IMPAIRMENT OF NON-PHAGOCYTOSIS-ASSOCIATED OXIDATIVE BURST TOACTINOBACILLUS PLEUROPNEUMONIAEIN PORCINE NEUTROPHILS INDUCED BY PSEUDORABIES VIRUS

Abstract

In industrial swine production, several important viral diseases are frequently complicated with bacterial infections, suggestive of virus–bacteria synergism. Although most virus-induced leukocyte dysfunctions are attributed to monocytes and lymphocytes, the role of polymorphonuclear cells (PMNs, mainly neutrophils) should not be excluded, because they are the first leukocytes to respond to inflammation. Previous studies indicated that pseudorabies virus (PrV) blocked the indirect recruitment of PMNs by inhibiting the production of interleukin-8 by primed peripheral blood mononuclear cells (PBMCs) and also reduced the phorbol 12-myristate 13-diacetate (PMA)-induced oxidative burst (OB) in PMNs. This study used PrV as a model to explore other possibilities of virus-induced PMN dysfunctions in pigs. The goals were: (1) to develop assay for simultaneous evaluation of phagocytosis and OB to Actinobacillus pleuropneumoniae (APP) and (2) to evaluate whether PrV could affect these responses to APP in an ex vivo setting. Approximately 12% of the PMNs underwent phagocytosis, as indicated by the presence of intracellular propidium iodide(PI)-labeled APP (PI-APP), and 32% of the PMNs launched OB to APP, as detected by dihydrorhodamine (DHR). Approximately 86% of those OB responsive cells did not contain engulfed PI-APP, and the OB was presumably induced by the bacteria lipopolysaccharide (LPS). Only 5 ± 1% of the cells underwent simultaneous phagocytosis and OB. Under certain conditions, PrV reduced the non-phagocytosis-associated OB by approximately 40% (p < 0.05), while the phagocytosis was unaffected overall. These results suggest that PrV may interfere with bacteria LPS-mediated signaling, suggesting a possibility of PrV-APP synergism in causing pneumonia.