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Communication between nostril/skin microbiome bacteria can influence pathogen behavior

Date:
July 22, 2014
Source:
Forsyth Institute
Summary:
Scientists have 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.
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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 bacterial species 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 invasive infections.

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 skin infections 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."


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The above post is reprinted from materials provided by Forsyth Institute. Note: Materials may be edited for content and length.


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Forsyth Institute. "Communication between nostril/skin microbiome bacteria can influence pathogen behavior." ScienceDaily. ScienceDaily, 22 July 2014. <www.sciencedaily.com/releases/2014/07/140722130652.htm>.
Forsyth Institute. (2014, July 22). Communication between nostril/skin microbiome bacteria can influence pathogen behavior. ScienceDaily. Retrieved July 28, 2015 from www.sciencedaily.com/releases/2014/07/140722130652.htm
Forsyth Institute. "Communication between nostril/skin microbiome bacteria can influence pathogen behavior." ScienceDaily. www.sciencedaily.com/releases/2014/07/140722130652.htm (accessed July 28, 2015).

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