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Immune response to diphtheria toxin-mediated depletion complicates the use of the CD11c-DTRtg model for studies of bacterial gastrointestinal infections
Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
2012 (engelsk)Inngår i: Immunology, ISSN 0019-2805, E-ISSN 1365-2567, Vol. 137, nr S1, s. 271-271Artikkel i tidsskrift, Meeting abstract (Annet vitenskapelig) Published
sted, utgiver, år, opplag, sider
2012. Vol. 137, nr S1, s. 271-271
HSV kategori
Identifikatorer
URN: urn:nbn:se:umu:diva-61200DOI: 10.1111/imm.12002ISI: 000309189102005OAI: oai:DiVA.org:umu-61200DiVA, id: diva2:565723
Konferanse
European Congress of Immunology, SEP 05-08, 2012, Glasgow, SCOTLAND
Tilgjengelig fra: 2012-11-08 Laget: 2012-11-07 Sist oppdatert: 2018-06-08bibliografisk kontrollert
Inngår i avhandling
1. Yersinia-phagocyte interactions during early infection
Åpne denne publikasjonen i ny fane eller vindu >>Yersinia-phagocyte interactions during early infection
2013 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Pathogenic Gram-negative Yersinia species preferentially target and inactivate phagocytic cells of the innate immune defense by translocation of effector Yersinia outer proteins (Yops) into the cells via a type III secretion system. This indicates that inactivation and avoidance of the early innate immune response is an efficient way for Yersinia species to avoid elimination and to cause diseases ranging from mild gastroenteritis (Y. pseudotuberculosis and Y. enterocolitica) to plague (Y. pestis). In this project, we aimed to study the interaction between enteropathogenic Y. pseudotuberculosis and phagocytic cells during early infection.

In situ interaction studies on infected intestinal tissues showed that Y. pseudotuberculosis mainly interacts with dendritic cells (DCs) in lymphoid tissues of the intestine during initial infection. After massive recruitment of polymorphonuclear neutrophils (PMNs) to the infected tissues, wild-type (wt) bacteria also interacted with this phagocyte. In contrast to the wt, mutants lacking the anti-phagocytic effectors YopH and YopE are avirulent in mice and unable to spread systemically. Interestingly, our interaction assay showed that these mutants not only interacted with DCs, but also with PMNs during the initial stage of infection. Thus, indicating that Y. pseudotuberculosis can avoid interaction with PMNs during early infection and that this is Yop-dependent. In a phagocytosis assay Y. pseudotuberculosis was demonstrated to inhibit internalization by DCs in a YopE-dependent manner, while both YopH and YopE were shown to be involved in the blocking of phagocytosis by macrophages and PMNs. Thus, indicating that YopH has cell type-specific effects. To further investigate the role of DCs during initial stages of infection, a mouse DC depletion model (CD11c-DTRtg) was applied. However, the DTx-mediated depletion of DCs in CD11c-DTRtg mice induced neutrophilia and the model could not give a definite answer to whether DCs play an important role in either restricting or stimulating progression of Y. pseudotuberculosis infection. To investigate involvement of PMNs during early infection mice were injected with the depleting antibody α-Ly6G. In absence of PMNs wt, as well as yopH and yopE mutants became more virulent, which further supports the importance of these Yops for the ability of Y. pseudotuberculosis to disseminate from the initial infection sites in the intestine to cause systemic disease.

In summary, our studies show that inhibiting internalization and maturation of DCs and avoiding phagocytosis by and interaction with macrophages and PMNs during the early stages of infection are important virulence strategies for Y. pseudotuberculosis to be able to colonize tissues, proliferate and disseminate systemically.

sted, utgiver, år, opplag, sider
Umeå: Umeå universitet, 2013. s. 59
Serie
Umeå University medical dissertations, ISSN 0346-6612 ; 1591
Emneord
Yersinia, dendritic cell, macrophage, neutrophil, T3SS
HSV kategori
Forskningsprogram
infektionssjukdomar
Identifikatorer
urn:nbn:se:umu:diva-79852 (URN)978-91-7459-713-4 (ISBN)
Disputas
2013-09-27, N320, Naturvetarhuset, Umeå universitet, Umeå, 13:00 (engelsk)
Opponent
Veileder
Forskningsfinansiär
Swedish Research Council
Tilgjengelig fra: 2013-09-05 Laget: 2013-09-03 Sist oppdatert: 2018-06-08bibliografisk kontrollert

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