scholarly journals OSTEOARTHRITIS AND IMMUNITY

2021 ◽  
Vol 29 (1) ◽  
pp. 44-51
Author(s):  
Irina Momcheva ◽  
I. Kazmin ◽  
S. Hristova ◽  
V. Madjova
Keyword(s):  
Complement System ◽  
Cell Membranes ◽  
Cartilage Damage ◽  
Joint Damage ◽  
Innate Immune ◽  
Low Grade ◽  
Complement Receptors ◽  
Molecular Patterns ◽  
Low Grade Inflammation ◽  
The Complement System

Abstract         Low-grade inflammation is part of the pathogenesis of osteoarthritis (OA) from its earliest stages and contributes to the acceleration of the degenerative process. Innate immunity has a leading role in it.        Activation of the innate immune response is initiated by stimulation of the receptors on the cell membrane to recognize the secreted PAMPs (pathogen-associated molecular patterns). However, PAMPs can also be activated by endogenous damage-related molecular patterns (DAMPs). The group of DAMPs also includes toll-like receptors (TLRs).The disruption of matrix homeostasis in the course of OA is an example of activation of these receptors in chronic damage.      The complement system is a key element of the innate immune system. It is one of the serum enzyme systems whose function is to opsonize antigens. The complement receptors on the surface of the cell membranes adhere to the targets for phagocytosis. The C3R fraction activates the complement cascade itself, as well as the oxygen metabolism of the cell, which is essential for the phagocytosis. The cartilage damage products released during joint damage are a separate class of potent complement modulators.     Complement fractions bind to complement receptors on the surface of the chondrocyte and the synoviocyte cell membranes by TLR. The complement system is involved in many processes in the course of osteoarthritis: chondrocyte degeneration, ECM degradation, low-grade inflammation in the osteoarthritis, cell lysis, unbalanced bone remodeling, osteophyte formation, and neoangiogenesis. Whether drug control of complement activation may be a future therapeutic strategy in the treatment of OA and prevent its progression is a subject of future studies.

scholarly journals Fcγand Complement Receptors and Complement Proteins in Neutrophil Activation in Rheumatoid Arthritis: Contribution to Pathogenesis and Progression and Modulation by Natural Products

2015 ◽  
Vol 2015 ◽  
pp. 1-22 ◽  
Author(s):  
Adriana Balbina Paoliello-Paschoalato ◽  
Larissa Fávaro Marchi ◽  
Micássio Fernandes de Andrade ◽  
Luciana Mariko Kabeya ◽  
Eduardo Antônio Donadi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Complement System ◽  
Proteolytic Enzymes ◽  
Joint Damage ◽  
Complement Receptors ◽  
Effector Functions ◽  
Extracellular Traps ◽  
Persistent Inflammation ◽  
The Complement System ◽  
Frustrated Phagocytosis

Rheumatoid arthritis (RA) is a highly disabling disease that affects all structures of the joint and significantly impacts on morbidity and mortality in RA patients. RA is characterized by persistent inflammation of the synovial membrane lining the joint associated with infiltration of immune cells. Eighty to 90% of the leukocytes infiltrating the synovia are neutrophils. The specific role that neutrophils play in the onset of RA is not clear, but recent studies have evidenced that they have an important participation in joint damage and disease progression through the release of proteolytic enzymes, reactive oxygen species (ROS), cytokines, and neutrophil extracellular traps, in particular during frustrated phagocytosis of immune complexes (ICs). In addition, the local and systemic activation of the complement system contributes to the pathogenesis of RA and other IC-mediated diseases. This review discusses (i) the participation of Fcγand complement receptors in mediating the effector functions of neutrophils in RA; (ii) the contribution of the complement system and ROS-dependent and ROS-independent mechanisms to joint damage in RA; and (iii) the use of plant extracts, dietary compounds, and isolated natural compounds in the treatment of RA, focusing on modulation of the effector functions of neutrophils and the complement system activity and/or activation.

Das Komplementsystem

2012 ◽  
Vol 32 (04) ◽  
pp. 276-285 ◽  
Author(s):  
V. Frauenknecht ◽  
V. Schroeder
Keyword(s):  
Coronary Artery Disease ◽  
Complement System ◽  
Innate Immune System ◽  
Innate Immune ◽  
The Other ◽  
Atherosclerotic Plaques ◽  
Inflammatory Processes ◽  
Artery Disease ◽  
The Complement System ◽  
Novel Therapeutic

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.

scholarly journals Rheumatic Diseases and Obesity: Adipocytokines as Potential Comorbidity Biomarkers for Cardiovascular Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Rossana Scrivo ◽  
Massimiliano Vasile ◽  
Ulf Müller-Ladner ◽  
Elena Neumann ◽  
Guido Valesini
Keyword(s):  
Cardiovascular Risk ◽  
Current Knowledge ◽  
Weight Bearing ◽  
Joint Damage ◽  
Positive Association ◽  
Experimental Models ◽  
Low Grade ◽  
Multifactorial Diseases ◽  
Systemic Factors ◽  
Low Grade Inflammation

Inflammation has been recognized as a common trait in the pathogenesis of multifactorial diseases including obesity, where a low-grade inflammation has been established and may be responsible for the cardiovascular risk related to the disease. Obesity has also been associated with the increased incidence and a worse outcome of rheumatoid arthritis (RA) and osteoarthritis (OA). RA is characterized by systemic inflammation, which is thought to play a key role in accelerated atherosclerosis and in the increased incidence of cardiovascular disease, an important comorbidity in patients with RA. The inflammatory process underlying the cardiovascular risk both in obesity and RA may be mediated by adipocytokines, a heterogeneous group of soluble proteins mainly secreted by the adipocytes. Many adipocytokines are mainly produced by white adipose tissue. Adipocytokines may also be involved in the pathogenesis of OA since a positive association with obesity has been found for weight-bearing and nonweight-bearing joints, suggesting that, in addition to local overload, systemic factors may contribute to joint damage. In this review we summarize the current knowledge on experimental models and clinical studies in which adipocytokines were examined in obesity, RA, and OA and discuss the potential of adipocytokines as comorbidity biomarkers for cardiovascular risk.

scholarly journals Replication-attenuated Human Adenoviral Type 4 vectors elicit capsid dependent enhanced innate immune responses that are partially dependent upon interactions with the complement system

Virology ◽  
2008 ◽  
Vol 374 (2) ◽  
pp. 453-467 ◽  
Author(s):  
Zachary C. Hartman ◽  
Daniel M. Appledorn ◽  
Delila Serra ◽  
Oliver Glass ◽  
Todd B. Mendelson ◽  
...  
Keyword(s):  
Immune Responses ◽  
Complement System ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
The Complement System

scholarly journals NLRP3 Inflammasome in Diabetic Cardiomyopathy and Exercise Intervention

2021 ◽  
Vol 22 (24) ◽  
pp. 13228
Author(s):  
Yi Sun ◽  
Shuzhe Ding
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Nlrp3 Inflammasome ◽  
Exercise Intervention ◽  
Inflammatory Responses ◽  
Innate Immune ◽  
Inflammasome Activation ◽  
Low Grade ◽  
Chronic Exercise ◽  
Nlrp3 Inflammasome Activation ◽  
Low Grade Inflammation

Diabetic cardiomyopathy (DCM), as a common complication of diabetes, is characterized by chronic low-grade inflammation. The NLRP3 inflammasome is a key sensor mediating innate immune and inflammatory responses. However, the mechanisms initiating and promoting NLRP3 inflammasome activation in DCM is largely unexplored. The aim of the present review is to describe the link between NLRP3 inflammasome and DCM, and to provide evidence highlighting the importance of exercise training in DCM intervention. Collectively, this evidence suggests that DCM is an inflammatory disease aggravated by NLRP3 inflammasome-mediated release of IL-1β and IL-18. In addition, chronic exercise intervention is an effective preventive and therapeutic method to alleviate DCM via modulating the NLRP3 inflammasome.

scholarly journals Protease-dependent mechanisms of complement evasion by bacterial pathogens

2012 ◽  
Vol 393 (9) ◽  
pp. 873-888 ◽  
Author(s):  
Michal Potempa ◽  
Jan Potempa
Keyword(s):  
Antibacterial Activity ◽  
Complement System ◽  
Antibacterial Activities ◽  
Immune Defense ◽  
Innate Immune ◽  
Human Pathogens ◽  
Human Immune System ◽  
Common Strategy ◽  
Human Immune ◽  
The Complement System

Abstract The human immune system has evolved a variety of mechanisms for the primary task of neutralizing and eliminating microbial intruders. As the first line of defense, the complement system is responsible for rapid recognition and opsonization of bacteria, presentation to phagocytes and bacterial cell killing by direct lysis. All successful human pathogens have mechanisms of circumventing the antibacterial activity of the complement system and escaping this stage of the immune response. One of the ways in which pathogens achieve this is the deployment of proteases. Based on the increasing number of recent publications in this area, it appears that proteolytic inactivation of the antibacterial activities of the complement system is a common strategy of avoiding targeting by this arm of host innate immune defense. In this review, we focus on those bacteria that deploy proteases capable of degrading complement system components into non-functional fragments, thus impairing complement-dependent antibacterial activity and facilitating pathogen survival inside the host.

scholarly journals Implication of Aging Related Chronic Neuroinflammation on COVID-19 Pandemic

2020 ◽  
Vol 10 (3) ◽  
pp. 102 ◽  
Author(s):  
Paola Bossù ◽  
Elisa Toppi ◽  
Valentina Sterbini ◽  
Gianfranco Spalletta
Keyword(s):  
Severe Disease ◽  
Severe Case ◽  
Innate Immune ◽  
Low Grade ◽  
Chronic Neuroinflammation ◽  
Low Grade Inflammation ◽  
The Brain ◽  
Neuropsychiatric Conditions

SARS-CoV-2, the virus responsible for the COVID-19 pandemic, leads to a respiratory syndrome and other manifestations. Most affected people show no or mild symptoms, but the risk of severe disease and death increases in older people. Here, we report a narrative review on selected studies targeting aging-related chronic neuroinflammation in the COVID-19 pandemic. A hyperactivation of the innate immune system with elevated levels of pro-inflammatory cytokines occurs during severe COVID-19, pointing to an important role of the innate immune dysregulation in the disease outcome. Aging is characterized by a general condition of low-grade inflammation, also connected to chronic inflammation of the brain (neuroinflammation), which is involved in frailty syndrome and contributes to several age-associated diseases, including neurodegenerative and neuropsychiatric disorders. Since neuroinflammation can be induced or worsened by the virus infection itself, as well as by stressful conditions like those linked to the recent pandemic, the role of neuroinflammatory mechanisms could be central in a vicious circle leading to an increase in the mortality risk in aged COVID-19 patients. Furthermore, triggered neuroinflammatory pathways and consequent neurodegenerative and neuropsychiatric conditions might be potential long-term complications of COVID-19. In order to provide insights to help clinicians in identifying patients who progress to a more severe case of the disease, this review underlines the potential implications of aging-related neuroinflammation in COVID-19 pandemic.

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