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WFRF:(Cook N)
 

Sökning: WFRF:(Cook N) > (2005-2009) > Nucleotide-binding ...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003717naa a2200445 4500
001oai:lup.lub.lu.se:56103d3e-c756-440c-999b-2798a50028c7
003SwePub
008160401s2006 | |||||||||||000 ||eng|
0247 a https://lup.lub.lu.se/record/4111712 URI
0247 a https://doi.org/10.1074/jbc.M5102752002 DOI
040 a (SwePub)lu
041 a engb eng
042 9 SwePub
072 7a art2 swepub-publicationtype
072 7a ref2 swepub-contenttype
1001 a Boughan, PK4 aut
2451 0a Nucleotide-binding oligomerization domain-1 and epidermal growth factor receptor - Critical regulators of beta-defensins during helicobacter pylori infection
264 1c 2006
520 a Host-pathogen interactions that allow Helicobacter pylori to survive and persist in the stomach of susceptible individuals remain unclear. Human beta-defensins ( hBDs), epithelial-derived antimicrobial peptides are critical components of host-defense at mucosal surfaces. The role of H. pylori-mediated NF-kappa B and epidermal growth factor receptor ( EGFR) activation on beta-defensin expression was investigated. Transient transfection studies utilizing beta-defensin promoter constructs were conducted in gastric cells with contribution of individual signaling events evaluated by the addition of specific inhibitors, small interference nucleotide-binding oligomerization domain 1( NOD1) RNA or plasmids encoding Vaccinia virus proteins that interrupt interleukin-1 and Toll-like receptor signaling. The role of individual MAPK pathways was further delineated in HEK-293 cells expressing conditional MAPK mutants. We found hBD2 expression exclusively dependent on the presence of the bacterial cag pathogenicity island, with NOD1 a critical host sensor. Impairment of murine beta-defensin 4( an orthologue of hBD2) expression in NOD1-deficient mice 7-days post-infection further confirmed the role of this cytoplasmic pattern-recognition receptor in eliciting host innate immunity. In contrast to hBD2, hBD3 expression was NOD1-independent but EGFR and ERK pathway-dependent. Importantly, Toll-like receptor signaling was not implicated in H. pylori-mediated hBD2 and hBD3 gene expression. The divergent signaling events governing hBD2 and hBD3 expression suggest temporal functional variation, such that hBD2 may contribute to antimicrobial barrier function during the inflammatory phase with hBD3 playing a greater role during the repair, wound healing phase of infection.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Infektionsmedicin0 (SwePub)302092 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Infectious Medicine0 (SwePub)302092 hsv//eng
7001 a Argent, RH4 aut
7001 a Body-Malapel, M4 aut
7001 a Park, JH4 aut
7001 a Ewings, KE4 aut
7001 a Bowie, AG4 aut
7001 a Ong, SJ4 aut
7001 a Cook, SJ4 aut
7001 a Sørensen, Ole Eu Lund University,Lunds universitet,Infektionsmedicin,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Infection Medicine (BMC),Section III,Department of Clinical Sciences, Lund,Faculty of Medicine4 aut0 (Swepub:lu)medk-oso
7001 a Manzo, BA4 aut
7001 a Inohara, N4 aut
7001 a Klein, NJ4 aut
7001 a Nunez, G4 aut
7001 a Atherton, JC4 aut
7001 a Bajaj-Elliott, M4 aut
7102 a Infektionsmedicinb Sektion III4 org
7730 t Journal of Biological Chemistryg 281:17, s. 11637-11648q 281:17<11637-11648x 1083-351X
8564 u http://dx.doi.org/10.1074/jbc.M510275200x freey FULLTEXT
8564 8u https://lup.lub.lu.se/record/411171
8564 8u https://doi.org/10.1074/jbc.M510275200

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