Immunity versus Inflammation
There is no doubt that some inflammation assists immunity. But those two mean different things. Inflammation is the body's response to injury and involves the contingency to remove devitalized tissue to enable repair to follow. This calls for some 'surgery' by the white cells. Who talks surgery talks extraordinary measures of invasiveness that necessitate degranulation which is then followed by phagocytosis. No such action goes without bystander consequences since it is often non specific and not well contained. Microbes and host cells then become victims. Leucotrienes that result from cellular damage act as chemoattractants of white cells to the injury site . They also help white cells to degranulate, at the same time that prostaglandins are producing and augmenting pain. Immunity on the other hand specifically targets invader microbes which themselves carry specific patterns that help the white cells locate, find and kill them.
Ideally, immunity should be specific and produce no bystander fallouts. But this is not often the case as infectious microbes also carry toxins that cause damage and divided attention between the microbial target and the (damaged)host cell and therefore necessitate inflammation. More so, even when specific guiding tags are put on these pathogen-associated patterns(PAMPs) by the white cells, some of these targets are too large, such as in the case of parasites and sessile microbial forms, to be engulfed by phagocytes, and call for inflammatory 'surgery ', which degranulation is. This means reactive species, free radicals, proteases, lipases, lyzozymes(hydrolases) are unleashed, this time much closer to the target, though not without nefarious consequences. At an intermediate position, less specific tags may be produced early on during an infection. This too can lead to injury and hence inflammation. Too much inflammation is therefore counter-immunity and must be suppressed in order for the immune cell to focus attention on defense proper.
When the immune cells on the spot cannot adequately use the arms available to them because of dysfunction or when such arms have been exhausted, they usually create deliberate damage with say TNF(proinflammatory cytokine) to call for help from blood ' progenies '.This additionally leads to fever.
Immunity is usually well regulated and focused to the target with the aid of microbial tags called antibodies and this alleviates inflammation. It should be borne in mind that too much cellular metabolic activity from an overtaxed immune system leads to increased production of reactive oxygen species which cause cellular damage and promote inflammation.
Inflammation can easily spiral out of control if the immune system is not well regulated since it is a self-perpetuating process and must be arrested to prevent damage, disease, and aging(senescence) .The goal is misdirected if attention is shifted from fighting the intruder to taking care of injury caused. The non-targeted slicing and dicing process, out of the controlled environment within the lysosome--whose contents are released externally instead--, not only leads to waste and exhaustion but more importantly harms, and limits phagocytosis by interfering with the immunological tags and patterns recognition.
Dr Oliver Verbe Birnso MD
Ideally, immunity should be specific and produce no bystander fallouts. But this is not often the case as infectious microbes also carry toxins that cause damage and divided attention between the microbial target and the (damaged)host cell and therefore necessitate inflammation. More so, even when specific guiding tags are put on these pathogen-associated patterns(PAMPs) by the white cells, some of these targets are too large, such as in the case of parasites and sessile microbial forms, to be engulfed by phagocytes, and call for inflammatory 'surgery ', which degranulation is. This means reactive species, free radicals, proteases, lipases, lyzozymes(hydrolases) are unleashed, this time much closer to the target, though not without nefarious consequences. At an intermediate position, less specific tags may be produced early on during an infection. This too can lead to injury and hence inflammation. Too much inflammation is therefore counter-immunity and must be suppressed in order for the immune cell to focus attention on defense proper.
When the immune cells on the spot cannot adequately use the arms available to them because of dysfunction or when such arms have been exhausted, they usually create deliberate damage with say TNF(proinflammatory cytokine) to call for help from blood ' progenies '.This additionally leads to fever.
Immunity is usually well regulated and focused to the target with the aid of microbial tags called antibodies and this alleviates inflammation. It should be borne in mind that too much cellular metabolic activity from an overtaxed immune system leads to increased production of reactive oxygen species which cause cellular damage and promote inflammation.
Inflammation can easily spiral out of control if the immune system is not well regulated since it is a self-perpetuating process and must be arrested to prevent damage, disease, and aging(senescence) .The goal is misdirected if attention is shifted from fighting the intruder to taking care of injury caused. The non-targeted slicing and dicing process, out of the controlled environment within the lysosome--whose contents are released externally instead--, not only leads to waste and exhaustion but more importantly harms, and limits phagocytosis by interfering with the immunological tags and patterns recognition.
Dr Oliver Verbe Birnso MD
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