2026-05-13T15:19:01Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/52032024-09-27T08:13:49Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605col_20.500.12105_19607
Repisalud
author
Villar, Margarita
author
Lopez, Vladimir
author
Ayllon, Nieves
author
Cabezas-Cruz, Alejandro
author
Lopez, Juan Antonio
author
Vazquez, Jesus
author
Alberdi, Pilar
author
de la Fuente, Jose
funder
Ministerio de Economía y Competitividad (España)
funder
Unión Europea
funder
Regional Government of Castile-La Mancha (España)
2017-10-30T13:15:40Z
2017-10-30T13:15:40Z
2016
Parasit Vectors. 2016; 9:467
10.1186/s13071-016-1747-3
1756-3305
Parasites & Vectors
27561965
http://hdl.handle.net/20.500.12105/5203
Background: The intracellular bacteria Anaplasma phagocytophilum are emerging zoonotic pathogens affecting human and animal health, and a good model for the study of tick-host-pathogen interactions. This tick-borne pathogen is transmitted by Ixodes scapularis in the United States where it causes human granulocytic anaplasmosis. Tick midguts and salivary glands play a major role during tick feeding and development, and in pathogen acquisition, multiplication and transmission. Vertebrate host proteins are found in tick midguts after feeding and have been described in the salivary glands of fed and unfed ticks, suggesting a role for these proteins during tick feeding and development. Furthermore, recent results suggested the hypothesis that pathogen infection affects tick metabolic processes to modify host protein digestion and persistence in the tick with possible implications for tick physiology and pathogen life-cycle. Methods: To address this hypothesis, herein we used I. scapularis female ticks fed on uninfected and A. phagocytophilum-infected sheep to characterize host protein content in midguts and salivary glands by proteomic analysis of tick tissues. Results: The results evidenced a clear difference in the host protein content between tick midguts and salivary glands in response to infection suggesting that A. phagocytophilum selectively manipulates the levels of vertebrate host proteins in ticks in a tissue-specific manner to facilitate pathogen infection, multiplication and transmission while preserving tick feeding and development. The mechanisms by which A. phagocytophilum manipulates the levels of vertebrate host proteins are not known, but the results obtained here suggested that it might include the modification of proteolytic pathways. Conclusions: The results of this study provided evidence to support that A. phagocytophilum affect tick proteolytic pathways to selectively manipulate the levels of vertebrate host proteins in a tissue-specific manner to increase tick vector capacity. Investigating the biological relevance of host proteins in tick biology and pathogen infection and the mechanisms used by A. phagocytophilum to manipulate host protein content is essential to advance our knowledge of tick-host-pathogen molecular interactions. These results have implications for the identification of new targets for the development of vaccines for the control of tick-borne diseases.
eng
Anaplasma
Tick
Ixodes
Proteomics
Hemoglobin
Immunology
QUANTITATIVE PROTEOMICS
EHRLICHIA-CHAFFEENSIS
GENE-EXPRESSION
SALIVARY-GLANDS
INFECTION
CELLS
INSIGHTS
DISEASE
IDENTIFICATION
ARTHROPODS
The intracellular bacterium Anaplasma phagocytophilum selectively manipulates the levels of vertebrate host proteins in the tick vector Ixodes scapularis
journal article
URL
https://repisalud.isciii.es/bitstreams/1dbe3a3c-bc09-4592-867f-61225b5ae8c8/download
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MD5
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application/pdf
IntracellularBacteriumAnaplasmaPhagocytophilum_2016
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https://repisalud.isciii.es/bitstreams/b06d6d49-e0c6-488d-990a-92075ccd14ca/download
File
MD5
07490e9738370ca658010aecc74e6746
70289
text/plain
IntracellularBacteriumAnaplasmaPhagocytophilum_2016.txt
URL
https://repisalud.isciii.es/bitstreams/a4d7b924-08f3-4236-8930-4116e0e2e12f/download
File
MD5
07490e9738370ca658010aecc74e6746
70289
text/plain
IntracellularBacteriumAnaplasmaPhagocytophilum_2016.txt