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1000 Titel
  • Lipopolysaccharide priming enhances expression of effectors of immune defence while decreasing expression of pro-inflammatory cytokines in mammary epithelia cells from cows
1000 Autor/in
  1. Günther, Juliane |
  2. Petzl, Wolfram |
  3. Zerbe, Holm |
  4. Schuberth, Hans-Joachim |
  5. Koczan, Dirk |
  6. Goetze, Leopold |
  7. Seyfert, Hans-Martin |
1000 Erscheinungsjahr 2012
1000 LeibnizOpen
1000 Art der Datei
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2012-01-12
1000 Erschienen in
1000 Quellenangabe
  • 13: 17
1000 FRL-Sammlung
1000 Copyrightjahr
  • 2012
1000 Lizenz
1000 Verlagsversion
  • https://dx.doi.org/10.1186/1471-2164-13-17 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3315725/ |
1000 Ergänzendes Material
  • http://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-13-17#Declarations |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • BACKGROUND: Udder infections with environmental pathogens like Escherichia coli are a serious problem for the dairy industry. Reduction of incidence and severity of mastitis is desirable and mild priming of the immune system either through vaccination or with low doses of immune stimulants such as lipopolysaccharide LPS was previously found to dampen detrimental effects of a subsequent infection. Monocytes/macrophages are known to develop tolerance towards the endotoxin LPS (endotoxin tolerance, ET) as adaptation strategy to prevent exuberant inflammation. We have recently observed that infusion of 1 μg of LPS into the quarter of an udder effectively protected for several days against an experimentally elicited mastitis. We have modelled this process in primary cultures of mammary epithelial cells (MEC) from the cow. MEC are by far the most abundant cells in the healthy udder coming into contact with invading pathogens and little is known about their role in establishing ET. RESULTS: We primed primary MEC cultures for 12 h with LPS (100 ng/ml) and stimulated three cultures either 12 h or 42 h later with 107/ml particles of heat inactivated E. coli bacteria for six hours. Priming-related alterations in the global transcriptome of those cells were quantified with Affymetrix microarrays. LPS priming alone caused differential expression of 40 genes and mediated significantly different response to a subsequent E. coli challenge of 226 genes. Expression of 38 genes was enhanced while that of 188 was decreased. Higher expressed were anti-microbial factors (β-defensin LAP, SLPI), cell and tissue protecting factors (DAF, MUC1, TGM1, TGM3) as well as mediators of the sentinel function of MEC (CCL5, CXCL8). Dampened was the expression of potentially harmful pro-inflammatory master cytokines (IL1B, IL6, TNF-α) and immune effectors (NOS2, matrix metalloproteases). Functional network analysis highlighted the reduced expression of IL1B and of IRF7 as key to this modulation. CONCLUSION: LPS-primed MEC are fitter to repel pathogens and better protected against misguided attacks of the immune response. Attenuated is the exuberant expression of factors potentially promoting immunopathological processes. MEC therefore recapitulate many aspects of ET known so far from professional immune cells.
1000 Fachgruppe
  1. Biologie |
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/creator/R8O8bnRoZXIsIEp1bGlhbmU=|https://frl.publisso.de/adhoc/creator/UGV0emwsIFdvbGZyYW0=|https://frl.publisso.de/adhoc/creator/WmVyYmUsIEhvbG0=|https://frl.publisso.de/adhoc/creator/U2NodWJlcnRoLCBIYW5zLUpvYWNoaW0=|https://frl.publisso.de/adhoc/creator/S29jemFuLCBEaXJr|https://frl.publisso.de/adhoc/creator/R29ldHplLCBMZW9wb2xk|https://frl.publisso.de/adhoc/creator/U2V5ZmVydCwgSGFucy1NYXJ0aW4=
1000 Förderer
  1. Pfizer Animal Health |
  2. Deutsche Forschungsgemeinschaft |
1000 Fördernummer
  1. -
  2. FOR585; Se 326/14
1000 Förderprogramm
  1. -
  2. -
1000 Dateien
1000 Förderung
  1. 1000 joinedFunding-child
    1000 Förderer Pfizer Animal Health |
    1000 Förderprogramm -
    1000 Fördernummer -
  2. 1000 joinedFunding-child
    1000 Förderer Deutsche Forschungsgemeinschaft |
    1000 Förderprogramm -
    1000 Fördernummer FOR585; Se 326/14
1000 Objektart article
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1000 @id frl:6403014.rdf
1000 Erstellt am 2017-06-13T11:07:10.226+0200
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1000 Bearbeitet von 218
1000 Zuletzt bearbeitet Mon May 28 10:58:05 CEST 2018
1000 Objekt bearb. Mon May 28 10:58:04 CEST 2018
1000 Vgl. frl:6403014
1000 Oai Id
  1. oai:frl.publisso.de:frl:6403014 |
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