Open AccessCyclic‐di‐ GMP signalling and biofilm‐related properties of the Shiga toxin‐producing 2011 German outbreak E scherichia coli O104:H4
Author(s) -
Richter Anja M,
Povolotsky Tatyana L,
Wieler Lothar H,
Hengge Regine
Publication year - 2014
Publication title -
embo molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.923
H-Index - 107
eISSN - 1757-4684
pISSN - 1757-4676
DOI - 10.15252/emmm.201404309
Subject(s) - biofilm , microbiology and biotechnology , shiga toxin , outbreak , proinflammatory cytokine , escherichia coli , virulence , biology , strain (injury) , virulence factor , chemistry , bacteria , inflammation , virology , immunology , biochemistry , gene , genetics , anatomy
In 2011, nearly 4,000 people in Germany were infected by Shiga toxin (Stx)‐producing E scherichia coli O104:H4 with > 22% of patients developing haemolytic uraemic syndrome ( HUS ). Genome sequencing showed the outbreak strain to be related to enteroaggregative E. coli ( EAEC ), suggesting its high virulence results from EAEC ‐typical strong adherence and biofilm formation combined to Stx production. Here, we report that the outbreak strain contains a novel diguanylate cyclase (DgcX)—producing the biofilm‐promoting second messenger c‐di‐ GMP —that shows higher expression than any other known E. coli diguanylate cyclase. Unlike closely related E. coli , the outbreak strain expresses the c‐di‐ GMP ‐controlled biofilm regulator CsgD and amyloid curli fibres at 37°C, but is cellulose‐negative. Moreover, it constantly generates derivatives with further increased and deregulated production of CsgD and curli. Since curli fibres are strongly proinflammatory, with cellulose counteracting this effect, high c‐di‐ GMP and curli production by the outbreak O104:H4 strain may enhance not only adherence but may also contribute to inflammation, thereby facilitating entry of Stx into the bloodstream and to the kidneys where Stx causes HUS .