Navigation überspringen
Universitätsbibliothek Heidelberg
Status: Bibliographieeintrag

Verfügbarkeit
Standort: ---
Exemplare: ---
heiBIB
 Online-Ressource
Verfasst von:Hemberger, Jacqueline [VerfasserIn]   i
 Ittensohn, Julia [VerfasserIn]   i
 Griffiths, Hannah-Miriam [VerfasserIn]   i
 Keller, Maren [VerfasserIn]   i
 Costina, Victor [VerfasserIn]   i
 Albrecht, Simone [VerfasserIn]   i
 Miethke, Thomas [VerfasserIn]   i
Titel:The promoter of the immune-modulating gene TIR-containing protein C of the uropathogenic escherichia coli strain CFT073 reacts to the pathogen’s environment
Verf.angabe:Jacqueline Hemberger, Julia Ittensohn, Hannah Griffiths, Maren Keller, Victor Costina, Simone Albrecht and Thomas Miethke
E-Jahr:2022
Jahr:20 January 2022
Umfang:21 S.
Fussnoten:Gesehen am 13.11.2023
Titel Quelle:Enthalten in: International journal of molecular sciences
Ort Quelle:Basel : Molecular Diversity Preservation International, 2000
Jahr Quelle:2022
Band/Heft Quelle:23(2022), 3, Artikel-ID 1148, Seite 1-21
ISSN Quelle:1422-0067
 1661-6596
Abstract:The TIR-containing protein C (TcpC) of the uropathogenic Escherichia coli strain CFT073 modulates innate immunity by interfering with the Toll-like receptor and NALP3 inflammasome signaling cascade. During a urinary tract infection the pathogen encounters epithelial and innate immune cells and replicates by several orders of magnitude. We therefore analyzed whether these cell types and also the density of the pathogen would induce the recently defined promoter of the CFT073 tcpC gene to, in time, dampen innate immune responses. Using reporter constructs we found that the uroepithelial cell line T24/83 and the monocytic cell line THP-1 induced the tcpC promoter. Differentiation of monocytic THP-1 cells to macrophages increased their potential to switch on the promoter. Cell-associated CFT073 displayed the highest promoter activity. Since potassium represents the most abundant intracellular ion and is secreted to induce the NLRP3 inflammasome, we tested its ability to activate the tcpC promoter. Potassium induced the promoter with high efficiency. Sodium, which is enriched in the renal cortex generating an antibacterial hypersalinity, also induced the tcpC promoter. Finally, the bacterial density modulated the tcpC promoter activity. In the search for promoter-regulating proteins, we found that the DNA-binding protein H-NS dampens the promoter activity. Taken together, different cell types and salts, present in the kidney, are able to induce the tcpC promoter and might explain the mechanism of TcpC induction during a kidney infection with uropathogenic E. coli strains.
DOI:doi:10.3390/ijms23031148
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

kostenfrei: Volltext: https://doi.org/10.3390/ijms23031148
 kostenfrei: Volltext: https://www.mdpi.com/1422-0067/23/3/1148
 DOI: https://doi.org/10.3390/ijms23031148
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:bacterial density
 host cell
 potassium
 sodium
 TcpC
 uropathogenic <i>Escherichia coli</i>
K10plus-PPN:1870149254
Verknüpfungen:→ Zeitschrift

Permanenter Link auf diesen Titel (bookmarkfähig):  https://katalog.ub.uni-heidelberg.de/titel/69142325   QR-Code
zum Seitenanfang