Tissue Cell SafelyTakes Care of Environmental Damage Garbage
Just as intrinsic immunity takes care of an internalized(intra-cellular) infection, each normal cell(non-professional phagocyte) is capable of 'eating' an apoptotic cell that results from environmental damage like UV radiation and mechanical shear strain and stress.
Repair, including the rapid reconstitution of the cell membrane, will prevent apoptosis, following such damage. However, for the most part, it is the availability of neighboring healthy cells, which recognize the 'eat me' signal on these damaged cells, that is responsible for clearing the mess in time before the damaged cells, themselves, become toxic, as they spill out their content. More severe damage, however, will permit some of the content to fleet about and this will allow the immune cells to sense, approach and mop up the mess, at the same time suffering injuries of their own, and causing more inflammation, by virtue of their stem-cell-like fragility and inherent ability to secrete harmful cytokines and enzymes when provoked or challenged.
Phagocytosis prevents inflammation and its accompanying pain by preventing damaged cells from releasing their toxic content in an unprotected manner, detrimental to the cell, unlike the case when it is captured safely and internally in the autophagolysomes.
The so-called immune-privileged organs, such as the eye, the testes and the brain, may simply be so well blessed with this local, non-immune cell phagocytosis ability that damaging inflammation will not be required and warranted for effective immunity. The cells and tissue infrastructure of the epithelium or tough connective tissue, are so tightly-held together that the effective penetration of immune cells is impossible, without a prior and substantial damage to the tissue. But with the presence of antigens sticking out but embedded between these cells, and therefore difficult to dislodge, it is possible to attract inflammatory cells that carry out 'frustrated phagocytosis', spilling their toxic content onto the intervening cells and committing them to die.
Increased metabolism, caused by cytokines from stress and other peroxisome proliferators like vitamins D and A and steroids, will lead, in an incrementally-determined manner, to phagocytosis and autophagy, cell repair, growth and death, respectively. But the dying cells are taken care of by the still active ones, to forestall inflammation. Cell death, and tissue damage from the loss of the integrity of the tissue architecture, will then have occurred, with minimal inflammatory pain. Inflammation returns when these autophagy stimuli are removed. Chronic inflammation responds more to growth than frank inflammatory cues, since some DNA hypermethylation sets in, in this state, in a bid to quell inflammation.
Dr. Oliver Verbe Birnso, MD
Repair, including the rapid reconstitution of the cell membrane, will prevent apoptosis, following such damage. However, for the most part, it is the availability of neighboring healthy cells, which recognize the 'eat me' signal on these damaged cells, that is responsible for clearing the mess in time before the damaged cells, themselves, become toxic, as they spill out their content. More severe damage, however, will permit some of the content to fleet about and this will allow the immune cells to sense, approach and mop up the mess, at the same time suffering injuries of their own, and causing more inflammation, by virtue of their stem-cell-like fragility and inherent ability to secrete harmful cytokines and enzymes when provoked or challenged.
Phagocytosis prevents inflammation and its accompanying pain by preventing damaged cells from releasing their toxic content in an unprotected manner, detrimental to the cell, unlike the case when it is captured safely and internally in the autophagolysomes.
The so-called immune-privileged organs, such as the eye, the testes and the brain, may simply be so well blessed with this local, non-immune cell phagocytosis ability that damaging inflammation will not be required and warranted for effective immunity. The cells and tissue infrastructure of the epithelium or tough connective tissue, are so tightly-held together that the effective penetration of immune cells is impossible, without a prior and substantial damage to the tissue. But with the presence of antigens sticking out but embedded between these cells, and therefore difficult to dislodge, it is possible to attract inflammatory cells that carry out 'frustrated phagocytosis', spilling their toxic content onto the intervening cells and committing them to die.
Increased metabolism, caused by cytokines from stress and other peroxisome proliferators like vitamins D and A and steroids, will lead, in an incrementally-determined manner, to phagocytosis and autophagy, cell repair, growth and death, respectively. But the dying cells are taken care of by the still active ones, to forestall inflammation. Cell death, and tissue damage from the loss of the integrity of the tissue architecture, will then have occurred, with minimal inflammatory pain. Inflammation returns when these autophagy stimuli are removed. Chronic inflammation responds more to growth than frank inflammatory cues, since some DNA hypermethylation sets in, in this state, in a bid to quell inflammation.
Dr. Oliver Verbe Birnso, MD
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