Wednesday, October 30, 2013
Martin McGavin, PhD, of the Departments of Medicine, and Microbiology and Immunology, is one of the authors on a new paper published by Nature looking at the possible connection between staph infections and eczema, a red, itchy skin condition. The University of Michigan-led research pinpoints molecules from bacteria that may play a key role in prompting skin inflammation, and could be a target for treatment.
Even before coming to Western in 2009, McGavin worked with clinicians towards understanding how epidemic strains of Staphylococcus aureus (S. aureus) colonize humans. While roughly 25% of the population is stably colonized by S. aureus, this can be much higher depending on both host- and microbe-specific factors. From the microbial perspective, community acquired methicillin resistant S. aureus (CA-MRSA) have become established in both the community and hospital setting. Of special concern, one strain of CA-MRSA that is endemic across North America, causes severe invasive skin and soft tissue infections that can quickly progress to systemic and fatal complications if not effectively treated, and it is more efficiently transmitted among household contacts compared to other strains.
From the human perspective, a significant portion of the population suffers from atopic dermatitis (eczema), where the skin produces reduced amounts of antimicrobial fatty acids, which would otherwise serve to limit growth of S. aureus. Consequently, eczema patients are normally heavily colonized by S. aureus, which in turn contributes to the severity of disease. This, combined with the prevalence of CA-MRSA, constitutes a potential threat to the health of eczema patients, and the general community.
“On this basis, we instigated a study to assess the prevalence of CA-MRSA among eczema patients,” says McGavin. “Fortunately, our findings revealed that this threat has not yet materialized in Canada, and when published, it drew the attention of Dr. Gabriel Nunez, a Clinician-Scientist at University of Michigan.”
Dr. Nunez was studying molecules produced by S. aureus, which trigger inflammation of the skin, and their efforts zeroed in on a previously known but poorly understood small peptide named delta toxin. They found that delta toxin could trigger immune cells known as mast cells, to release their inflammatory contents. We provided Dr. Nunez with a broad selection of S. aureus strains recovered from skin lesions of eczema patients, and his group found that they exhibited copious production of this toxin. Moreover, they were able to identify the toxin on the skin of eczema patients. Although more research needs to be done, the discovery that delta toxin aggravates mast cells in the skin offers eczema patients new hope for better treatment of the intensely irritating inflamed red itchy skin that is the hallmark of this disease. Click here to see the news release from U-M.
“It is very satisfying to see this type of study come to fruition”, says Dr. McGavin, “as my lab has had a long-standing interest in understanding how S. aureus strains colonize and persist on humans. In work funded by NSERC, we are evaluating factors that may contribute to persistence of S. aureus on the skin, in the presence of larger numbers of commensal bacteria, including Staphylococcus epidermidis, which compete with S. aureus for colonization of human skin. We are also excited over the prospects of a new initiative supported by Western’s CIHR-Strategic Success program, which allows us to evaluate how epidemic CA-MRSA alter their gene expression in response to the antimicrobial fatty acids that are present on skin. We believe that this will lead to new insight as to how S. aureus persists on the skin, and ultimately to better means of preventing the transmission of this pathogen in both the community and hospital setting.”
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