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ARS Home » Pacific West Area » Pullman, Washington » Animal Disease Research » Research » Publications at this Location » Publication #410467

Research Project: Identifying Effective Immune Responses and Vaccine Development for Bovine Anaplasmosis

Location: Animal Disease Research

Title: Identification of Anaplasma marginale adhesins for entry into Dermacentor andersoni tick cells using phage display

Author
item Noh, Susan
item Ujczo, Jessica
item ALPERIN, DEBRA - Washington State University
item Jarvis, Sheby
item SOLYMAN, MUNA - Washington State University
item KOKU, ROBERTA - Washington State University
item AKINSULIE, OLALEKAN - Washington State University
item HOFFMAN, ELIZABETH - Washington State University

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/15/2024
Publication Date: 5/10/2024
Citation: Noh, S.M., Ujczo, J.K., Alperin, D.C., Jarvis, S.M., Solyman, M.S., Koku, R., Akinsulie, O.C., Hoffman, E.E. 2024. Identification of Anaplasma marginale adhesins for entry into Dermacentor andersoni tick cells using phage display. Infection and Immunity. 92. Article e00540-23. https://doi.org/10.1128/iai.00540-23.
DOI: https://doi.org/10.1128/iai.00540-23

Interpretive Summary: Anaplasma marginale, a tick-borne pathogen that causes bovine anaplasmosis, negative impacts cattle health worldwide, and thus global food security. A safe and effective recombinant vaccine would greatly reduce the severe economic impacts of this disease. This work identifies a complement of outer membrane proteins that adhere to tick cells and thus play a key role in entry of the pathogen into the tick. Because entry into the host cells is essential for tick transmission of A. mariginale, these identified proteins will be essential components of a vaccine that blocks tick transmission of A. marginale.

Technical Abstract: Anaplasma marginale, is an obligate intracellular tick-borne bacterial pathogen that causes bovine anaplasmosis, an often severe, production-limiting disease of cattle found worldwide. Methods to control this disease are lacking, in large part due to major knowledge gaps in our understanding of the molecular underpinnings of basic host-pathogen interactions. For example, the surface proteins that serve as adhesins and thus likely play a role in pathogen entry into tick cells are largely unknown. To address this knowledge gap, we developed a phage display library and screened 66 A. marginale proteins for their ability to adhere to Dermacentor andersoni tick cells. From this screen, 17 candidate adhesins were identified including OmpA, and multiple members of the Msp1 family including Msp1b, Mlp3, and Mlp4. We then measured transcript of ompA and all members of the msp1 gene family through time and determined that msp1b, mlp2, and mlp4 have increased transcript during tick cell infection, suggesting a possible role in host cell binding or entry. Finally, Msp1a, Msp1b, Mlp3, and OmpA were expressed as recombinant protein. When added to cultured tick cells prior to A. marginale infection, all proteins except the C-terminus of Msp1a reduced A. marginale entry by 2.2 to 4.7-fold. Except OmpA, these adhesins lack orthologs in related pathogens of humans and animals, including A. phagocytophilum and the Ehrlichia spp., thus limiting their utility in a universal tick transmission blocking vaccine. However, this work greatly advances efforts toward developing methods to control bovine anaplasmosis and thus may help improve global food security.