scholarly journals A pathogenic role of complement in arterial hypertension and hypertensive end organ damage

2017 ◽  
Vol 312 (3) ◽  
pp. H349-H354 ◽  
Author(s):  
Ulrich O. Wenzel ◽  
Marlies Bode ◽  
Jörg Köhl ◽  
Heimo Ehmke
Keyword(s):  
Immune Responses ◽  
Arterial Hypertension ◽  
Complement Activation ◽  
Atypical Hemolytic Uremic Syndrome ◽  
Organ Damage ◽  
Recent Experimental Data ◽  
Adaptive Immune Responses ◽  
End Organ Damage ◽  
Adaptive Immune ◽  
Malignant Nephrosclerosis

The self-amplifying cascade of messenger and effector molecules of the complement system serves as a powerful danger-sensing system that protects the host from a hostile microbial environment, while maintaining proper tissue and organ function through effective clearance of altered or dying cells. As an important effector arm of innate immunity, it also plays important roles in the regulation of adaptive immunity. Innate and adaptive immune responses have been identified as crucial players in the pathogenesis of arterial hypertension and hypertensive end organ damage. In line with this view, complement activation may drive the pathology of hypertension and hypertensive injury through its impact on innate and adaptive immune responses. It is well known that complement activation can cause tissue inflammation and injury and complement-inhibitory drugs are effective treatments for several inflammatory diseases. In addition to these proinflammatory properties, complement cleavage fragments of C3 and C5 can exert anti-inflammatory effects that dampen the inflammatory response to injury. Recent experimental data strongly support a role for complement in arterial hypertension. The remarkably similar clinical and histopathological features of malignant nephrosclerosis and atypical hemolytic uremic syndrome, which is driven by complement activation, suggest a role for complement also in the development of malignant nephrosclerosis. Herein, we will review canonical and noncanonical pathways of complement activation as the framework to understand the multiple roles of complement in arterial hypertension and hypertensive end organ damage.

scholarly journals Protective immune responses against West Nile virus are primed by distinct complement activation pathways

2006 ◽  
Vol 203 (5) ◽  
pp. 1371-1381 ◽  
Author(s):  
Erin Mehlhop ◽  
Michael S. Diamond
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
West Nile Virus ◽  
Immune Responses ◽  
Complement Activation ◽  
Adaptive Immune Responses ◽  
Cell Responses ◽  
Adaptive Immune ◽  
The Central Nervous System ◽  
Activation Pathways

West Nile virus (WNV) causes a severe infection of the central nervous system in several vertebrate animals including humans. Prior studies have shown that complement plays a critical role in controlling WNV infection in complement (C) 3−/− and complement receptor 1/2−/− mice. Here, we dissect the contributions of the individual complement activation pathways to the protection from WNV disease. Genetic deficiencies in C1q, C4, factor B, or factor D all resulted in increased mortality in mice, suggesting that all activation pathways function together to limit WNV spread. In the absence of alternative pathway complement activation, WNV disseminated into the central nervous system at earlier times and was associated with reduced CD8+ T cell responses yet near normal anti-WNV antibody profiles. Animals lacking the classical and lectin pathways had deficits in both B and T cell responses to WNV. Finally, and somewhat surprisingly, C1q was required for productive infection in the spleen but not for development of adaptive immune responses after WNV infection. Our results suggest that individual pathways of complement activation control WNV infection by priming adaptive immune responses through distinct mechanisms.

scholarly journals The role of inflammation and oxidative stress in cardiovascular pathology

2013 ◽  
Vol 17 (1 (65)) ◽  
pp. 156-162
Author(s):  
T. V. Talayeva ◽  
V. V. Shishkin ◽  
L. L. Vavilova
Keyword(s):  
Oxidative Stress ◽  
Immune Responses ◽  
Arterial Hypertension ◽  
Vascular Wall ◽  
Adaptive Immune Responses ◽  
Cardiovascular Pathology ◽  
Immune Systems ◽  
Adaptive Immune ◽  
And Oxidative Stress

The paper is devoted to an analysis of the problem of the significance and mechanisms of inflammation and oxidative stress participation in the development of cardiovascular pathology, first of all – in heart and vascular wall damaging and remodeling and in the development of arterial hypertension. An interrelation is traced between the reninangiotensin, sympathoadrenal and immune systems in the development of oxidative stress as a component of innate and adaptive immune responses.

scholarly journals Patients with COVID-19: in the dark-NETs of neutrophils

2021 ◽  
Author(s):  
Maximilian Ackermann ◽  
Hans-Joachim Anders ◽  
Rostyslav Bilyy ◽  
Gary L. Bowlin ◽  
Christoph Daniel ◽  
...  
Keyword(s):  
Immune Responses ◽  
Organ Dysfunction ◽  
Tissue Injury ◽  
Organ Damage ◽  
Therapeutic Strategies ◽  
Neutrophil Extracellular Trap ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Major Threat ◽  
Extracellular Trap

AbstractSARS-CoV-2 infection poses a major threat to the lungs and multiple other organs, occasionally causing death. Until effective vaccines are developed to curb the pandemic, it is paramount to define the mechanisms and develop protective therapies to prevent organ dysfunction in patients with COVID-19. Individuals that develop severe manifestations have signs of dysregulated innate and adaptive immune responses. Emerging evidence implicates neutrophils and the disbalance between neutrophil extracellular trap (NET) formation and degradation plays a central role in the pathophysiology of inflammation, coagulopathy, organ damage, and immunothrombosis that characterize severe cases of COVID-19. Here, we discuss the evidence supporting a role for NETs in COVID-19 manifestations and present putative mechanisms, by which NETs promote tissue injury and immunothrombosis. We present therapeutic strategies, which have been successful in the treatment of immunο-inflammatory disorders and which target dysregulated NET formation or degradation, as potential approaches that may benefit patients with severe COVID-19.

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