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Comparative Proteomics Identifies Host Immune System Proteins Affected by Infection with Mycobacterium bovis

AutorLópez, Vladimir; Villar, Margarita ; Queirós, João ; Vicente, Joaquín ; Mateos-Hernández, Lourdes ; Díez-Delgado, Iratxe ; Contreras, Marinela; Alves, Paulo C.; Alberdi, Pilar ; Gortázar, Christian ; Fuente, José de la
Fecha de publicación30-mar-2016
EditorPublic Library of Science
CitaciónPLoS Neglected Tropical Diseases 10(3): e0004541 (2016)
Resumen[Abstract] Mycobacteria of the Mycobacterium tuberculosis complex (MTBC) greatly impact human and animal health worldwide. The mycobacterial life cycle is complex, and the mechanisms resulting in pathogen infection and survival in host cells are not fully understood. Eurasian wild boar (Sus scrofa) are natural reservoir hosts for MTBC and a model for mycobacterial infection and tuberculosis (TB). In the wild boar TB model, mycobacterial infection affects the expression of innate and adaptive immune response genes in mandibular lymph nodes and oropharyngeal tonsils, and biomarkers have been proposed as correlates with resistance to natural infection. However, the mechanisms used by mycobacteria to manipulate host immune response are not fully characterized. Our hypothesis is that the immune system proteins under-represented in infected animals, when compared to uninfected controls, are used by mycobacteria to guarantee pathogen infection and transmission. To address this hypothesis, a comparative proteomics approach was used to compare host response between uninfected (TB-) and M. bovis-infected young (TB+) and adult animals with different infection status [TB lesions localized in the head (TB+) or affecting multiple organs (TB++)]. The results identified host immune system proteins that play an important role in host response to mycobacteria. Calcium binding protein A9, Heme peroxidase, Lactotransferrin, Cathelicidin and Peptidoglycan-recognition protein were under-represented in TB+ animals when compared to uninfected TB- controls, but protein levels were higher as infection progressed in TB++ animals when compared to TB- and/or TB+ adult wild boar. MHCI was the only protein over-represented in TB+ adult wild boar when compared to uninfected TB- controls. The results reported here suggest that M. bovis manipulates host immune response by reducing the production of immune system proteins. However, as infection progresses, wild boar immune response recovers to limit pathogen multiplication and promote survival, facilitating pathogen transmission.
[Author Summary] Mycobacteria of the Mycobacterium tuberculosis complex (MTBC) are zoonotic pathogens representing a serious health problem for humans and animals worldwide. The life cycle of mycobacteria is complex, and the mechanisms resulting in pathogen infection and survival in host cells are not fully understood. Eurasian wild boar are natural reservoir hosts for MTBC and a model for mycobacterial infections and tuberculosis. The results of this study broaden our understanding of the molecular epidemiology of zoonotic tuberculosis and fill important gaps in knowledge of this topic. The results suggested that mycobacteria manipulate host immune response by reducing the production of immune system proteins. However, as infection progresses, wild boar immune response recovers to limit pathogen multiplication and promote survival, facilitating pathogen transmission. As previously reported in other obligate intracellular bacteria, host-mycobacteria interactions probably reflect a co-evolutionary process in which pathogens evolved mechanisms to subvert host response to establish infection, but hosts also evolved mechanisms to limit pathogen infection and promote survival. Subsequently, mycobacteria benefit from host survival by increasing the probability for transmission to continue their life cycle. These results provide relevant information to develop tools to evaluate risks for tuberculosis caused by MTBC and for disease control in humans and animals.
Versión del editorhttps://doi.org/10.1371/journal.pntd.0004541
URIhttp://hdl.handle.net/10261/171852
DOI10.1371/journal.pntd.0004541
ISSN1935-2727
E-ISSN1935-2735
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