Anaplasma phagocytophilum inhibe la apoptosis y promueve la reorganización del citoesqueleto para la infección de células de garrapata

Anaplasma phagocytophilum causes human granulocytic anaplasmosis. Infection with this zoonotic pathogen affects gene expression in both vertebrate host and the tick vector, Ixodes scapularis. Here, we identified new genes, including spectrin alpha chain or alpha-fodrin (CG8) and voltage-dependent anion-selective channel or mitochondrial porin (T2), that are involved in A. phagocytophilum infection/multiplication and the tick cell response to infection. The pathogen downregulated the expression of CG8 in tick salivary glands and T2 in both the gut and salivary glands to inhibit apoptosis as a mechanism to subvert host cell defenses and increase infection. In the gut, tick response to infection through CG8 upregulation was used by the pathogen to increase infection due to cytoskeleton rearrangement that is required for pathogen infection. These results increased our understanding of the role of tick genes during A. phagocytophilum infection and multiplication and demonstrated that the pathogen uses similar strategies to establish infection in both vertebrate and invertebrate hosts.

tick cell infestation anaplasma

 Mitochondrially-induced apoptosis pathway showing the effect of A. phagocytophilum infection on reducing T2 levels which results in the inhibition of tick cell apoptosis.

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Ayllón, N., Villar, M., Busby, A.T., Kocan, K.M., Blouin, E.F., Bonzón-Kulichenko, E., Galindo, R.C., Mangold, A.J., Alberdi, P., Pérez de la Lastra, J.M., Vázquez, J., de la Fuente, J. 2013. Anaplasma phagocytophilum inhibits apoptosis and promotes cytoskeleton rearrangement for infection of tick cells. Infection and Immunity 81: 2415-2425.

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