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. 2017 Jul 5;7:307. doi: 10.3389/fcimb.2017.00307

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Copyright © 2017 Contreras, Alberdi, Mateos-Hernández, Fernández de Mera, García-Pérez, Vancová, Villar, Ayllón, Cabezas-Cruz, Valdés, Stuen, Gortazar and de la Fuente.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Anaplasma phagocytophilum HSP70 and MSP4 are necessary for pathogen infection of host cells. Based on the results of this study, a model was developed to explain the role of HSP70 and MSP4 during pathogen infection of host cells. HSP70 and MSP4 form a complex on the bacterial membrane where MSP4 probably acts a doking protein for HSP70. The incubation of HL60 human cells with recombinant HSP70 or MSP4-HSP70 interacting proteins inhibits infection by interfering with pathogen interaction with host cells mediated by HSP70, which is necessary for infection. However, the addition of recombinant MSP4 does not affect infection because the interaction of bacterial HSP70 with host cells occurs and is sufficient for infection. The anti-MSP4 antibodies probably inhibit infection through binding to MSP4 at the MSP4-HSP70 interaction site, thus preventing HSP70 adhesion to host cells. The anti-HSP70 antibodies bind to HSP70 and prevent the interaction with host cells required for pathogen infection.