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Communication between bacteria from nostril and skin microbiome can influence pathogen behavior

CAMBRIDGE, Mass., 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 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.”

Overview of Study

This study, “Propionibacterium-produced Coproporphyrin III induces Staphylococcus aureus aggregation and biofilm formation,” will be published in mBio on July 22, 2014. It was a collaborative, multidisciplinary effort of two research groups. The work was led by Dr. Katherine P. Lemon, Department of Microbiology, Forsyth, Cambridge, MA and members of her lab, in particular, the lead author Dr. Michael Wollenberg, along with Dr. Isabel Fernandez Escapa and Ms. Kelly Aldridge. The chemistry side was led by Dr. Michael A. Fischbach and, his postdoctoral fellow, Dr. Jan Claesen from the Department of Bioengineering and Therapeutic Sciences and the California Institute for Quantitative Biosciences at the University of California, San Francisco. In addition to overseeing her lab at Forsyth, Dr. Lemon serves on the clinical staff of the Division of Infectious Diseases at Boston Children’s Hospital.

This research was supported in part by NIH through the National Institute of Dental and Craniofacial Research and the National Institute of Allergy and Infectious Diseases and through a Boston Children’s Hospital Career Development Fellowship, a Fundación Ramón Areces Fellowship, a Medical Research Program Grant from the W.M. Keck Foundation, and a Fellowship for Science and Engineering from the David and Lucile Packard Foundation.

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