Research

 

The skin microbiome response to systemic isotretinoin acne therapy

Resident: William H. McCoy IV, M.D., Ph.D.
Medical Student: Elaine Otchere B.S.
Faculty Mentors: Caroline M. Mann, M.D. and Makedonka Mitreva, Ph.D.
Research Support: American Acne and Rosacea Society Clinical Research
Grant 2015

 

Acne vulgaris results in >5 million office visits per year and annual direct
healthcare costs of >$2 billion in the United States. This enormous healthcare
cost is due in a large part to the fact that >85% of adolescents suffer from acne
and, though incidence decreases with age, it continues to significantly affect
>10% of adults in their 5th decade of life. Further, effective therapy usually
requires prolonged trial-and-error with various treatments (benzoyl peroxide,
antibiotics, oral contraceptives, laser therapy, etc.) leading to frequent
medication noncompliance. This circuitous and costly route to "clear skin" is a
consequence of our as yet incomplete understanding of acne pathogenesis.

 

The role of the skin commensal bacterium Propionibacterium acnes in acne
pathogenesis has been the subject of intense investigation for half a century,
and not surprisingly the majority of acne treatments are antimicrobial with
many clinicians commonly prescribing systemic antibiotics. Unfortunately, the feared consequence of such practices, the development of antibiotic resistant P. acnes strains, has already been documented. Collateral damage of the normal human microflora may lead to serious human ailments, as has already been seen in the emergence of methicillin-resistant Staphylococcus aureus and Clostridium difficile infections. Recent skin microbiome work has described P. acnes strains distinctly associated with normal skin versus the skin of acne vulgaris patients and further identified genomic regions unique to acneassociated strains, thus suggesting that we may be able to narrow our
antimicrobial treatment of acne to only the pathogenic P. acnes strains.

 

This previous work provided a snapshot of the skin microflora, but the
response of P. acnes or any other part of the skin microbiome to acne
treatment has yet to be investigated. We hypothesize that symptomatic acne
patients will have P. acnes communities that will shift towards those observed
in normal skin following successful clinical treatment. We are currently
collecting microbiomes samples to compare the microbiomes of subjects
without acne to patients with acne undergoing isotretinoin treatment. The
results of this work will both add to our knowledge of acne pathogenesis and
support research into targeted acne treatments that spare commensal flora
essential for skin health, thus minimizing the "collateral damage" enacted via
the treatment of acne.


For additional information or questions, please contact Dr. William H. McCoy

bmccoy@wustl.edu.