Yersiniabactin Siderophore of Crohn's Disease-Associated Adherent-Invasive
AIEC
Crohn’s disease
HIF-1alpha
autophagy
siderophore
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
29 Mar 2021
29 Mar 2021
Historique:
received:
04
03
2021
revised:
25
03
2021
accepted:
26
03
2021
entrez:
3
4
2021
pubmed:
4
4
2021
medline:
11
5
2021
Statut:
epublish
Résumé
Adherent-invasive Intestinal epithelial T84 cells and CEABAC10 transgenic mice were infected with LF82 or its mutants deficient in yersiniabactin expression. Autophagy was assessed by Western blot analysis for p62 and LC3-II expression. Loss of yersiniabactin decreased the growth of LF82 in competitive conditions, reducing the ability of LF82 to adhere to and invade T84 cells and to colonize the intestinal tract of CEABAC10 mice. However, yersiniabactin deficiency increased LF82 intracellular replication. Mechanistically, a functional yersiniabactin is necessary for LF82-induced expression of HIF-1α, which is implicated in autophagy activation in infected cells. Our study highlights a novel role for yersiniabactin siderophore in AIEC-host interaction. Indeed, yersiniabactin, which is an advantage for AIEC to growth in a competitive environment, could be a disadvantage for the bacteria as it activates autophagy, a key host defense mechanism, leading to bacterial clearance.
Sections du résumé
BACKGROUND
BACKGROUND
Adherent-invasive
METHODS
METHODS
Intestinal epithelial T84 cells and CEABAC10 transgenic mice were infected with LF82 or its mutants deficient in yersiniabactin expression. Autophagy was assessed by Western blot analysis for p62 and LC3-II expression.
RESULTS
RESULTS
Loss of yersiniabactin decreased the growth of LF82 in competitive conditions, reducing the ability of LF82 to adhere to and invade T84 cells and to colonize the intestinal tract of CEABAC10 mice. However, yersiniabactin deficiency increased LF82 intracellular replication. Mechanistically, a functional yersiniabactin is necessary for LF82-induced expression of HIF-1α, which is implicated in autophagy activation in infected cells.
CONCLUSION
CONCLUSIONS
Our study highlights a novel role for yersiniabactin siderophore in AIEC-host interaction. Indeed, yersiniabactin, which is an advantage for AIEC to growth in a competitive environment, could be a disadvantage for the bacteria as it activates autophagy, a key host defense mechanism, leading to bacterial clearance.
Identifiants
pubmed: 33805299
pii: ijms22073512
doi: 10.3390/ijms22073512
pmc: PMC8037853
pii:
doi:
Substances chimiques
Phenols
0
Thiazoles
0
yersiniabactin
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : IDEX-ISITE
ID : 16-IDEX-0001
Organisme : Inserm
ID : U1071
Organisme : European Union FP7 People Marie Curie International Incoming Fellowship
ID : FP7 Marie Curie
Organisme : Association François Aupetit
ID : Association François Aupetit
Organisme : Ministère de la Recherche et de la Technologie
ID : Ministère de la Recherche et de la Technologie
Organisme : INRAE
ID : USC-2018
Références
Free Radic Biol Med. 2017 Apr;105:68-78
pubmed: 27780750
J Exp Med. 2009 Sep 28;206(10):2179-89
pubmed: 19737864
Microbiol Res. 2018 Jul - Aug;212-213:103-111
pubmed: 29103733
Sci Rep. 2019 Feb 18;9(1):2175
pubmed: 30778122
Int J Mol Sci. 2020 May 25;21(10):
pubmed: 32466328
Autophagy. 2016 May 3;12(5):770-83
pubmed: 26986695
Cells. 2019 Jan 09;8(1):
pubmed: 30634511
Inflamm Bowel Dis. 2014 Nov;20(11):1919-32
pubmed: 25230163
Infect Immun. 1997 May;65(5):1659-68
pubmed: 9125544
Infect Immun. 2019 Oct 18;87(11):
pubmed: 31481410
Gastroenterology. 2014 Feb;146(2):508-19
pubmed: 24148619
Int J Med Microbiol. 2004 Sep;294(2-3):83-94
pubmed: 15493818
Mol Cell Biol. 1996 Sep;16(9):4604-13
pubmed: 8756616
World J Gastroenterol. 2014 Sep 14;20(34):12102-17
pubmed: 25232246
Cell Microbiol. 2012 Jun;14(6):791-807
pubmed: 22309232
Nat Med. 2003 Jun;9(6):677-84
pubmed: 12778166
Nat Rev Gastroenterol Hepatol. 2010 Nov;7(11):599-610
pubmed: 20924367
J Clin Invest. 2007 Jun;117(6):1566-74
pubmed: 17525800
Cell Microbiol. 2016 May;18(5):617-31
pubmed: 26499863
Gastroenterology. 2008 Mar;134(3):756-67
pubmed: 18325389
Nucleic Acids Res. 2000 Nov 15;28(22):E97
pubmed: 11071951
Gastroenterology. 2013 Sep;145(3):602-12.e9
pubmed: 23684751
Cell. 2001 Oct 5;107(1):1-3
pubmed: 11595178
Nat Genet. 2011 Mar;43(3):242-5
pubmed: 21278745
Gut Microbes. 2020 Nov 1;11(6):1677-1694
pubmed: 32583714
Gastroenterology. 1998 Dec;115(6):1405-13
pubmed: 9834268
Mol Microbiol. 1993 Apr;8(2):397-408
pubmed: 8316088
BMC Genomics. 2017 Jul 19;18(1):544
pubmed: 28724357
Front Microbiol. 2017 May 24;8:639
pubmed: 28596755
J Innate Immun. 2013;5(5):434-43
pubmed: 23328432
Inflamm Bowel Dis. 2016 Mar;22(3):516-28
pubmed: 26595556
Autophagy. 2020 Jan;16(1):38-51
pubmed: 31286804
Infect Immun. 2011 Aug;79(8):3309-16
pubmed: 21576334
Sci Rep. 2018 Aug 17;8(1):12301
pubmed: 30120269
Proc Natl Acad Sci U S A. 2000 Jun 6;97(12):6640-5
pubmed: 10829079
Infect Immun. 2001 Sep;69(9):5529-37
pubmed: 11500426
Inflamm Bowel Dis. 2015 Jun;21(6):1219-28
pubmed: 25844959
Immunol Lett. 2014 Dec;162(2 Pt A):48-53
pubmed: 24803011
Gut. 2012 Jun;61(6):933-52
pubmed: 22016365
Autophagy. 2021 Jan;17(1):1-382
pubmed: 33634751
Cell Microbiol. 2010 Jan;12(1):99-113
pubmed: 19747213
Gut. 2017 Aug;66(8):1382-1389
pubmed: 27196580
Nucleic Acids Res. 1999 Nov 15;27(22):4409-15
pubmed: 10536150
Trends Mol Med. 2016 Dec;22(12):1077-1090
pubmed: 27825668
Gut. 2018 Mar;67(3):574-587
pubmed: 29141957
Infect Immun. 1999 Sep;67(9):4499-509
pubmed: 10456892
PLoS Pathog. 2013 Jan;9(1):e1003141
pubmed: 23358328
Gastroenterology. 2004 Aug;127(2):412-21
pubmed: 15300573
Inflamm Bowel Dis. 2009 Jun;15(6):872-82
pubmed: 19235912
PLoS One. 2010 Sep 17;5(9):
pubmed: 20862302
Gastroenterology. 2004 Jul;127(1):80-93
pubmed: 15236175
Mol Microbiol. 2001 Mar;39(5):1272-84
pubmed: 11251843
Gut Microbes. 2020 May 3;11(3):364-380
pubmed: 29494278