Gene expression in pigs (Sus scrofa) infected with Anaplasma phagocytophilum

Abstract

Anaplasma phagocytophilum infects a wide variety of hosts and causes granulocytic anaplasmosis in humans, horses and dogs and tick-borne fever in ruminants. Infection with A. phagocytophilum results in the modification of host gene expression and immune response. The objective of this research was to characterize gene expression in pigs (Sus scrofa) naturally and experimentally infected with A. phagocytophilum. For gene expression analysis in naturally infected pigs, microarray hybridization was used. Differential expression of immune response genes was analyzed by real-time RT-PCR in naturally and experimentally infected pigs. A. phagocytophilum infection affected cytoskeleton rearrangement and increased both innate and adaptive immune responses by upregulation of interleukin 1 receptor accessory protein-like 1 (IL1RAPL1), T-cell receptor alpha chain (TCR-alpha), hrombospondin 4 (TSP-4) and Gap junction protein alpha 1 (GJA1) genes. These results suggested that pigs are susceptible to A. phagocytophilum while be able to control infection, particularly through activation of innate immune responses, phagocytosis and autophagy. This fact may account for the low infection prevalence detected in pigs and thus their low or lack of impact as a reservoir host for this pathogen. These results advanced our understanding of the molecular mechanisms at the host-pathogen interface and suggested a role for newly reported genes in the protection of pigs against A. phagocytophilum.