Das Komplementsystem

2012 ◽  
Vol 32 (04) ◽  
pp. 276-285 ◽  
Author(s):  
V. Frauenknecht ◽  
V. Schroeder

SummaryAtherosclerotic diseases such as coronary artery disease and ischaemic stroke are caused by chronic inflammation in arterial vessel walls. The complement system is part of the innate immune system. It is involved in many processes contributing to onset and development of atherosclerotic plaques up to the final stage of acute thrombotic events. This is due to its prominent role in inflammatory processes. In addition, there is increasing evidence that interactions between complement and coagulation provide a link between inflammation and thrombosis. On the other hand, the complement system also has an atheroprotective function through the clearance of apoptotic material.The knowledge of these complex mechanisms will become increasingly important, also for clinicians, since it may lead to novel therapeutic and diagnostic options. Therapies targeting the complement system have the potential to reduce tissue damage caused by acute ischaemic events. Whether early anti-inflammatory and anti-complement therapy may be able to prevent atherosclerosis, remains a hot topic for research.

2017 ◽  
Vol 2 (4) ◽  
pp. 174-186 ◽  
Author(s):  
Kirsten M. Pondman ◽  
Carolina Salvador-Morales ◽  
Basudev Paudyal ◽  
Robert B. Sim ◽  
Uday Kishore

The complement system can interact with nanoparticles and alter the intended therapeutic targeting.


2015 ◽  
Vol 7 (3) ◽  
Author(s):  
S. Moein Moghimi ◽  
Peter P. Wibroe ◽  
Linping Wu ◽  
Z. Shadi Farhangrazi

AbstractThe lectin pathway of the complement system is an integral component of the innate immune system recognizing pathogens through patterns of sugar moieties displayed on their surfaces and neutralizing them through an antibody-independent reaction cascade. Many engineered nanoparticles incite complement through the lectin pathway, but these nanoparticles inherently do not express surface-exposed sugars. However, the projected polymeric surface architecture of nanoparticles may transiently resemble structural motifs of peptidoglycan constituents of pathogens and trigger the lectin pathway. We discuss these issues in relation to nanomedicine design and immune safety.


2021 ◽  
Vol 14 (4) ◽  
pp. 835-840
Author(s):  
Taline Scalco Picetti ◽  
Lucas de Figueiredo Soveral ◽  
Rovian Miotto ◽  
Luana Marina Scheer Erpen ◽  
Yasmin Kreutz ◽  
...  

Background and Aim: Immune-modulating molecules mainly act on innate immune cells, which are central to early defense against invading pathogens and contribute to developing adaptive immunity. Yeast-extracted β-glucan, a model immune-modulating molecule, is widely used in several animal species; however, its effect on horse immune parameters has not been thoroughly investigated yet. This study aimed to evaluate the effects of orally administered β-glucan on selected innate immune parameters in horses. Materials and Methods: Eighteen thoroughbred horses were assigned equally into three groups as follows: One control group (no β-glucan) and two β-glucan experimental groups (one received 125 mg and the other 2 g of β-glucan per day for 28 days). Blood samples were collected before and at the end of the experiment for hematological analysis, whole blood phagocytosis, respiratory burst assays, and to assess the serum lysozyme and complement hemolytic activities. Results: At the end of the experiment, significant decreases (p<0.05) in monocyte numbers were observed in the control horses (258.8±45.9 vs. 115.3±41.5) and in those fed 125 mg/day of β-glucan (208.8±72.3 vs. 99.2±60.7), whereas a significant increase in numbers was noted in the horses that were fed 2 g/day of β-glucan (303.5±45.8 vs. 429.8±86.0; p<0.05). The natural hemolytic activity of the complement was higher only in horses fed 2 g/day of β-glucan (p=0.018) compared to the other groups. The hemolytic activity in the classical pathway was higher in those fed 125 mg/day (p=0.0035) and 2 g/day of β-glucan (p=0.0001). Conclusion: β-glucan improves important innate immune parameters and might be fed to horses before stressful events.


Author(s):  
Marina Botto ◽  
Mark J. Walport

The complement system consists of over 20 distinct proteins and is an essential component of the innate immune system. It is a major effector mechanism of host defence against infection and inflammatory responses, has an important role in the physiological removal of immune complexes and dying cells, and plays an accessory role in the induction of antibody responses....


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Masayuki Aoyama ◽  
Yoshimi Kishimoto ◽  
Emi Saita ◽  
Yukinori Ikegami ◽  
Reiko Ohmori ◽  
...  

Aims. Talin-1 is a cytoskeletal protein that binds integrin, thereby leading to integrin activation and affecting focal adhesions. Recently, talin-1 expression was reported to be downregulated in human atherosclerotic plaques. However, blood levels of soluble talin-1 (sTalin-1) in patients with atherosclerotic disease, such as coronary artery disease (CAD), have not been elucidated. Methods. We measured plasma sTalin-1 levels in 349 patients undergoing elective coronary angiography. The severity of CAD was represented as the number of stenotic coronary vessels and segments. Results. Of the 349 study patients, CAD was found in 194 patients, of whom 88 had 1-vessel disease (1-VD), 60 had 2-vessel disease (2-VD), and 46 had 3-vessel disease (3-VD). Plasma sTalin-1 levels were higher in 194 patients with CAD than in 155 without CAD (CAD(-) group) (median 0.30 vs. 0.23 ng/mL, P<0.005). A stepwise increase in sTalin-1 levels was found depending on the number of >50% stenotic coronary vessels: 0.23 in CAD(-), 0.29 in 1-VD, 0.30 in 2-VD, and 0.32 ng/mL in 3-VD group, respectively, (P<0.05). High sTalin-1 level (>0.28 ng/mL) was found in 36% of CAD(-), 51% of 1-VD, 53% of 2-VD, and 59% of 3-VD group (P<0.025). sTalin-1 levels also correlated with the number of >50% stenotic segments (r=0.14, P<0.02). The multivariate analysis revealed that sTalin-1 levels were independently associated with CAD. The odds ratio for CAD was 1.83 (95%CI=1.14−2.93) for high sTalin-1 level (>0.28 ng/mL) (P<0.02). Conclusions. Plasma sTalin-1 levels in patients with CAD were found to be high and to be associated with the presence and severity of CAD, suggesting a role of sTalin-1 in the progression of coronary atherosclerosis.


Atherosclerosis: pathophysiology 212Development of atherosclerotic plaques 214Epidemiology 216Assessment of atherosclerotic risk 218Risk factors for coronary artery disease 220Hypertension 226Treatment of high blood pressure 228Combining antihypertensive drugs 230Lipid management in atherosclerosis 232Lipid-lowering therapy 236When to treat lipids ...


1992 ◽  
Vol 65 ◽  
pp. S10
Author(s):  
E. Arbustini ◽  
M. Grasso ◽  
M. Diegoli ◽  
M. Bramerio ◽  
A. Aguzzi ◽  
...  

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