A Zebrafish Model for Chlamydia Infection with the Obligate Intracellular Pathogen Waddlia chondrophila.

Détails

Ressource 1Télécharger: fmicb-07-01829.pdf (4657.24 [Ko])
Etat: Serval
Version: Final published version
ID Serval
serval:BIB_DA358C63BE7A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
A Zebrafish Model for Chlamydia Infection with the Obligate Intracellular Pathogen Waddlia chondrophila.
Périodique
Frontiers in microbiology
Auteur(s)
Fehr A.G., Ruetten M., Seth-Smith H.M., Nufer L., Voegtlin A., Lehner A., Greub G., Crosier P.S., Neuhauss S.C., Vaughan L.
ISSN-L
1664-302X
Statut éditorial
Publié
Date de publication
2016
Peer-reviewed
Oui
Volume
7
Pages
1829
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish

Résumé
Obligate intracellular chlamydial bacteria of the Planctomycetes-Verrucomicrobia-Chlamydiae (PVC) superphylum are important pathogens of terrestrial and marine vertebrates, yet many features of their pathogenesis and host specificity are still unknown. This is particularly true for families such as the Waddliacea which, in addition to epithelia, cellular targets for nearly all Chlamydia, can infect and replicate in macrophages, an important arm of the innate immune system or in their free-living amoebal counterparts. An ideal pathogen model system should include both host and pathogen, which led us to develop the first larval zebrafish model for chlamydial infections with Waddlia chondrophila. By varying the means and sites of application, epithelial cells of the swim bladder, endothelial cells of the vasculature and phagocytosing cells of the innate immune system became preferred targets for infection in zebrafish larvae. Through the use of transgenic zebrafish, we could observe recruitment of neutrophils to the infection site and demonstrate for the first time that W. chondrophila is taken up and replicates in these phagocytic cells and not only in macrophages. Furthermore, we present evidence that myeloid differentiation factor 88 (MyD88) mediated signaling plays a role in the innate immune reaction to W. chondrophila, eventually by Toll-like receptor (TLRs) recognition. Infected larvae with depleted levels of MyD88 showed a higher infection load and a lower survival rate compared to control fish. This work presents a new and potentially powerful non-mammalian experimental model to study the pathology of chlamydial virulence in vivo and opens up new possibilities for investigation of other members of the PVC superphylum.

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Création de la notice
12/12/2016 20:39
Dernière modification de la notice
03/03/2018 21:54
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