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Uropathogenic Escherichia coli AL511 requires flagellum to enter renal collecting duct cells
Authors:Christophe Pichon,Cé  line Hé  chard,Laurence du Merle,Christelle Chaudray,Isabelle Bonne,Sté  phanie Guadagnini,Alain Vandewalle, Chantal Le Bougué  nec
Affiliation:Institut Pasteur, UnitéPathogénie Bactérienne des Muqueuses, 28 Rue du Docteur Roux, 75724, Paris Cedex 15, France.;
Institut Pasteur, Plateforme de microscopie électronique, 25 Rue du Docteur Roux, 75724, Paris Cedex 15, France.;
INSERM, U773, Centre de Recherche Biomédicale Bichat-Beaujon (CRB3), BP 416, 75018, Paris, France;UniversitéParis 7 –Denis Diderot, site Bichat, Paris, 75870, Paris, France.
Abstract:Escherichia coli is the leading cause of urinary tract infections, but the mechanisms governing renal colonization by this bacterium remain poorly understood. We investigated the ability of 13 E. coli strains isolated from the urine of patients with pyelonephritis and cystitis and normal stools to invade collecting duct cells, which constitute the first epithelium encountered by bacteria ascending from the bladder. The AL511 clinical isolate adhered to mouse collecting duct mpkCCDcl4 cells, used as a model of renal cell invasion, and was able to enter and persist within these cells. Previous studies have shown that bacterial flagella play an important role in host urinary tract colonization, but the role of flagella in the interaction of E. coli with renal epithelial cells remains unclear. An analysis of the ability of E. coli AL511 mutants to invade renal cells showed that flagellin played a key role in bacterial entry. Both flagellum filament assembly and the motor proteins MotA and MotB appeared to be required for E. coli AL511 uptake into collecting duct cells. These findings indicate that pyelonephritis-associated E. coli strains may invade renal collecting duct cells and that flagellin may act as an invasin in this process.
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