Tensegrity and immunology part 2. Jon Trister MD

Cellular components of the organs and tissues, vascular and neurological structures are parts of tensegrity arrangement; Microbiome is an equal part of this ecosystem. Tensegrity is influenced by the microbiome. At the same time, mechanical properties of the connective tissue will influence microbiome composition and pathogenicity.

Cellular components of the organs and tissues, vascular and neurological structures are suspended in the tensegrity network and actually part of this network. Their form and function regulated by mechanical properties of the ecosystem they reside (Pre-stress).

Pre-stress  is  influenced by  microbiome and microbiome is regulated by pre-stress.

 Microbiota are ecological communities of commensal, 

symbiotic and pathogenic microorganisms

 found in and on all multicellular organisms. Microbiota includes bacteria, archaea, protists, fungi and viruses. Microbiota have a  crucial role for immunologic, hormonal and metabolic

 homeostasis of their host. The synonymous term microbiome describes either the collective genomes of the microorganisms that reside in an environmental niche or the microorganisms themselves

Microbiome  persist in nearly every human body site, including tissue and blood. The genomes of these microbes continually interact with the human genome in order to regulate host metabolism.

Many components of this microbiome are capable of both commensal and pathogenic activity. This activity is determined by environment they reside (viscoelasticity -pre-stress): immunological cells responsible for innate and adaptive responses. They are additionally able to persist in both “acute” and chronic forms. Inflammatory conditions historically studied separately (autoimmune, neurological and malignant) are now repeatedly tied to a common trend: imbalance or dysbiosis of these microbial ecosystems.

Collective activity of the microbiome that drives inflammatory processes via complex microbe-microbe and host-microbe interactions. Many microbes survive as polymicrobial entities in order to evade the immune response. Pathogens in these communities alter their gene expression in ways that promote community-wide virulence. Other microbes persist inside the cells of the immune system (Cell Wall Deficient bacteria -CWD), where they directly interfere with host transcription, translation, and DNA repair mechanisms. The numerous proteins and metabolites expressed by these pathogens further dysregulate human gene expression in a manner that promotes imbalance and immunosuppression. Molecular mimicry, or homology between host and microbial proteins, complicates the nature of this interference. When taken together, these microbe-microbe and host-microbe interactions are capable of driving the large-scale failure of human metabolism characteristic of many different inflammatory conditions.

Microbiota are “ecological communities of commensal, symbiotic and pathogenic microorganisms” found in and on all multicellular organisms. Microbiota includes bacteria, archaea, protists, fungi and viruses. Microbiota have been found to be crucial for immunologic, hormonal and metabolic homeostasis of their host. The synonymous term microbiome describes either the collective genomes of the microorganisms that reside in an environmental niche or the microorganisms themselves

Microbiome  persist in nearly every human body site, including tissue and blood. The genomes of these microbes continually interact with the human genome in order to regulate host metabolism.

Many components of this microbiome are capable of both commensal and pathogenic activity. They are additionally able to persist in both “acute” and chronic forms. Inflammatory conditions historically studied separately (autoimmune, neurological and malignant) are now repeatedly tied to a common trend: imbalance or dysbiosis of these microbial ecosystems.The collective activity of the microbiome that drives inflammatory processes via complex microbe-microbe and host-microbe interactions. Many microbes survive as polymicrobial entities in order to evade the immune response. Pathogens in these communities alter their gene expression in ways that promote community-wide virulence. Other microbes persist inside the cells of the immune system, where they directly interfere with host transcription, translation, and DNA repair mechanisms. The numerous proteins and metabolites expressed by these pathogens further dysregulate human gene expression in a manner that promotes imbalance and immunosuppression. Molecular mimicry, or homology between host and microbial proteins, complicates the nature of this interference. When taken together, these microbe-microbe and host-microbe interactions are capable of driving the large-scale failure of human metabolism characteristic of many different inflammatory conditions. (Amy D Proal)

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