Increased Production of Proinflammatory Cytokines following Infection with Porcine Reproductive and Respiratory Syndrome Virus and Mycoplasma hyopneum

30-09-2004


Article by:
R Thanawongnuwech, Brad Thacker, [...], and Eileen L. Thacker.

This study was performed in order to characterize the interaction between PRRSv and M. hyopneumoniae in pigs. It was designed to better understand the pathogenesis of PRRSV and M.hyo their effects on the respiratory immune system. The study investigated the induction of proinflammatory cytokines produced by macrophages after an infection with PRRSV and/or M. hyopneumoniae.

6 piglets were euthanized at 7 weeks of age for the in-vitro studies: tracheal rings were cultured and inoculated as well.
70 piglets of 10-12 days of selected (PRRSV and M.hyo negative) and used for the in vivo studies: they were assigned to 4 different groups (Control, M.hyo+, PRRS+ and M.hyo-PRRS+) and inoculated at 6 weeks of age. Clinical evaluation was performed daily from 0 to 10dpi and every other day from 11 to 20dpi, and pigs from each group were euthanized on days 10, 28 and 42 in order to necropsy them. BAL was performed to collect epithelial lining fluid and PAMs.
The results suggest that the two pathogens have a great effect on cytokine production, which may play a role in the induction of disease and the persistence of the organisms in the host.

In general, it was seen in the in vivo and in vitro studies that when pigs or tracheal cultures were inoculated/incubated with M. hyopneumoniae and PRRSV, the induced levels of proinflammatory cytokines were higher than the levels detected when only one pathogen was present.
The presence of PRRSV amplified the severity of mycoplasmal pneumonia. The severity of viral pneumonia did not depend on the degree of mycoplasmal pneumonia, pigs with low mycoplasmal pneumonia lesions had increased viral pneumonia compared to pigs only infected with PRRSv.

The specific mechanisms, by which M. hyopneumoniae enhances PRRSV pneumonia are not determined. One example could be that M. hyopneumoniae enhances production of IL-10, which inhibits the apoptosis of PAMs, and this increases the number of macrophages susceptible to infection by the virus.

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