Biofilm-Host Interaction in Chronic Infection

Biofilms, bacterial communities surrounded by protecting extracellular matrix, are resistant to antibiotics and the host defense systems. Most recent research results suggest that the inter-kingdom signaling between biofilm forming bacteria and the host cells might elucidate the different phases in chronic biofilm infection. The aim of our studies is to illuminate the molecular mechanisms of biofilm-host crosstalk in periodontitis, a chronic infection destroying the tooth supporting tissues.
We are part of the European Network of Aggregatibacter actinomycetemcomitans research


In natural environment, bacteria form communities, biofilms, on surfaces. In biofilms, bacteria are more resistant than their planktonic forms to antimicrobials and host defense factors. Reasons for biofilm resistance to external forces include a protective extracellular matrix and formation of non-dividing persister cells. In humans, bacterial biofilms cause chronic infections. A common biofilm diseases in humans is periodontitis, a persistent multispecies infection triggering chronic inflammation in tooth-supporting tissues. Periodontitis is characterized by active and less active phases in inflammation and tissue destruction suggesting that there might be certain type of pathogen-host crosstalk. It has been suggested that bacteria growing in biofilms could exploit pro-inflammatory cytokines produced by the host. Thus cytokine network aimed to enhance the clearance of pathogens might actually promote bacterial survival in protective biofilm.


Our research is focused on studying a novel virulence mechanism of an aggressive periodontal pathogen Aggregatibacter actinomycetemcomitans: how the opportunistic pathogen is sensing the host response in inflammation. The research includes molecular- and structural biology methods, flow cytometry and electron microscopy. In addition, we study the biofilm-host interaction by using cell culture model which mimics the gingival tissue.


This research opens possibilities to search for novel treatments to chronic biofilm infections, such as periodontitis. Molecular level information about bacterial virulence mechanisms is needed in battle against pathogenic bacteria, especially in the era of increasing amount of antimicrobial resistance which threatens modern medicine, including cancer treatments and organ transplants. Targeting virulence mechanisms instead of bacterial molecules essential for growth and viability, decreases the risk of development of resistance to novel antimicrobials.