Mycobacterium tuberculosis ADK protein sepsis treatment

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Solution Overview

Problem

Current treatments for sepsis and septic shock are inadequate, particularly against antibiotic-resistant pathogens, and there is a need for an effective therapeutic agent that can address the excessive inflammatory response and mortality associated with these conditions.

Innovation Solution

A pharmaceutical and food composition containing an adenosine kinase (ADK) protein derived from Mycobacterium tuberculosis, which binds to lipopolysaccharide (LPS) to inhibit its binding to cells, thereby reducing inflammatory responses and enhancing viability in sepsis animal models.

Engineering Contradictions & Design Principles

VSEngineering Contradiction Analysis

1Reliability

If antibiotic treatment is used for sepsis, then infection control is achieved, but treatment effectiveness decreases due to antibiotic resistance

Engineering Contradiction:

Improvetreatment effectivenessVSAvoidantibiotic resistance

Core Design Contradiction:

ReliabilityVSObject-generated harmful factors

Solution Approach 1:

The patent introduces an ADK protein as an intermediary substance that binds to LPS and prevents it from activating immune cells. This mediator approach allows treatment of sepsis without relying on antibiotics, thereby overcoming antibiotic resistance while maintaining treatment effectiveness through a different mechanism (LPS binding rather than bacterial killing).

Inventive Principle:

Principle #24Intermediary (Mediator)

Solution Approach 2:

The patent converts the harmful LPS (which causes sepsis) into a beneficial interaction by using the ADK protein to bind it. The LPS that would normally trigger harmful inflammatory responses is instead captured by the ADK protein, transforming the harmful stimulus into a controlled interaction that protects against sepsis without requiring antibiotics.

Inventive Principle:

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

2Reliability

If excessive immune response is activated against LPS, then pathogen clearance is improved, but tissue damage and mortality increase

Engineering Contradiction:

Improvepathogen clearanceVSAvoidtissue damage

Core Design Contradiction:

ReliabilityVSObject-affected harmful factors

Solution Approach 1:

The ADK protein performs preliminary binding to LPS before LPS can activate immune cells and trigger harmful inflammatory responses. By pre-neutralizing the harmful LPS molecule through binding, the system prevents the cascade of harmful immune responses while still allowing controlled immune activity to clear pathogens, thus protecting tissues from damage.

Inventive Principle:

Principle #9Preliminary anti-action

Applied Scientific Principles

This section explains which scientific principles are used to turn an abstract innovation direction into a practical engineering solution.

Function Achieved in This Case

The ADK protein effectively suppresses inflammatory responses and cell death in the lung and spleen, demonstrating a therapeutic effect against sepsis and septic shock by enhancing animal model viability and reducing inflammatory cell infiltration and cytokine secretion.

Implementation Method 1

an ADK protein derived from Mycobacterium tuberculosis binds to LPS to show an excellent therapeutic effect against sepsis

Methodology Applied

Scientific EffectBinding:

Data Source

PatentUS10736944B2Compositions for preventing or treating sepsis or septic shock compromising ADK protein as active ingredient

Publication Date: 2020.08.11 KONKUK UNIV GLOCAL IND ACADEMIC COLLABORATION FOUND

AI summary

The present invention relates to a composition for preventing or treating sepsis or septic shock including a Mycobacterium tuberculosis-derived adenosine kinase (ADK) protein as an active ingredient. The Mycobacterium tuberculosis-derived ADK protein according to one exemplary embodiment of the present invention has an effect of inhibit binding between the LPS and cells by binding to LPS, and also has an excellent therapeutic effect against sepsis by enhancing viability in a sepsis animal model and suppressing inflammatory response in the lung and cell death in the spleen.