JMM Editor's Choice: investigating host responses to infection by Staphylococcus aureus and/or Burkholderia cenocepacia

Posted on December 9, 2019   by Microbiology Society

The Journal of Medical Microbiology (JMM) is a journal published by the Microbiology Society, focused on providing comprehensive coverage of medical, dental and veterinary microbiology and infectious diseases, including bacteriology, virology, mycology and parasitology. This month, Dr Marcello Riggio has selected ‘Staphylococcus aureus products subvert the Burkholderia cenocepacia-induced inflammatory response in airway epithelial cells’.

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This article by Ji et al. is a well-executed, interesting and novel mechanistic study that investigates the host response to mono- and co-infection with Staphylococcus aureus and Burkholderia cenocepacia in epithelial cells of the human airway. The key finding was that S. aureus can attenuate the pro-inflammatory response induced by B. cenocepacia The major benefit of the study is that there is potential for the development of improved treatments for patients with chronic pulmonary infections and for reducing excessive inflammation.

Staphylococcus aureus products subvert the Burkholderia cenocepacia-induced inflammatory response in airway epithelial cells

Long-term infection of the lungs is usually associated with multiple micro-organisms. To improve understanding of the interactions between these micro-organisms and the host, this study investigated host responses to infection with the bacteria Staphylococcus aureus and/or Burkholderia cenocepacia.

Using a cell model of human epithelial cells, cell signalling and inflammatory responses were measured following co-infection with S. aureus and B. cenocepacia. The results showed that when human epithelial cells were infected with B. cenocepacia alone, MAPK and NF-κB pathways were activated, leading to the production of interleukin-8 (IL-8). However, co-infection with both B. cenocepacia and S. aureus did not illicit as strong an anti-inflammatory response.

These findings provide insight into a staphylococcal immune evasion mechanism, as well as identifying a potential therapeutic intervention for excessive inflammation.