Pretreatment of epithelial cells with rifaximin alters bacterial attachment and internalization profiles

Eric L Brown1, Qiong Xue, Zhi-Dong Jiang

  • 1The University of Texas School of Public Health, 1200 Herman Pressler, Houston, TX 77030, USA. eric.l.brown@uth.tmc.edu

Insights

Rifaximin, an antibiotic for traveler's diarrhea, alters epithelial cells to reduce bacterial attachment and inflammatory responses. This mechanism impacts bacterial adhesion differently based on their specific mechanisms.

Area of Science:

  • Microbiology
  • Pharmacology
  • Cell Biology

Background:

  • Rifaximin is a poorly absorbed antibiotic used for traveler's diarrhea.
  • It reduces enteric infection symptoms with limited impact on gut flora.
  • Its effects on host-pathogen interactions are not fully understood.

Purpose of the Study:

  • To investigate how rifaximin pretreatment affects bacterial adherence to epithelial cells.
  • To explore rifaximin's influence on bacterial internalization into host cells.
  • To determine if rifaximin modulates host cell inflammatory responses.

Main Methods:

  • Epithelial cell lines (HEp-2, HCT-8, A549, HeLa) were pretreated with rifaximin.
  • Pretreated cells were exposed to enteroaggregative Escherichia coli (EAEC), Bacillus anthracis, or Shigella sonnei.
  • Bacterial attachment and internalization were quantified.
  • Cytokine release from uninfected cells was measured.

Main Results:

  • Rifaximin pretreatment significantly reduced EAEC adherence to three of four cell lines.
  • Bacterial attachment and internalization of Bacillus anthracis were significantly reduced.
  • Rifaximin did not affect attachment or internalization of Shigella sonnei.
  • Rifaximin pretreatment reduced inflammatory cytokine release in HEp-2 cells.

Conclusions:

  • Rifaximin alters epithelial cell physiology, impacting bacterial attachment and internalization.
  • The effect of rifaximin varies depending on the bacteria's specific adhesion mechanisms.
  • Rifaximin exhibits anti-inflammatory properties by reducing cytokine release from epithelial cells.

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