Expression of cellulose and curli fimbriae by Escherichia coli isolated from the gastrointestinal tract.

Escherichia coli colonizes the gastrointestinal tract of humans; however, little is known about the features of commensal strains. This study investigated whether expression of the biofilm extracellular matrix components cellulose and curli fimbriae is found among commensal isolates. Fifty-two E. coli strains were isolated from faecal samples and, as a control, 24 strains from urinary tract infections were also used. Faecal isolates were characterized by serotyping and phylogenetically grouped by PCR. The genotype was determined by PFGE and the presence of virulence factors was assessed. Co-expression of cellulose and curli fimbriae at 28 degrees C and 37 degrees C was typical for faecal isolates, while urinary tract infection strains typically expressed the extracellular matrix components at 28 degrees C only. Knockout studies in a representative faecal isolate revealed that the response regulator CsgD regulated cellulose and curli fimbriae, as found previously in Salmonella enterica. In contrast to S. enterica, at 37 degrees C pellicle formation occurred in the absence of cellulose and curli fimbriae. The gastrointestinal tract represents a source of biofilm-forming bacteria, which can spread to susceptible sites.

[1]  F. Cassels,et al.  Colonization factors of diarrheagenicE. coli and their intestinal receptors , 1995, Journal of Industrial Microbiology.

[2]  J. Preston,et al.  The pgaABCD Locus of Escherichia coli Promotes the Synthesis of a Polysaccharide Adhesin Required for Biofilm Formation , 2004, Journal of bacteriology.

[3]  U. Römling,et al.  The csgD promoter, a control unit for biofilm formation in Salmonella typhimurium. , 2003, Research in microbiology.

[4]  U. Römling,et al.  Production of Cellulose and Curli Fimbriae by Members of the Family Enterobacteriaceae Isolated from the Human Gastrointestinal Tract , 2003, Infection and Immunity.

[5]  F. Guarner,et al.  Gut flora in health and disease , 2003, The Lancet.

[6]  W. Rabsch,et al.  Occurrence and regulation of the multicellular morphotype in Salmonella serovars important in human disease. , 2003, International journal of medical microbiology : IJMM.

[7]  L. Björck,et al.  Identification of Two Protein-binding and Functional Regions of Curli, a Surface Organelle and Virulence Determinant ofEscherichia coli * , 2002, The Journal of Biological Chemistry.

[8]  J. Keen,et al.  Variations in the csgD Promoter of Escherichia coli O157:H7 Associated with Increased Virulence in Mice and Increased Invasion of HEp-2 Cells , 2002, Infection and Immunity.

[9]  M. Woodward,et al.  The role of type 1 and curli fimbriae of Shiga toxin-producing Escherichia coli in adherence to abiotic surfaces. , 2002, International journal of medical microbiology : IJMM.

[10]  E. Denamur,et al.  Commensal Escherichia coli isolates are phylogenetically distributed among geographically distinct human populations. , 2001, Microbiology.

[11]  J. Keen,et al.  Mutations in the csgD Promoter Associated with Variations in Curli Expression in Certain Strains ofEscherichia coli O157:H7 , 2001, Applied and Environmental Microbiology.

[12]  U. Gophna,et al.  Curli Fibers Mediate Internalization ofEscherichia coli by Eukaryotic Cells , 2001, Infection and Immunity.

[13]  M. Rohde,et al.  The multicellular morphotypes of Salmonella typhimurium and Escherichia coli produce cellulose as the second component of the extracellular matrix , 2001, Molecular microbiology.

[14]  J. Boudeau,et al.  Type 1 pili‐mediated adherence of Escherichia coli strain LF82 isolated from Crohn's disease is involved in bacterial invasion of intestinal epithelial cells , 2001, Molecular microbiology.

[15]  F. Nowrouzian,et al.  P fimbriae, capsule and aerobactin characterize colonic resident Escherichia coli , 2001, Epidemiology and Infection.

[16]  U. Römling.  Genetic and phenotypic analysis of multicellular behavior in Salmonella typhimurium. , 2001, Methods in enzymology.

[17]  I. Blomfield.  The regulation of pap and type 1 fimbriation in Escherichia coli. , 2001, Advances in microbial physiology.

[18]  S. Edberg,et al.  Advances in the bacteriology of the coliform group: their suitability as markers of microbial water safety. , 2001, Annual review of microbiology.

[19]  O. Clermont,et al.  Rapid and Simple Determination of theEscherichia coli Phylogenetic Group , 2000, Applied and Environmental Microbiology.

[20]  B. Wanner,et al.  One-step inactivation of chromosomal genes in Escherichia coli K-12 using PCR products. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[21]  C. Sasakawa,et al.  Curli Loci of Shigella spp , 2000, Infection and Immunity.

[22]  S. Normark,et al.  AgfD, the checkpoint of multicellular and aggregative behaviour in Salmonella typhimurium regulates at least two independent pathways , 2000, Molecular microbiology.

[23]  S. Normark,et al.  Expression of and cytokine activation by Escherichia coli curli fibers in human sepsis. , 2000, The Journal of infectious diseases.

[24]  T. Pál,et al.  Thin aggregative fimbriae on urinary Escherichia coli isolates. , 2000, Advances in experimental medicine and biology.

[25]  Wangxue Chen,et al.  The intestinal microflora and inflammatory bowel disease , 1999 .

[26]  N. Barnich,et al.  Presence of adherent Escherichia coli strains in ileal mucosa of patients with Crohn's disease. , 1998, Gastroenterology.

[27]  R. Kolter,et al.  Genetic analysis of Escherichia coli biofilm formation: roles of flagella, motility, chemotaxis and type I pili , 1998, Molecular microbiology.

[28]  D. Dykhuizen,et al.  Pathogenic adaptation of Escherichia coli by natural variation of the FimH adhesin. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[29]  W. Kay,et al.  Thin aggregative fimbriae enhance Salmonella enteritidis biofilm formation. , 1998, FEMS microbiology letters.

[30]  W. Sierralta,et al.  Multicellular and aggregative behaviour of Salmonella typhimurium strains is controlled by mutations in the agfD promoter , 1998, Molecular microbiology.

[31]  T. Russo,et al.  Colonization with and acquisition of uropathogenic Escherichia coli as revealed by polymerase chain reaction-based detection. , 1998, The Journal of infectious diseases.

[32]  L. Björck,et al.  Activation of the contact-phase system on bacterial surfaces—a clue to serious complications in infectious diseases , 1998, Nature Medicine.

[33]  W. Sierralta,et al.  Curli Fibers Are Highly Conserved between Salmonella typhimurium and Escherichia coli with Respect to Operon Structure and Regulation , 1998, Journal of bacteriology.

[34]  J. Macfie,et al.  Microbiology of bacterial translocation in humans , 1998, Gut.

[35]  M. Struelens.  Consensus guidelines for appropriate use and evaluation of microbial epidemiologic typing systems. , 1996, Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases.

[36]  S. Normark,et al.  Expression of two csg operons is required for production of fibronectin‐ and Congo red‐binding curli polymers in Escherichia coli K‐12 , 1995, Molecular microbiology.

[37]  R. Berg.  Bacterial translocation from the gastrointestinal tract. , 1990, Trends in microbiology.

[38]  B. Tümmler,et al.  Epidemiology of chronic Pseudomonas aeruginosa infections in cystic fibrosis. , 1994, The Journal of infectious diseases.

[39]  A. Olsén,et al.  Plasminogen, absorbed by Escherichia coli expressing curli or by Salmonella enteritidis expressing thin aggregative fimbriae, can be activated by simultaneously captured tissue‐type plasminogen activator (t‐PA) , 1994, Molecular microbiology.

[40]  S. Normark,et al.  The RpoS Sigma factor relieves H‐NS‐mediated transcriptional repression of csgA, the subunit gene of fibronectin‐binding curli in Escherichia coli , 1993, Molecular microbiology.

[41]  D. Caugant,et al.  Resident colonic Escherichia coli strains frequently display uropathogenic characteristics. , 1992, The Journal of infectious diseases.

[42]  T. Trust,et al.  Purification and characterization of thin, aggregative fimbriae from Salmonella enteritidis , 1991, Journal of bacteriology.

[43]  A. Brauner,et al.  Characterization of Escherichia coli isolated in blood, urine and faeces from bacteraemic patients and msible smead of infection , 1991 .

[44]  C. Bloch,et al.  Impaired colonization by and full invasiveness of Escherichia coli K1 bearing a site-directed mutation in the type 1 pilin gene , 1990, Infection and immunity.

[45]  B. McCormick,et al.  Type 1 pili are not necessary for colonization of the streptomycin-treated mouse large intestine by type 1-piliated Escherichia coli F-18 and E. coli K-12 , 1989, Infection and immunity.

[46]  B. McCormick,et al.  Type 1 pili are not necessary for colonization of the streptomycin-treated mouse large intestine by type 1-piliated Escherichia coli F-18 and E. coli K-12 , 1989 .

[47]  S. Normark,et al.  Fibronectin binding mediated by a novel class of surface organelles on Escherichia coll , 1989, Nature.

[48]  D. Hartl,et al.  The population genetics of Escherichia coli. , 1984, Annual review of genetics.

[49]  F. Ørskov.  Virulence Factors of the Bacterial Cell Surface , 1978 .

[50]  F. Orskov.  Virulence factors of the bacterial cell surface. , 1978, The Journal of infectious diseases.

[51]  Cooke Em,et al.  Properties of Strains of Escherichia Coli Isolated from a Variety of Sources , 1975 .

[52]  E. Cooke,et al.  Properties of strains of Escherichia coli isolated from a variety of sources. , 1975, Journal of medical microbiology.

[53]  S. O'farrell,et al.  The origin of O serotypes of Escherichia coli in babies after normal delivery , 1974, Journal of Hygiene.

[54]  D. Updegraff.  Semimicro determination of cellulose in biological materials. , 1969, Analytical biochemistry.