#FEMSmicroBlog: Pathogenic bacteria become stronger together


Just like humans in society, microbes form communities to interact with each other. These interactions can be of a competitive nature, assist in the growth of one partner, or provide a mutual benefit. The study “Enterococcus faecalis suppresses Staphylococcus aureus-induced NETosis and promotes bacterial survival in poly-microbial infections” in FEMS Microbes investigates how two human pathogens interact and impact each other in infection sites, as explained in this #FEMSmicroBlog by Patrick Hsien-Neng Kao. #FascinatingMicrobes


Microbes stronger together

Many disease-inducing infections are poly-microbial in nature as microbes rarely live in isolation. Often, several pathogens infect wounds and surgical sites, lungs in cystic fibrosis patients, or the urinary tract after catheter-induced abrasions.

In chronic infections, microbes sustain growth by adapting to their environment and forming stable biofilms. These survival mechanisms make infections harder to treat and enhance the exchange of antibiotic-resistant traits between the pathogens.

Poly-microbial infections are associated with increased severity in the progression of the disease. Currently, options to treat poly-microbial infections are limited and mainly rely on broad-spectrum antibiotics to reduce the overall microbial population. To develop novel therapeutic strategies, it is thus crucial to gain insights into how microbes interact and benefit from each other in poly-microbial infections.

 A well-known pathogen causing infections on various body sites is Staphylococcus aureus. This opportunistic pathogen escapes the human immune system using multiple mechanisms and is often co-isolated from wound infections with other bacteria, in particular Enterococcus faecalis.

In laboratory conditions, E. faecalis can transfer resistance to antibiotics to S. aureus, making the pathogen a potential reservoir for antibiotic-resistant superbugs. Yet, so far it is not clear how the interactions between both pathogens impact their survival.


E. faecalis interferes with NETosis formation and promotes the survival of S. aureus

The study Enterococcus faecalis suppresses Staphylococcus aureus-induced NETosis and promotes bacterial survival in poly-microbial infections” in FEMS Microbes investigates how E. faecalis and S. aureus impact each other and the host immune responses during co-infection.

As part of the immune mechanism against pathogens, neutrophils release DNA. This extracellular DNA forms web-like structures, the neutrophil extracellular trap (NET), aimed to trap microbes in a process called NETosis.

Previous studies showed that S. aureus infection induces NETosis while disrupting NETosis enhances the survival of S. aureus. Yet, little is known about how neutrophils respond to E. faecalis infections.

The study presented here identified the neutrophil responses against E. faecalis and investigated how they differ from the responses induced by S. aureus. Shown for the first time, neutrophils recognise E. faecalis and respond by producing reactive oxygen species in large amounts as well as with phagocytosis.

But unlike S. aureus, E. faecalis does not trigger the formation of NETs. Instead, co-infection of E. faecalis reduces the level of NETosis induced by S. aureus, which correlates with reduced killing rates of S. aureus by neutrophils.

Co-infection with Enterococcus faecalis promotes Staphylococcus aureus survival. From Kao et al. (2023).

As multiple cellular pathways regulate NET-formation, the study looked into how E. faecalis would interfere with this process. Results show that E. faecalis inhibits histone citrullination thus preventing histone decondensation, a prerequisite to loosening the chromatin before its release.

Furthermore, co-infection of both S. aureus and E. faecalis leads to stronger growth of E. faecalis, indicating that a poly-microbial community is more resistant than a single species causing an infection. These findings highlight the complexity of the immune response to poly-microbial infections and suggest that co-infection can alter the pathogen-specific immune responses, contributing to the pathogenesis of one or both co-infecting species.


About the author of this blog

Dr Patrick Hsien-Neng Kao completed his Master’s education at the National Taiwan University and received his Ph.D. from Nanyang Technological University. He is an immunologist focusing on host-microbe interactions, particularly the mechanisms of how bacteria evade the immune system. Intrigued by the widespread antibiotic resistance problem, he aims to discover alternative options to fight infectious diseases.

About this blog section

The section #FascinatingMicrobes for the #FEMSmicroBlog explains the science behind a paper and highlights the significance and broader context of a recent finding. One of the main goals is to share the fascinating spectrum of microbes across all fields of microbiology.

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