The human skin is home to many types of bacteria, fungi, and viruses that compose the skin microbiome. These 1,000s of different organisms and species have an important role in protecting from pathogens, influences immune functions and the ability of the skin to form a protective barrier, which in turn either promote or disrupt human health (1).
In some disease states, an altered balance of the skin microbiome can occur, a condition known as dysbiosis. This state of dysbiosis contributes to the disruption of immune homeostasis and worsens disease symptoms (1).
For example, atopic dermatitis is often characterized by dysbiosis of the skin microbiome, with an over-abundance of Staphylococcus aureus bacteria (2).
Our work has discovered mechanisms for how selected bacteria cause or prevent diseases and has shown that reintroducing specifically selected beneficial bacterial strains from healthy skin can alleviate disease symptoms as well as kill or inhibit harmful species (3).
Using the discovery platform based on leading research from the Gallo Laboratory at the University of California San Diego, MatriSys is able to screen thousands of microbes on the skin to identify beneficial bacteria that can treat skin disorders and restore homeostasis to the skin microbiome.
The team at Matrisys then optimizes the beneficial bacteria with the goal to identify and clinically develop a topical prescription formulation.
MatriSys leverages a deep clinical pipeline to treat the millions of children and adults suffering from difficult to treat chronic skin diseases.
Our lead clinical development program, MSB-0221, is for the treatment of Atopic Dermatitis (AD), a common skin condition which affects more than 18 million patients in the US alone. Current therapies include moisturizers, topical corticosteroids, anti-inflammatory agents (PED4i) and immunosuppressants (topical and systemic), but can be associated with skin thinning and other safety concerns. Given the existing high unmet medical need, new therapies are needed to address the root cause of the disease. The mechanisms by which MSB-0221 may help AD is depicted in the cartoon below.
Antimicrobial activity via production of 2 lantibiotics that directly kill S. aureus.
AIP (autoinducing peptides) production inhibiting the aggressive proteases and PSMs produced by S. aureus, as well as the damaging proteases and toxins from S. epidermis, which degrade the skin barrier and trigger an immune reaction.
Helps the commensal bacterial community recreate itself, preventing further S. aureus, colonization, and has potential to directly act on human skin to improve its defense and decrease inflammation.