Abstract
Almost every kind of inflammation in the human body is accompanied by rising C-reactive protein (CRP) concentrations. This can include bacterial and viral infection, chronic inflammation and so-called sterile inflammation triggered by (internal) acute tissue injury. CRP is part of the ancient humoral immune response and secreted into the circulation by the liver upon respective stimuli. Its main immunological functions are the opsonization of biological particles (bacteria and dead or dying cells) for their clearance by macrophages and the activation of the classical complement pathway. This not only helps to eliminate pathogens and dead cells, which is very useful in any case, but unfortunately also to remove only slightly damaged or inactive human cells that may potentially regenerate with more CRP-free time. CRP action severely aggravates the extent of tissue damage during the acute phase response after an acute injury and therefore negatively affects clinical outcome. CRP is therefore a promising therapeutic target to rescue energy-deprived tissue either caused by ischemic injury (e.g., myocardial infarction and stroke) or by an overcompensating immune reaction occurring in acute inflammation (e.g., pancreatitis) or systemic inflammatory response syndrome (SIRS; e.g., after transplantation or surgery). Selective CRP apheresis can remove circulating CRP safely and efficiently. We explain the pathophysiological reasoning behind therapeutic CRP apheresis and summarize the broad span of indications in which its application could be beneficial with a focus on ischemic stroke as well as the results of this therapeutic approach after myocardial infarction.
Highlights
Inflammatory processes involve a plethora of signaling pathways and affect the whole body, even if their origin is most often locally restricted in an acute setting
During acute pancreatitis, a systemic inflammatory response syndrome (SIRS), or an acute bacterial or viral infection (Sepsis) the inflammation might cause widespread tissue injury, which might result in multiple organ failure [6]
One of the acute-phase mediators directly involved in these pro-inflammatory processes is C-reactive protein (CRP) which was discovered by Tillett and Francis in 1930 [7]
Summary
Inflammatory processes involve a plethora of signaling pathways and affect the whole body, even if their origin is most often locally restricted in an acute setting. Mounting an inflammatory response is the body’s strategy to primarily eliminate any cause of tissue damage and subsequently repair the injury [1] This is rooted in the evolutionary background that damage is mainly caused by pathogens or at least exacerbated by them within an external wound. Whenever an injury is “sterile”, meaning it occurred internally without pathogen involvement, inflammation aggravates deterioration by elimination of additional cells, which were either vital or only slightly and reversibly impaired. This happens for example after ischemic injury like stroke or myocardial infarction, leading to a larger extent of organ damage, increased scarring and thereby worsening clinical outcome [3,4]. CRP has to be regarded as a marker, and as an active pro-inflammatory protein
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