Communication between nostril/skin microbiome bacteria can influence pathogen behavior

July 22, 2014

A team of scientists has made an important discovery about the molecular interactions that occur between generally benign species of Propionibacterium bacteria and the pathogenic bacterium Staphylococcus aureus, the cause of most "staph" infections.

These are commonly found in the human nostrils and, also, on human skin. S. aureus is a potential pathogen that inhibits the nostrils of about a quarter of all adults. It is also a common cause of skin and more . The team, led by Forsyth scientists, discovered that a small molecule secreted by skin/nostril-associated Propionibacterium species impacts the behavior of S. aureus in the lab. This research may lead to new and sustainable ways to manage the nostril-associated bacterial community to decrease infection.

S. aureus infections range in severity from mild to life threatening invasive infections. Although many people live with the bacteria in their nostrils and never get sick, having S. aureus present in the nostrils is a risk for infection. In recent years, the emergence of an antibiotic resistant form (methicillin-resistant S. aureus, or MRSA) has been a vexing problem. According to the Centers for Disease Control and Prevention, MRSA caused over 80,000 cases of invasive disease and over 10,000 annual deaths from 2005 through 2011. Community-associated or CA-MRSA imposes an annual burden of $478 million to 2.2 billion on third-party payers and $1.4-13.8 billion on society (Clinical Microbiology and Infection, June 19,2013).

In spite of the known importance of nostril colonization as a risk for S. aureus infection, little is known about the interactions between the benign bacteria that inhabit the adult nostril and S .aureus, and what might cause this bacterium to become pathogenic. In this study, the team of researchers found that a small molecule, coproporphyrin III (CIII), excreted by Propionibacterium species found on nostril and skin surfaces causes S. aureus to aggregate and stick together, i.e., form biofilms, when grown in the laboratory. CIII induction of S. aureus aggregation is dependent on dose, the bacterium's growth phase and an acidic pH in the normal range for skin surfaces. The biofilm formation occurs in the absence of plasma proteins, which suggests that it could occur on human skin surfaces, like the lining of the nostrils. "The emergence of antibiotic resistant S. aureus has accentuated the need to understand how the generally benign bacteria that live side-by-side with S. aureus might influence its ability to reside in the nose and on the skin where it has the opportunity to initiate infection," said Dr. Katherine Lemon, Associate Member of the Staff, Department of Microbiology at the Forsyth Institute. "This study is exciting because it is the first time that it's been demonstrated that there is a role for CIII in bacterial interspecies interactions and it shows that nostril microbiota are influenced by small-molecule-mediated interactions."

Explore further: Staphylococcus aureus: Why it just gets up your nose

More information: This study, "Propionibacterium-produced Coproporphyrin III induces Staphylococcus aureus aggregation and biofilm formation," will be published in mBio on July 22, 2014.

Related Stories

Staphylococcus aureus: Why it just gets up your nose

December 27, 2012

A collaboration between researchers at the School of Biochemistry and Immunology and the Department of Microbiology at Trinity College Dublin has identified a mechanism by which the bacterium Staphylococcus aureus (S. aureus) ...

MRSA strain gained dominance with help from skin bacteria

December 17, 2013

Scientists believe they have an explanation for how the most common strain of methicillin-resistant Staphylococcus aureus (MRSA) rapidly rose to prominence. Research published in mBio, the online open-access journal of the ...

Recommended for you

Ebola virus mutations may help it evade drug treatment

September 11, 2015

Genetic mutations called "escape variants" in the deadly Ebola virus appear to block the ability of antibody-based treatments to ward off infection, according to a team of U.S. Army scientists and collaborators. Their findings, ...


Please sign in to add a comment. Registration is free, and takes less than a minute. Read more

Click here to reset your password.
Sign in to get notified via email when new comments are made.