective of this study was to elucidate the pathogenic mechanisms of how Mycoplasma hyopneumoniae enhances secondary Pasteurella multocida type A infection which leads to porcine enzootic pneumonia in infected pigs. Altered composition of glycoconjugates as the result of mycoplasmal infection may be one factor that predisposes pigs to enhance secondary P. multocida type A infection in the lung. It has been reported that infection with M. hyopneumoniae enhances Ulex europaeus agglutinin-I (UEA-I), which has affinity of glycoconjugates for L-fucose residues, in ciliated epithelium of the respiratory tract in infected pigs [10]. These results suggest that M. hyopneumoniae infection can alter the composition of glycoconjugates to render the lungs susceptible to P. multocida type A infection
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