Co-existence between Microbes and Host Cells
There is much difficulty clearing an infection with prolonged sub-lethal arsenal of an antibiotic and the immunity, and this promotes tolerance with a resultant co-existence between the pathogen and the host cell. The pathogen would be slow-growing, usually intracellularly or extra-cellularly as biofilm. T-reg is upregulated as fewer antigens are shed, and even then not exposed as buried in the biofilm. Nutrients requirements are met by apoptosis from low grade inflammation. Adulthood stress-related inflammation is therefore supportive.
An attempt to mount further and much forceful attack on the pathogen, by cutting through the biofilm, will only lead to toxin production and inflammation with little killing. Antibiotic peptide, TNF and amyloid production, meant to kill microbes, only promote further inflammation. The persistent pathogen, slowly-growing or dormant, has become less metabolically and structurally sensitive to further antibiotic stress and the host immune response, when these normally would be lethal tto the microbe in ordinary times.
This co-existence can last the host's lifetime, and through re-infection and a bolster of oxygen and nutrients, such as when the host experiences some stress and mobilizes energy from stores and produces cytokines(the cytokine storm is derived from free radical production) the pathogens reactivate, produce toxins and acute infection (a flare) sets in motion.
A correspondingly well-fed immune system can then clear the infection. Failing to do so, granulomas are formed from TNF and amyloid that damage tissue and activate mast cells to generate stem-cell proliferative factor that promotes adhesion molecules, cellular proliferation and fibrosis with mucinosis(lupus) as well as the upregulation of metalloproteases that in turn activate lipases. Panniculitis and a switch from type I to type III collage are observable features. Fibroblasts, in turn, activate mast cells. Exocytosis of indigestible materials from phagosomes, including host materials, being difficult to be removed, become enclosed in granuloma. With enhanced immune stimulation, T-suppressor(T-reg) cells are becoming T-heper cells.
There's autoimmunity. Oxidation and cross-linking modify macromolecules, making them look 'foreign' and prevent normal hydrolysis, rendering breakdown difficult and promoting persistence, autoimmunity and formation of granulomas with an enclosing palisade. Upregulated vitamin D, antibiotic,TNF, amyloid, free radical production and calcium uptake are observed. These events may eventually produce calcium carbonate, calcium oxalate and compounds of sulfur from anaerobiosis. .
In latency, this residual infection is still doing harm to the patient host in ways different from the classical pathophysiology that the acute infection itself would present; usually as low-grade chronic inflammation, with intracellular microbes in host cells and sometimes infections sealed up in granuloma.The released toxins scramble the host cell metabolism and promote aging.When a toxin subdues the host defense, and the pathogens themselves, it may kill or weaken some host cells and prevent them from mounting an attack, and the red flag tags, carried by the pathogens and used by the host as indicator(signal) for a counterattack, are lost from decreased protein translation.
Yet there is another type of a tolerant co-existence between microbes and the host that would not cause disease if the needs of the micro-organisms are catered for by the host and which microbes will cater for the host's needs if an immune response is not mounted against them. These are normal flora that, and like pathogens, have a toxin/anti-toxin system. They have foreign antigens but the immune system deems them innocuous or less of a threat and causes the synthesis of tolerant Treg rather than T-helper cells which normally fend off the intruder.
Anything that helps those less threatening microbes to live in harmony, such as the shedding of the host epithelium, rich in proteins, fats and carbohydrates or exogenous fiber from consumed food will be a boon, since the dilemma of dependence on viable host cells for food, and by extension the need for the secretion of toxins, will not be posed. It should be noted that stress produces toxic metabolic waste in every cell, be it a microbial or host cell.
They are normal flora, found on the skin, in the gut, the respiratory tract and reproductive cannal.They ferment soluble fiber into short-chain carboxylic(organic) acids that, themselves, limit microbial growth. Excess normal flora can become pathogenic when growth is not controlled, wherein the increased number will make additional demands for nutrient that may not be met, for being scarce, and lead to toxin production, tissue damage(in the search for nutrients) and inflammation.
Dr. Oliver Verbe Birnso, MD.
An attempt to mount further and much forceful attack on the pathogen, by cutting through the biofilm, will only lead to toxin production and inflammation with little killing. Antibiotic peptide, TNF and amyloid production, meant to kill microbes, only promote further inflammation. The persistent pathogen, slowly-growing or dormant, has become less metabolically and structurally sensitive to further antibiotic stress and the host immune response, when these normally would be lethal tto the microbe in ordinary times.
This co-existence can last the host's lifetime, and through re-infection and a bolster of oxygen and nutrients, such as when the host experiences some stress and mobilizes energy from stores and produces cytokines(the cytokine storm is derived from free radical production) the pathogens reactivate, produce toxins and acute infection (a flare) sets in motion.
A correspondingly well-fed immune system can then clear the infection. Failing to do so, granulomas are formed from TNF and amyloid that damage tissue and activate mast cells to generate stem-cell proliferative factor that promotes adhesion molecules, cellular proliferation and fibrosis with mucinosis(lupus) as well as the upregulation of metalloproteases that in turn activate lipases. Panniculitis and a switch from type I to type III collage are observable features. Fibroblasts, in turn, activate mast cells. Exocytosis of indigestible materials from phagosomes, including host materials, being difficult to be removed, become enclosed in granuloma. With enhanced immune stimulation, T-suppressor(T-reg) cells are becoming T-heper cells.
There's autoimmunity. Oxidation and cross-linking modify macromolecules, making them look 'foreign' and prevent normal hydrolysis, rendering breakdown difficult and promoting persistence, autoimmunity and formation of granulomas with an enclosing palisade. Upregulated vitamin D, antibiotic,TNF, amyloid, free radical production and calcium uptake are observed. These events may eventually produce calcium carbonate, calcium oxalate and compounds of sulfur from anaerobiosis. .
In latency, this residual infection is still doing harm to the patient host in ways different from the classical pathophysiology that the acute infection itself would present; usually as low-grade chronic inflammation, with intracellular microbes in host cells and sometimes infections sealed up in granuloma.The released toxins scramble the host cell metabolism and promote aging.When a toxin subdues the host defense, and the pathogens themselves, it may kill or weaken some host cells and prevent them from mounting an attack, and the red flag tags, carried by the pathogens and used by the host as indicator(signal) for a counterattack, are lost from decreased protein translation.
Yet there is another type of a tolerant co-existence between microbes and the host that would not cause disease if the needs of the micro-organisms are catered for by the host and which microbes will cater for the host's needs if an immune response is not mounted against them. These are normal flora that, and like pathogens, have a toxin/anti-toxin system. They have foreign antigens but the immune system deems them innocuous or less of a threat and causes the synthesis of tolerant Treg rather than T-helper cells which normally fend off the intruder.
Anything that helps those less threatening microbes to live in harmony, such as the shedding of the host epithelium, rich in proteins, fats and carbohydrates or exogenous fiber from consumed food will be a boon, since the dilemma of dependence on viable host cells for food, and by extension the need for the secretion of toxins, will not be posed. It should be noted that stress produces toxic metabolic waste in every cell, be it a microbial or host cell.
They are normal flora, found on the skin, in the gut, the respiratory tract and reproductive cannal.They ferment soluble fiber into short-chain carboxylic(organic) acids that, themselves, limit microbial growth. Excess normal flora can become pathogenic when growth is not controlled, wherein the increased number will make additional demands for nutrient that may not be met, for being scarce, and lead to toxin production, tissue damage(in the search for nutrients) and inflammation.
Dr. Oliver Verbe Birnso, MD.
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