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Periodontal pathogen Aggregatibacter actinomycetemcomitans JP2 correlates with colonic leukocytes decrease and gut

André L A da Costa1,2, Mariana A Soares3, Talita G B Lourenço1

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Summary

Oral pathogen Aggregatibacter actinomycetemcomitans (Aa) alters gut microbiota and reduces immune cells in mice. This oral-gut axis disruption shows increased pathobionts and decreased commensals without significant gut inflammation.

Keywords:
Aggregatibacter actinomycetemcomitans JP2gut dysbiosisgut microbiomehomeostasisoral–gut axisperiodontal pathogen

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Area of Science:

  • Microbiology
  • Immunology
  • Gastroenterology

Background:

  • Oral pathogens may translocate to the gut, potentially causing intestinal dysbiosis via the oral-gut axis.
  • Highly leukotoxic strains of Aggregatibacter actinomycetemcomitans (Aa) are implicated in periodontal disease.

Purpose of the Study:

  • To investigate the effects of a highly leukotoxic Aa strain (JP2) on the gut microbiota, intestinal mucosal integrity, and immune system in healthy mice.
  • To evaluate the impact of oral pathogen translocation on the gut ecosystem.

Main Methods:

  • Eight-week-old male C57BL6 mice were gavaged with Aa JP2 or PBS for 4 weeks.
  • Analyses included colonic lamina propria, fecal material, serum, gingival tissues, and mandibles.
  • Parameters assessed: leukocyte populations, inflammatory mediators, mucosal integrity, alveolar bone loss, and gut microbiota.

Main Results:

  • Aa JP2 infection reduced gut microbial richness and colonic myeloid cells (macrophages, neutrophils, monocytes).
  • Increased abundance of Clostridiaceae, Lactobacillus taiwanensis, and Helicobacter rodentium was observed in infected mice.
  • Infected mice showed higher colonic IL-6 expression, splenic MPO activity, and slight alveolar bone loss.

Conclusions:

  • Intragastric Aa JP2 administration alters the gut ecosystem in healthy mice.
  • Changes include reduced myeloid cells, enrichment with pathobionts, and a decrease in commensals.
  • No significant disruption of mucosal barrier or colonic inflammation was observed.