Figure 5

Effect of A. phagocytophilum infection on host cells. A. phagocytophilum (Ap) infection causes cytoskeleton rearrangement required for infection, but in pigs it may also promote phagocytosis and autophagy for effective pathogen clearance. Ap delays the apoptotic death of neutrophils to increase infection, but different and complementary mechanisms may operate in human and pig cells. Pathogen infection stimulates innate immune and pro-inflammatory responses in both humans and pigs. IL-8 is likely secreted by infected neutrophils but monocytes, rather than neutrophils, are probably responsible for proinflammatory IL-1 beta and TNF-alpha cytokine production. The expression of genes involved in adaptive immunity was not impaired in pigs. ROS production is inhibited by pathogen infection of human neutrophils but although this mechanism was not found in pigs, upregulation of TGF-beta in infected pigs may inhibits NO production by suppressing STAT1 activation and accelerating iNOS protein degradation. The effect on lipid metabolism required for pathogen infection of human neutrophils was not found in pigs. Data for human neutrophils was obtained from the recent review by Severo et al. [43]