Interaction of the SXT/R391 element ICEPmiJpn1 with its natural host Proteus mirabilis

Douglas Lyra de Holanda Fonseca1, Gaby Soares Scheunemann1, Bruna Nakanishi Fortes1

  • 1Department of Microbiology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.

PubMed

Insights

Integrative and conjugative elements (ICEs) like ICEPmiJpn1 do not harm their host bacteria, Proteus mirabilis, but their spread depends on bacterial strain factors. This research clarifies ICE-host interactions and antibiotic resistance gene mobility.

Area of Science:

  • Microbiology
  • Genetics
  • Molecular Biology

Background:

  • Integrative and conjugative elements (ICEs) are mobile genetic elements that can spread antimicrobial resistance genes.
  • The SXT/R391 family of ICEs are widespread and integrate into bacterial chromosomes.
  • Understanding the host-bacterium relationship is crucial for controlling antibiotic resistance.

Purpose of the Study:

  • To investigate the relationship between ICEPmiJpn1 and its natural host, Proteus mirabilis.
  • To evaluate the impact of ICEPmiJpn1 on P. mirabilis physiology and pathogenicity.
  • To determine how P. mirabilis genetic background influences ICE transfer.

Main Methods:

  • Used isogenic P. mirabilis strains (with and without ICEPmiJpn1).
  • Assessed bacterial fitness, self-recognition, swarming, pathogenicity, persistence, and biofilm formation.
  • Conducted mating assays to study conjugative transfer to Escherichia coli using different P. mirabilis donors.

Main Results:

  • ICEPmiJpn1 did not significantly affect P. mirabilis fitness, self-recognition, swarming, pathogenicity, or persistence.
  • Biofilm formation was increased in one P. mirabilis strain harboring ICEPmiJpn1.
  • Conjugative transfer efficiency of ICEPmiJpn1 varied significantly depending on the P. mirabilis donor strain.

Conclusions:

  • ICEPmiJpn1 exhibits a stable association with P. mirabilis, showing no adverse physiological or pathogenicity effects.
  • ICE transfer is influenced by both element-specific regulators and host strain-specific factors.
  • Further research into host-dependent mechanisms is needed to combat antibiotic resistance spread.

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