Abstract
C-reactive protein (CRP) is the best-known acute phase protein. In humans, almost every type of inflammation is accompanied by an increase of CRP concentration. Until recently, the only known physiological function of CRP was the marking of cells to initiate their phagocytosis. This triggers the classical complement pathway up to C4, which helps to eliminate pathogens and dead cells. However, vital cells with reduced energy supply are also marked, which is useful in the case of a classical external wound because an important substrate for pathogens is disposed of, but is counterproductive at internal wounds (e.g., heart attack or stroke). This mechanism negatively affects clinical outcomes since it is established that CRP levels correlate with the prognosis of these indications. Here, we summarize what we can learn from a clinical study in which CRP was adsorbed from the bloodstream by CRP-apheresis. Recently, it was shown that CRP can have a direct effect on blood pressure in rabbits. This is interesting in regard to patients with high inflammation, as they often become tachycardic and need catecholamines. These two physiological effects of CRP apparently also occur in COVID-19. Parts of the lung become ischemic due to intra-alveolar edema and hemorrhage and in parallel CRP increases dramatically, hence it is assumed that CRP is also involved in this ischemic condition. It is meanwhile considered that most of the damage in COVID-19 is caused by the immune system. The high amounts of CRP could have an additional influence on blood pressure in severe COVID-19.
Highlights
Inflammation in humans is deeply evolutionary rooted
While it has been shown that blood pressure and heart rate as well as adrenergic receptor (AR) signaling can affect C-reactive protein (CRP) concentrations [62,63,64], a direct influence of CRP on hemodynamic variables has hardly been investigated so far
It has been suggested earlier to target CRP in acute myocardial infarction (AMI), but the therapeutic approaches were not clinically relevant or sufficiently rapid [16, 92,93,94]. This changed when it was shown that specific extracorporeal removal of CRP by CRP apheresis resulted in a significant reduction of the infarct area and stabilization of the left ventricular ejection fraction (LVEF) in a preclinical trial in pigs [22, 50]
Summary
Vogt B (2021) C-Reactive Protein Triggers Cell Death in Ischemic Cells. C-reactive protein (CRP) is the best-known acute phase protein. The only known physiological function of CRP was the marking of cells to initiate their phagocytosis This triggers the classical complement pathway up to C4, which helps to eliminate pathogens and dead cells. Vital cells with reduced energy supply are marked, which is useful in the case of a classical external wound because an important substrate for pathogens is disposed of, but is counterproductive at internal wounds (e.g., heart attack or stroke) This mechanism negatively affects clinical outcomes since it is established that CRP levels correlate with the prognosis of these indications. It was shown that CRP can have a direct effect on blood pressure in rabbits This is interesting in regard to patients with high inflammation, as they often become tachycardic and need catecholamines.
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