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Adherent invasive Escherichia coli strains from patients with Crohn's disease survive and replicate within

A L Glasser1, J Boudeau, N Barnich

  • 1Pathogénie Bactérienne Intestinale, Laboratoire de Bactériologie, Université d'Auvergne, 63001 Clermont-Ferrand, France.

Infection and Immunity
|August 14, 2001
PubMed

Insights

Adherent invasive Escherichia coli (AIEC) strains from Crohn's disease (CD) replicate within macrophages without causing cell death. These AIEC strains promote high levels of tumor necrosis factor alpha (TNF-alpha) secretion, potentially linking to CD pathogenesis.

Area of Science:

  • Microbiology
  • Immunology
  • Gastroenterology

Background:

  • Crohn's disease (CD) is a chronic inflammatory bowel disease.
  • Adherent invasive *Escherichia coli* (AIEC) strains are frequently isolated from CD lesions.
  • The interaction between AIEC and host immune cells is not fully understood.

Purpose of the Study:

  • To investigate the behavior of AIEC strains within macrophages.
  • To determine if AIEC can survive, replicate, and induce cell death in macrophages.
  • To assess the inflammatory cytokine response of macrophages infected with AIEC.

Main Methods:

  • Infection of macrophage cell lines (J774-A1) and primary macrophages (murine peritoneal and human monocyte-derived) with AIEC strains.
  • Quantification of intracellular bacterial replication over time.
  • Assessment of macrophage cell death using LDH release, DNA fragmentation, and Annexin V binding assays.
  • Measurement of cytokine secretion (TNF-alpha, IL-1beta) using ELISA.

Main Results:

  • All 15 tested AIEC strains replicated extensively within J774-A1 cells (2.2- to 74.2-fold increase in 48h).
  • The reference AIEC strain LF82 survived and replicated within murine and human macrophages, forming large vacuoles.
  • AIEC LF82 infection did not induce macrophage cell death (no LDH release, DNA fragmentation, or Annexin V binding).
  • LF82-infected macrophages secreted significantly higher levels of TNF-alpha (2.7-fold) compared to LPS stimulation.
  • No interleukin-1beta release was observed in LPS-prestimulated macrophages infected with AIEC LF82.

Conclusions:

  • AIEC strains can survive and multiply within macrophages.
  • AIEC LF82 replication within macrophages does not trigger host cell death.
  • AIEC-infected macrophages exhibit elevated TNF-alpha production.
  • These properties may contribute to the pathogenesis of Crohn's disease, including granuloma formation.

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