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PubMed · 2858808

Bacterial adherence.

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D C Old. 1985. Bacterial adherence.. https://pubmed.ncbi.nlm.nih.gov/2858808/

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Binding of Escherichia coli adhesin AfaE to CD55 triggers cell-surface expression of the MHC class I-related molecule MICA.

MICA are distant homologs of MHC class I molecules expressed in the normal intestinal epithelium. They are ligands of the NKG2D activating receptor expressed on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer cells and therefore play a critical role in innate immune responses. We investigated MICA cell-surface expression on infection of epithelial cell lines by enteric bacteria and show here that MICA expression can be markedly increased by bacteria of the diffusely adherent Escherichia coli diarrheagenic group. This effect is mediated by the specific interaction between bacterial adhesin AfaE and its cellular receptor, CD55, or decay-accelerating factor. It is extremely rapid after AfaE binding, consistent with a stress-induced signal. MICA induction on epithelial cells triggered IFN-gamma release by the NKG2D expressing natural killer cell line NKL. This host-bacteria interaction pathway could play a role in the pathogenesis of inflammatory bowel disease, a condition that implicates a bacterial trigger in genetically susceptible individuals. This was supported by the increased MICA expression at the surface of epithelial cells in colonic biopsies from Crohn's disease-affected patients compared with controls.

Adhesins, Escherichia coli↗

Genotypic prevalence of the fimbrial adhesins (F4, F5, F6, F41 and F18) and toxins (LT, STa, STb and STx2e) in Escherichia coli isolated from postweaning pigs with diarrhoea or oedema disease in Korea.

A PCR was used to determine the genotypic prevalence of five fimbrial adhesins (F4, F5, F6, F41 and F18), two heat-stable enterotoxins (STa and STb), the heat-labile enterotoxin (LT), and the shiga toxin 2e (Stx2e) in 230 isolates of Escherichia coli from postweaning pigs with diarrhoea or oedema disease. Ninety-four (40.9 per cent) of the isolates carried genes for at least one of the fimbrial adhesins or toxins. Genes for the F18 fimbrial adhesin were detected in 18.3 per cent, and genes for F4, F6, F5 and F41 were detected in 10.0 per cent, 4.3 per cent, 1.7 per cent and 0.8 per cent of the isolates, respectively. Genes for STa, STb and LT were detected in 25.7 per cent, 15.2 per cent and 8.7 per cent of the isolates, respectively. Genes for Stx2e were detected in 36 (15.6 per cent) of the isolates, and among them 24 also contained the gene for F18ab and four also contained the gene for F18ac.

Adhesins, Escherichia coli↗

Recurrent urinary tract infections in infancy: relapses or reinfections?

Seventeen infants with an index episode of pyelonephritis caused by Escherichia coli were monitored for 18 months for recurrent urinary tract infections (UTIs). All the infants had at least 1 recurrent UTI caused by the same pathogen. Twenty-six recurrent UTI episodes were recorded. The 40 E. coli strains available were analyzed by multiplex polymerase chain reaction for 3 alleles (classes I-III) of the papG gene and by pulsed-field gel electrophoresis (PFGE) after genomial digestion by XbaI. Of the 17 index strains, 12 (71%) carried the papG gene; 67% of these strains had class II alleles. In recurrent UTI isolates, the papG-positive E. coli appeared in 16 (70%) of 23 isolates. The proportion of all recurrent isolates available that represented a strain previously encountered (indistinguishable or highly similar in PFGE) in the same infant was 65%. Our results suggest that most recurrent UTIs in infants are endogenous relapses rather than reinfections caused by new organisms.

Adhesins, Escherichia coli↗