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Decreased expression of mannose-specific adhesins by Escherichia coli in the colonic microflora of immunoglobulin A-deficient individuals.

Artikel i vetenskaplig tidskrift
Författare Vanda Friman
Ingegerd Adlerberth
H Connell
Catharina Svanborg
Lars Åke Hanson
Agnes E Wold
Publicerad i Infection and immunity
Volym 64
Nummer/häfte 7
Sidor 2794-8
ISSN 0019-9567
Publiceringsår 1996
Publicerad vid Institutionen för laboratoriemedicin, Avdelningen för klinisk immunologi
Institutionen för invärtesmedicin, Avdelningen för infektionssjukdomar
Sidor 2794-8
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Adhesins, Bacterial, genetics, metabolism, Adult, Aged, Binding Sites, Case-Control Studies, Colon, microbiology, Enterobacteriaceae, isolation & purification, Escherichia coli, genetics, isolation & purification, metabolism, Female, Fimbriae, Bacterial, genetics, metabolism, Genes, Bacterial, Genotype, Humans, IgA Deficiency, metabolism, microbiology, Male, Mannose, metabolism, Middle Aged
Ämneskategorier Gastroenterologi, Infektionsmedicin, Mikrobiologi inom det medicinska området

Sammanfattning

Most Escherichia coli isolates can express type 1 fimbriae with mannose-specific adhesins. These adhesins bind to the oligosaccharide chains of secretory immunoglobulin A (IgA). Thus, in addition to specific antibody activity, secretory IgA possesses a broad reactivity with bacteria expressing type 1 fimbriae. The absence of secretory IgA in colonic secretions, as seen in IgA deficiency, might therefore alter the ability of type 1-fimbriated E. coli to colonize the large intestines of these individuals. In the present study, 10 E. coli isolates from each of 17 IgA-deficient and 17 age-matched control individuals were assessed for the carriage of the fim gene cluster by DNA-DNA hybridization and for the expression of type 1 fimbriae by hemagglutination of guinea pig erythrocytes. The contribution of type 1-fimbria-mediated adherence to HT-29 colonic cells was also analyzed. The proportion of fim+ E. coli isolates was lower in IgA-deficient than in control individuals (74 versus 94%, P < 0.05), as was the proportion of isolates expressing type 1 fimbriae in vitro (69% versus 85%, P < 0.05). The median mannose-sensitive adherence to HT-29 cells was lower for isolates from IgA-deficient individuals than from the controls (9 versus 26 bacteria per cell, P < 0.05). Isolates expressing type 1 fimbriae showed lower adherence to HT-29 cells when they were derived from IgA-deficient individuals than when they were derived from control individuals (15 versus 27 bacteria per cell, P < 0.05). The results suggest that the interaction of type 1 fimbriae with secretory IgA contributes to the large intestinal colonization by these bacteria.

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