Prevalence of Mycobacteriumavium subsp. paratuberculosis and Escherichia coli in blood samples from patients with inflammatory bowel disease
Mycobacterium avium subsp. paratuberculosis (MAP) and adherent-invasive Escherichia coli (AIEC) have been implicated as primary triggers in Crohn’s disease (CD). In this study, we evaluated the prevalence of MAP and E. coli (EC) DNA in peripheral blood from 202 inflammatory bowel disease (IBD) patie...
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Veröffentlicht in: | Medical microbiology and immunology 2015-05, Vol.204 (6), p.681-692 |
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Zusammenfassung: | Mycobacterium avium
subsp.
paratuberculosis
(MAP) and adherent-invasive
Escherichia coli
(AIEC) have been implicated as primary triggers in Crohn’s disease (CD). In this study, we evaluated the prevalence of MAP and
E. coli
(EC) DNA in peripheral blood from 202 inflammatory bowel disease (IBD) patients at various disease periods and compared against 24 cirrhotic patients with ascites (CIR) (non-IBD controls) and 29 healthy controls (HC). MAP DNA was detected by IS900-specific nested PCR, EC DNA by
mal
B-specific nested PCR and AIEC identity, in selected samples, by sequencing of
fimH
gene. CD patients with active disease showed the highest MAP DNA prevalence among IBD patients (68 %). Infliximab treatment resulted in decreased MAP detection. CIR patients had high individual and coinfection rates (75 % MAP, 88 % EC and 67 % MAP and EC), whilst HC controls had lower MAP prevalence (38 %) and EC was undetectable in this control group. EC DNA prevalence in IBD patients was highly associated with CD, and 80 % of EC from the selected samples of CD patients analyzed carried the
fimH30
allele, with a mutation strongly associated with AIEC. Our results show that coinfection with MAP and AIEC is common and persistent in CD, although the high MAP and EC detection in CIR patients suggested that colonization is, at least, partially dependent on increased gut permeability. Nevertheless, facilitative mechanisms between a susceptible host and these two potential human pathogens may allow their implication in CD pathogenesis. |
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ISSN: | 0300-8584 1432-1831 |
DOI: | 10.1007/s00430-015-0420-3 |