Mannose-Equipped Nanogels Disrupt Pathogen Shields
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Solution Overview
Problem
Mannose residues on pathogens form clusters that self-interact and create a 'shield' of structured water, making it difficult for mannose-binding lectins to recognize and target these pathogens, thereby hindering the immune system's ability to effectively respond to infections.
Innovation Solution
Delivering mannose-equipped nanogels that disrupt mannose self-interactions and water structuring on pathogen surfaces, allowing mannose receptors on immune cells to more easily recognize pathogens, which includes mannose-coated or filled nanogels that release mannobiose cargo to interfere with mannose clusters and enhance lectin recognition.
Engineering Contradictions & Design Principles
Engineering Contradiction Analysis
1Reliability
If mannose residues are present in clusters on pathogen surfaces, then the pathogen can resist lectin binding and immune recognition, but this self-interaction creates a shield that prevents effective immune response
Solution Approach 1:
The patent introduces mannobiose as an intermediary substance that binds to mannose clusters on pathogen surfaces. This intermediary molecule disrupts the self-interaction shield formed by mannose residues, making the pathogen surface more accessible to lectins and immune receptors. The mannobiose acts as a mediator that translates the harmful mannose clustering into a beneficial state for immune recognition.
Solution Approach 2:
The patent changes the chemical and physical parameters of the mannose surface by introducing mannobiose, which alters the self-interaction properties of mannose residues. This parameter change disrupts the structured water moat and mannose-mannose bonding, transforming the surface from a protective shield to an accessible target for immune recognition.
2Reliability
If concentrated lectins are introduced to bind mannose-containing viruses, then immune recognition is enhanced, but the mannose clusters self-latch and prevent lectin access
Solution Approach 1:
Mannobiose serves as a mediator that interferes with the self-latching mechanism of mannose clusters. By binding to the mannose residues, mannobiose prevents the clusters from forming protective self-latched structures, thereby enabling lectins to access and bind to mannose-containing pathogens effectively.
Solution Approach 2:
The patent applies preliminary action by introducing mannobiose before lectin binding occurs. This preliminary disruption of mannose self-interactions prepares the pathogen surface to be more receptive to lectin binding, effectively preventing the self-latching barrier from forming in the first place.
3Reliability
If free mannose is delivered to disrupt mannose self-interactions, then lectin recognition is enhanced, but the delivery mechanism must overcome the protective water structuring moat
Solution Approach 1:
Mannobiose acts as an intermediary that penetrates or disrupts the structured water moat surrounding mannose clusters. By introducing mannobiose into this protected environment, the patent enables disruption of mannose self-interactions without requiring direct delivery of lectins through the water barrier.
Solution Approach 2:
The patent changes the physical chemistry parameters of the water-mannose interface by introducing mannobiose, which alters the structured water moat's properties. This parameter change allows mannose self-interactions to be disrupted while maintaining effective delivery mechanisms.
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
This approach enhances the immune system's ability to recognize and destroy pathogens by making mannose residues on pathogens more accessible, thereby preventing or reducing infections caused by a broad spectrum of diseases, including Ebola, Marburg, SARS, Dengue, and HIV, and potentially cancer cells.
Implementation Method 1
Mannose residues on pathogens form clusters that self-interact
Implementation Method 2
mannose residues to bind to one another
Implementation Method 3
Mannose clusters also appear to build a 'moat' of structured water over them interfering with access to the mannose residues
Implementation Method 4
Free forms of mannobiose interfere with ordered packing between anchored mannose residues, disrupting both self-stickiness and water-structuring
Data Source
AI summary
Methods and compositions are provided for preventing and/or treating infection by disrupting interactions at or near the surface of mannosylated pathogens or other pathogens exhibiting carbohydrate-carbohydrate self-interaction, thus enhancing the immune system's ability to recognize and destroy such pathogens. In some forms, carrier molecules are provided to delivering polymers or other molecules capable of disrupting intra-cellular interaction and/or self-interaction of surface markers on cells.