Commensal Bacteria Modulate Staphylococcus aureus Protease Activity

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Solution Overview

Problem

Current treatments for dermatological disorders such as atopic dermatitis and Netherton syndrome are inadequate in addressing the increased protease activity and skin barrier disruption caused by Staphylococcus aureus colonization, which exacerbates disease severity.

Innovation Solution

A purified polypeptide and recombinant microorganisms, such as Staphylococcus epidermidis and Staphylococcus hominis, are used to inhibit protease production and activity, modulate the agr quorum sensing system of Staphylococcus aureus, and maintain skin barrier integrity through topical formulations and probiotic compositions.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Object-affected harmful factors

If Staphylococcus aureus colonization is present, then skin barrier disruption and protease activity increase, but disease severity worsens

Engineering Contradiction:
Improveskin barrier disruptionVSAvoiddisease severity
Core Design Contradiction:
Object-affected harmful factorsVSObject-generated harmful factors

Solution Approach 1:

The patent uses commensal bacteria (Staphylococcus epidermidis and Staphylococcus hominis) that naturally inhibit pathogenic S. aureus through quorum sensing interference. The commensal bacteria convert the harmful effect of S. aureus colonization into a beneficial outcome by producing auto-inducing peptides that block S. aureus virulence factors, thereby reducing protease activity and skin barrier disruption while improving disease outcomes in atopic dermatitis and Netherton syndrome

Inventive Principle:
Principle #22Blessing in disguise (Convert harm into benefit)

Solution Approach 2:

The patent introduces commensal bacteria as intermediary organisms that mediate between the host skin and pathogenic S. aureus. These commensal bacteria produce auto-inducing peptides (AIPs) that act as signaling molecules to interfere with S. aureus quorum sensing, preventing the pathogen from activating virulence genes. This intermediary mechanism reduces protease production and protects skin barrier integrity without directly attacking the pathogen

Inventive Principle:
Principle #24Intermediary (Mediator)

2Reliability

If protease activity is increased by S. aureus, then skin barrier function deteriorates, but current treatments are inadequate

Engineering Contradiction:
Improveskin barrier functionVSAvoidprotease activity
Core Design Contradiction:
ReliabilityVSObject-generated harmful factors

Solution Approach 1:

The patent applies commensal bacteria topically to the skin before or during S. aureus colonization to preemptively establish protective microbial communities. The commensal bacteria colonize the skin surface and continuously produce auto-inducing peptides that inhibit S. aureus quorum sensing, preventing the activation of protease genes before they can cause significant skin barrier damage. This preliminary protective action maintains skin barrier function more effectively than treating established infections

Inventive Principle:
Principle #10Preliminary action

Data Source

PatentUS20240325460A1Molecular bacteriotherapy to control skin enzymatic activity
Publication Date: 2024.10.03 RGT UNIV OF CALIFORNIA
  • US20240325460A1 patent drawing
  • US20240325460A1 patent drawing
  • US20240325460A1 patent drawing

AI summary

The disclosure relates to composition and methods to treat dermatological diseases and disorders and to composition that modulate skin barrier permeability.