Publications by authors named "Clara Douadi"

We investigated the role of ChiA and its associated polymorphisms in the interaction between Crohn's disease (CD)-associated adherent-invasive (AIEC) and intestinal mucosa. We observed a higher abundance of among the metagenome of CD patients compared to healthy subjects. In dextran sulfate sodium-induced colitis mice model, AIEC-LF82∆ colonization was reduced in ileal, colonic and fecal samples compared to wild-type LF82.

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Background And Aims: The mechanism of action of anti-tumour necrosis factor [anti-TNF] agents could implicate macrophage modulation in Crohn's disease [CD]. As CD macrophages are defective in controlling CD-associated adherent-invasive Escherichia coli [AIEC], anti-TNF agents could limit AIEC replication within macrophages. We assessed the effect of anti-TNF agents on AIEC survival within monocyte-derived macrophages [MDMs] from CD patients and attempted to identify the proteins involved.

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The macrophages from Crohn's Disease (CD) patients are defective to control the replication of CD-associated adherent-invasive (AIEC). We aimed to identify the host factors associated with AIEC replication focusing on polymorphisms related to autophagy. Peripheral blood monocyte-derived macrophages (MDM), obtained from 95 CD patient, 30 ulcerative colitis (UC) patients and 15 healthy subjects, were genotyped for several CD-associated polymorphisms.

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Synopsis of recent research by authors named "Clara Douadi"

  • - Clara Douadi's research primarily focuses on the interactions between adherent-invasive Escherichia coli (AIEC) and the immune response in Crohn's disease (CD), revealing implications for disease virulence through factors like ChiA and macrophage modulation.
  • - Recent studies show that ChiA plays a significant role in AIEC's ability to colonize intestinal mucosa, with affected metagenomic profiles in CD patients compared to healthy individuals, suggesting a link between microbiome composition and disease severity.
  • - Douadi's work also highlights the potential of anti-TNF agents to limit AIEC replication within macrophages by modulating specific proteins, underscoring the importance of autophagy-related genetic factors in the immune response of CD patients.