Actinobacillus pleuropneumoniae triggers IL-10 expression in tonsils to mediate colonisation and persistence of infection in pigs.

Actinobacillus pleuropneumoniae (APP) persisting in clinically healthy pigs may be the causative agent of sudden outbreaks of severe respiratory disease in swine herds. During the course of acute disease, the pathogen is eliminated from inflamed lung tissue, which is characterized by the expression of pro-inflammatory cytokines and an influx of neutrophils. However, if clearance by the porcine immune system fails, APP may switch to a persistent form. At later stages of infection, the pathogen may reside in tonsillar tissue without being eliminated by the host immune defence. To better understand the host immune response at different stages of infection, expression pattern of cytokines in tonsils and lung were recorded. In contrast to lung tissue, in which APP presence was associated with a pronounced pro-inflammatory character, APP presence in the tonsils elicited an increased IL-10 expression. In both organs of infected animals, a marked reciprocal correlation of the pro-inflammatory IL-17A and the anti-inflammatory IL-10 was found, supporting the idea that both cytokines are produced in highly associated, but reciprocal differentiated cell types, possibly APP-specific Th17 subsets. It appears that a persistent phenotype of APP triggers the anti-inflammatory immune response in tonsillar tissue in an attempt to evade the porcine immune defence.

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