Inflammatory potential of monospecies biofilm matrix components

T Ramirez1, A Shrestha2, A Kishen2

  • 1Faculty of Dentistry, Universidad de Costa Rica, San José, Costa Rica.

Abstract

Insights

Biofilm matrix components from Enterococcus faecalis and Pseudomonas aeruginosa induce low-grade inflammation. Exopolysaccharides (EPS) and extracellular DNA (eDNA) showed less inflammatory potential than planktonic bacteria.

Area of Science:

  • Microbiology
  • Immunology
  • Biochemistry

Background:

  • Bacterial biofilms are a significant challenge in healthcare settings.
  • The inflammatory potential of biofilm matrix components is not fully understood.
  • Enterococcus faecalis and Pseudomonas aeruginosa are common pathogens associated with biofilm formation.

Purpose of the Study:

  • To evaluate the inflammatory response induced by exopolysaccharides (EPS) and extracellular DNA (eDNA) from monospecies biofilms of E. faecalis and P. aeruginosa.
  • To compare the inflammatory potential of biofilm matrix components with planktonic bacteria and lipopolysaccharide (LPS).

Main Methods:

  • In vitro biofilms of E. faecalis and P. aeruginosa were cultured under aerobic and anaerobic conditions.
  • EPS and eDNA were extracted and quantified from the biofilms.
  • The inflammatory potential was assessed on macrophage cell lines by measuring nitric oxide (NO), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) levels.

Main Results:

  • EPS levels were higher than eDNA in both growth conditions for both bacterial strains.
  • Biofilm matrix components exhibited lower inflammatory potential compared to planktonic bacteria and LPS.
  • EPS induced a greater inflammatory response than eDNA for both strains.
  • P. aeruginosa EPS and eDNA significantly increased IL-6 levels compared to TNF-α and NO.

Conclusions:

  • Monospecies biofilm matrix EPS and eDNA can induce a low-grade inflammatory response.
  • These findings suggest that bacterial biofilm matrix components, even without live bacteria, may contribute to chronic inflammation.

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