Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/32251
Appears in Collections:Biological and Environmental Sciences Journal Articles
Peer Review Status: Refereed
Title: Defective phagocyte association during infection of Galleria mellonella with Yersinia pseudotuberculosis is detrimental to both insect host and microbe
Author(s): Krachler, Anne Marie
Sirisaengtaksin, Natalie
Monteith, Pauline
Paine, C E Timothy
Coates, Christopher J
Lim, Jenson
Keywords: Yersinia
Galleria
adhesin
innate immunity
melanogenesis
damage response framework
Issue Date: 2021
Date Deposited: 8-Feb-2021
Citation: Krachler AM, Sirisaengtaksin N, Monteith P, Paine CET, Coates CJ & Lim J (2021) Defective phagocyte association during infection of Galleria mellonella with Yersinia pseudotuberculosis is detrimental to both insect host and microbe. Virulence, 12 (1), pp. 638-353. https://doi.org/10.1080/21505594.2021.1878672
Abstract: Adhesins facilitate bacterial colonization and invasion of host tissues and are considered virulence factors, but their impact on immune-mediated damage as a driver of pathogenesis remains unclear. Yersinia pseudotuberculosis encodes for a multivalent adhesion molecule (MAM), a mammalian cell entry (MCE) family protein and adhesin. MAMs are widespread in Gram-negative bacteria and enable enteric bacteria to colonize epithelial tissues. Their role in bacterial interactions with the host innate immune system and contribution to pathogenicity remains unclear. Here, we investigated how Y. pseudotuberculosis MAM contributes to pathogenesis during infection of the Galleria mellonella insect model. We show that Y. pseudotuberculosis MAM is required for efficient bacterial binding and uptake by hemocytes, the host phagocytes. Y. pseudotuberculosis interactions with insect and mammalian phagocytes are determined by bacterial and host factors. Loss of MAM, and deficient microbe–phagocyte interaction, increased pathogenesis in G. mellonella. Diminished phagocyte association also led to increased bacterial clearance. Furthermore, Y. pseudotuberculosis that failed to engage phagocytes hyperactivated humoral immune responses, most notably melanin production. Despite clearing the pathogen, excessive melanization also increased phagocyte death and host mortality. Our findings provide a basis for further studies investigating how microbe- and host-factors integrate to drive pathogenesis in a tractable experimental system.
DOI Link: 10.1080/21505594.2021.1878672
Rights: © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Licence URL(s): http://creativecommons.org/licenses/by/4.0/

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