Influence of internalin a murinisation on host resistance to orally acquired listeriosis in mice.

Bergmann, Silke; Beard, Philippa M; Pasche, Bastian; Lienenklaus, Stefan; Weiss, Siegfried; Gahan, Cormac G M; Schughart, Klaus; Lengeling, Andreas

dc.contributor.author	Bergmann, Silke
dc.contributor.author	Beard, Philippa M
dc.contributor.author	Pasche, Bastian
dc.contributor.author	Lienenklaus, Stefan
dc.contributor.author	Weiss, Siegfried
dc.contributor.author	Gahan, Cormac G M
dc.contributor.author	Schughart, Klaus
dc.contributor.author	Lengeling, Andreas
dc.date.accessioned	2013-05-30T14:12:07Z	en
dc.date.available	2013-05-30T14:12:07Z	en
dc.date.issued	2013	en
dc.identifier.citation	Influence of internalin a murinisation on host resistance to orally acquired listeriosis in mice. 2013, 13:90 BMC Microbiol.	en_GB
dc.identifier.issn	1471-2180	en
dc.identifier.pmid	23617550	en
dc.identifier.doi	10.1186/1471-2180-13-90	en
dc.identifier.uri	http://hdl.handle.net/10033/293072	en
dc.description.abstract	The bacterial surface protein internalin (InlA) is a major virulence factor of the food-born pathogen Listeria monocytogenes. It plays a critical role in the bacteria crossing the host intestinal barrier by a species-specific interaction with the cell adhesion molecule E-cadherin. In mice, the interaction of InlA with murine E-cadherin is impaired due to sequence-specific binding incompatibilities. We have previously used the approach of 'murinisation' to establish an oral listeriosis infection model in mice by exchanging two amino acid residues in InlA. This dramatically increases binding to mouse E-cadherin. In the present study, we have used bioluminescent murinised and non-murinised Listeria strains to examine the spatiotemporal dissemination of Listeria in four diverse mouse genetic backgrounds after oral inoculation.
dc.language.iso	en	en
dc.rights	Archived with thanks to BMC microbiology	en_GB
dc.title	Influence of internalin a murinisation on host resistance to orally acquired listeriosis in mice.	en
dc.type	Article	en
dc.contributor.department	Infection and Immunity Division, The Roslin Institute and R(D)SVS, University of Edinburgh, Easter Bush Veterinary Campus, Edinburgh EH25 9RG, UK. andreas.lengeling@roslin.ed.ac.uk.	en_GB
dc.identifier.journal	BMC microbiology	en_GB
refterms.dateFOA	2018-06-13T00:40:20Z
html.description.abstract	The bacterial surface protein internalin (InlA) is a major virulence factor of the food-born pathogen Listeria monocytogenes. It plays a critical role in the bacteria crossing the host intestinal barrier by a species-specific interaction with the cell adhesion molecule E-cadherin. In mice, the interaction of InlA with murine E-cadherin is impaired due to sequence-specific binding incompatibilities. We have previously used the approach of 'murinisation' to establish an oral listeriosis infection model in mice by exchanging two amino acid residues in InlA. This dramatically increases binding to mouse E-cadherin. In the present study, we have used bioluminescent murinised and non-murinised Listeria strains to examine the spatiotemporal dissemination of Listeria in four diverse mouse genetic backgrounds after oral inoculation.