Matthew Garth Brewer, Ph.D.

My background in science began in 2006 when I enrolled at the Rochester Institute of Technology (RIT) and studied Biotechnology. During my undergraduate studies I focused on developing a cyclopropene backbone molecule that could be easily modified to develop derivatives that prevent crop ripening. I...

My background in science began in 2006 when I enrolled at the Rochester Institute of Technology (RIT) and studied Biotechnology. During my undergraduate studies I focused on developing a cyclopropene backbone molecule that could be easily modified to develop derivatives that prevent crop ripening. I worked on this project under Dr. Michael Coleman until my graduation in 2010.
Upon graduating from RIT, I started a technical position under Dr. Stephen Dewhurst at the University of Rochester (UoR). During that time, I investigated novel platforms for HIV vaccines. Specifically, I worked on using lambda phage to display HIV-1 envelope (Env) protein. I discovered that this delivery platform, while displaying a dense distribution of protein, was no better than soluble Env at initiating an anti-HIV immune response. I then joined the PhD program at the UoR in 2011 and continued to work under Dr. Dewhurst. I transitioned my studies from lambda phage to nanoparticle-based vaccine platforms to avoid the problems inherent to biological vectors. Through my studies on nanoparticles displaying either Env or Influenza hemagglutinin (HA) protein, I discovered that a sparse display of vaccine antigen was more efficient in stimulating an immune response. This was a truly unique finding since the general belief in the scientific community is that highly dense, multivalent vectors are the most ideal for vaccine candidates. Clearly, from my work, this was not always true. When I achieved my Masters of Science in 2014, I then began to teach (adjunct professor) at Saint John Fisher College, which I maintained up to the fall of 2021.
I finished my PhD in 2017 and then transitioned to a Postdoctoral Associate position working with Drs. Lisa Beck and Ben Miller. I utilized my knowledge on vaccine platforms and delivery to develop a new skin-based method of vaccination through targeting a microdomain (tight junctions) in the epidermis important for barrier formation. With this method I demonstrated that epicutaneous delivery of vaccine antigens was able to stimulate an immune response similar in magnitude to intramuscular administration.
In August 2021 I was promoted to Research Assistant Professor in the Department of Dermatology. My research currently focuses on continuing the epicutaneous vaccine delivery studies. Additionally, I have become intensely interested in chronic inflammatory skin diseases (such as atopic dermatitis and psoriasis) and pathogenesis studies. The reason for this is during my Postdoctoral position I was made aware that patients with inflammatory skin diseases, such as atopic dermatitis, were overly susceptible to skin infections from both bacteria and viruses. Importantly, the mechanism behind this observation is not known. I now focus on identifying how epidermal cells become infected by different pathogens (vaccinia virus, herpes simplex virus-1, S. aureus) and the affects that skin inflammation has on this process.
I am currently a member of the Society of Investigative Dermatology and serve as an ad hoc reviewer for the following journals: International Journal of Molecular Sciences, BBA-Biomembranes, Frontiers in Cellular and Infection Microbiology, and the Journal of Clinical Medicine.

My research focuses on the intersection between chronic inflammatory skin diseases (such as atopic dermatitis and psoriasis) and the underlying immune environment during times of stimulation (such as vaccination) and disease (both viral and bacterial pathogens).
Utilizing the skin as the primary ...

My research focuses on the intersection between chronic inflammatory skin diseases (such as atopic dermatitis and psoriasis) and the underlying immune environment during times of stimulation (such as vaccination) and disease (both viral and bacterial pathogens).
Utilizing the skin as the primary site of antigen delivery represents an underappreciated practice in vaccine biology. To correct this lack of knowledge, I am working on methods enabling antigen delivery into the epidermis. My unique approach targets a microdomain in the epidermis called tight junctions, which serve as a critical source of skin barrier. I have demonstrated that disruption of tight junctions via a targeted peptide delivers influenza antigens into the skin and elicits an anti-influenza humoral response similar to intramuscular delivery. Ongoing studies include how this technology alters the cellular and inflammatory environment of the skin. Importantly, antigen type (protein, carbohydrate, lipid) and source (bacterial, viral, protozoan) can cause alterations in acquisition, processing, and presentation from different cell types of the immune system. Whether these attributes affect the efficacy of an immune response initiated in the skin are unknown and the focus of ongoing studies. Finally, drug delivery into the epidermis represents a safer route due to diminished side effects, which typically arise after systemic delivery. Unfortunately, drug delivery into the skin is usually inefficient because of the molecular characteristics of most therapeutics. Current studies using small molecule inhibitors delivered into the skin by tight junction disruption are expected to support this technique as a method to enhance cutaneous drug delivery and decrease the necessity of oral or intravenous routes.
Individuals with chronic inflammatory skin diseases have been shown to be overly susceptible to bacterial and viral infections. The underlying mechanism behind this occurrence is poorly understood. To address this gap in knowledge, my group has developed a number of models including CRISPR/Cas9 knockout cell lines, primary cell cultures from neonatal/adult skin tissue, a mouse AD model, and an adult skin explant infection platform. I focus my viral pathogenesis studies on skin-specific viruses (vaccinia and herpes simplex, respectively). In addition, I have been studying how bacterial pathogens (S. aureus, S. epidermidis, etc.) are able to invade, persist, and disseminate in the skin. These studies are expected to identify host factors or pathways in epidermal cells (i.e. keratinocytes) that are critical for protection against or susceptibility to pathogens, which would open up new druggable targets to prevent cutaneous infections.