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Medicina
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The Role of the Complement System in Chronic Inflammation
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The Role of the Complement System in Chronic Inflammation

A special issue of Medicina (ISSN 1648-9144).

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 23959

Special Issue Editor

Dr. Cordula Stover

E-Mail Website
Guest Editor
Department of Respiratory Sciences, College of Life Sciences, University of Leicester, Leicester, UK
Interests: obesity; autoimmune disease; atherosclerosis; chronic kidney disease; tumour immunology; inflammation, senescence; persistence of infection; complement

Special Issue Information

Dear Colleagues,

Chronic inflammation has moved into the limelight of public opinion when concern is expressed about the quality of life. Often unseen, the socioeconomic burden is substantial and a feature of modern, developed societies, where long life expectancy has become the new norm. This issue will study the role complement has been characterised to play in a diverse range of chronic inflammatory conditions. Complement was originally described as a plasma protein system involved in innate imune defence but has in recent years advanced to a modulator of mechanisms important in disease pathogenesis and a fine-tuner of cell activities. These new advances in understanding will be evidenced in original work and review submissions to this Special Issue.

Dr. Cordula Stover
Guest Editor

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Keywords

  • Obesity
  • Autoimmune disease
  • Atherosclerosis
  • Chronic kidney disease
  • Tumour immunology
  • Senescence
  • Persistence of infection

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Published Papers (6 papers)

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Research

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8 pages, 816 KiB  
Article
Properdin Is a Modulator of Tumour Immunity in a Syngeneic Mouse Melanoma Model
by Izzat A. M. Al-Rayahi, Lee R. Machado and Cordula M. Stover
Medicina 2021, 57(2), 85; https://doi.org/10.3390/medicina57020085 - 21 Jan 2021
Cited by 3 | Viewed by 2437
Abstract
Background and Objectives: Tumours are often low immunogenic. The role of complement, an innate immune defence system, in tumour control has begun to be elucidated, but findings are conflicting. A role for properdin, an amplifier of complement activation, in tumour control has [...] Read more.
Background and Objectives: Tumours are often low immunogenic. The role of complement, an innate immune defence system, in tumour control has begun to be elucidated, but findings are conflicting. A role for properdin, an amplifier of complement activation, in tumour control has recently been implicated. Materials and Methods: Properdin-deficient and congenic wildtype mice were injected subcutaneously with B16F10 melanoma cells. Tumour mass and chemokine profile were assessed. The frequencies of CD45+CD11b+ Gr-1+ cells were determined from tumours and spleens, and CD206+ F4/80+ cells were evaluated in spleens. Sera were analysed for C5a, sC5b-9, and CCL2. Results: Whilst there was no difference in tumour growth at study endpoint, properdin-deficient mice had significantly fewer myeloid-derived suppressor cells (MDSCs) in their tumours and spleens. Splenic M2 type macrophages and serum levels of C5a, sC5b-9, and CCL2 were decreased in properdin-deficient compared to wildtype mice. Conclusions: The presence of intact complement amplification sustains an environment that lessens potential anti-tumour responses. Full article
(This article belongs to the Special Issue The Role of the Complement System in Chronic Inflammation)
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25 pages, 6937 KiB  
Article
Complement Properdin Regulates the Metabolo-Inflammatory Response to a High Fat Diet
by Rόisín C. Thomas, Ramiar Kheder, Hasanain Alaridhee, Naomi Martin and Cordula M. Stover
Medicina 2020, 56(9), 484; https://doi.org/10.3390/medicina56090484 - 22 Sep 2020
Cited by 3 | Viewed by 3377
Abstract
Background and objectives: Overnutrition leads to a metabolic and inflammatory response that includes the activation of Complement. Properdin is the only amplifier of complement activation and increases the provision of complement activation products. Its absence has previously been shown to lead to increased [...] Read more.
Background and objectives: Overnutrition leads to a metabolic and inflammatory response that includes the activation of Complement. Properdin is the only amplifier of complement activation and increases the provision of complement activation products. Its absence has previously been shown to lead to increased obesity in mice on a high fat diet. The aim of this study was to determine ways in which properdin contributes to a less pronounced obese phenotype. Materials and Methods: Wild type (WT) and properdin deficient mice (KO) were fed a high-fat diet (HFD) for up to 12 weeks. Results: There was a significant increase in liver triglyceride content in the KO HFD group compared to WT on HFD. WT developed steatosis. KO had an additional inflammatory component (steatohepatitis). Analysis of AKT signalling by phosphorylation array supported a decrease in insulin sensitivity which was greater for KO than WT in liver and kidney. There was a significant decrease of C5L2 in the fat membranes of the KO HFD group compared to the WT HFD group. Circulating microparticles in KO HFD group showed lower presence of C5L2. Expression of the fatty acid transporter CD36 in adipose tissue was increased in KO on HFD and was also significantly increased in plasma of KO HFD mice compared to WT on HFD. CD36 was elevated on microparticles from KO on HFD. Ultrastructural changes consistent with obesity-associated glomerulopathy were observed for both HFD fed genotypes, but tubular strain was greater in KO. Conclusion: Our work demonstrates that complement properdin is a dominant factor in limiting the severity of obesity-associated conditions that impact on liver and kidney. The two receptors, C5L2 and CD36, are downstream of the activity exerted by properdin. Full article
(This article belongs to the Special Issue The Role of the Complement System in Chronic Inflammation)
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11 pages, 1991 KiB  
Article
Complement Properdin Determines Disease Activity in MRL/lpr Mice
by Hasanain Alaridhee, Azzah Alharbi, Zeayd Saeed, Róisín C. Thomas and Cordula M. Stover
Medicina 2020, 56(9), 430; https://doi.org/10.3390/medicina56090430 - 27 Aug 2020
Cited by 3 | Viewed by 3315
Abstract
Background and objects: In systemic lupus erythematosus, circulating immune complexes activate complement and, when trapped in renal capillaries, cause glomerulonephritis. Mouse models have been used in the preclinical assessment of targeting complement activation pathways to manage chronic inflammation in lupus. Properdin is the [...] Read more.
Background and objects: In systemic lupus erythematosus, circulating immune complexes activate complement and, when trapped in renal capillaries, cause glomerulonephritis. Mouse models have been used in the preclinical assessment of targeting complement activation pathways to manage chronic inflammation in lupus. Properdin is the only known positive regulator of complement activation, but its role in the severity of lupus nephritis has not been studied yet. Materials and Methods: Fully characterized properdin-deficient mice were crossed with lupus prone MRL/lpr mice on C57Bl/6 background. Results: Compared to MRL/lpr properdin wildtype mice, MRL/lpr properdin-deficient mice had significantly lower anti-DNA antibody titres, TNFα and BAFF levels in serum. The qualitative glomerulonephritic score was less severe and there was significantly less serum creatinine in MRL/lpr properdin-deficient mice compared to MRL/lpr properdin wildtype littermate mice. Conclusion: Properdin plays a significant role in the severity of lupus overall and specifically in the extent of glomerulonephritis observed in MRL/lpr mice. Because MRL/lpr properdin-deficient mice had lower levels of anti-DNA antibodies, inflammatory mediators and markers of renal impairment, the study implies that properdin could constitute a novel therapy target in lupus disease. Full article
(This article belongs to the Special Issue The Role of the Complement System in Chronic Inflammation)
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Review

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18 pages, 2165 KiB  
Review
The Role of Complement System and the Immune Response to Tuberculosis Infection
by Heena Jagatia and Anthony G. Tsolaki
Medicina 2021, 57(2), 84; https://doi.org/10.3390/medicina57020084 - 20 Jan 2021
Cited by 20 | Viewed by 8459
Abstract
The complement system orchestrates a multi-faceted immune response to the invading pathogen, Mycobacterium tuberculosis. Macrophages engulf the mycobacterial bacilli through bacterial cell surface proteins or secrete proteins, which activate the complement pathway. The classical pathway is activated by C1q, which binds to [...] Read more.
The complement system orchestrates a multi-faceted immune response to the invading pathogen, Mycobacterium tuberculosis. Macrophages engulf the mycobacterial bacilli through bacterial cell surface proteins or secrete proteins, which activate the complement pathway. The classical pathway is activated by C1q, which binds to antibody antigen complexes. While the alternative pathway is constitutively active and regulated by properdin, the direct interaction of properdin is capable of complement activation. The lectin-binding pathway is activated in response to bacterial cell surface carbohydrates such as mannose, fucose, and N-acetyl-d-glucosamine. All three pathways contribute to mounting an immune response for the clearance of mycobacteria. However, the bacilli can reside, persist, and evade clearance by the immune system once inside the macrophages using a number of mechanisms. The immune system can compartmentalise the infection into a granulomatous structure, which contains heterogenous sub-populations of M. tuberculosis. The granuloma consists of many types of immune cells, which aim to clear and contain the infection whilst sacrificing the affected host tissue. The full extent of the involvement of the complement system during infection with M. tuberculosis is not fully understood. Therefore, we reviewed the available literature on M. tuberculosis and other mycobacterial literature to understand the contribution of the complement system during infection. Full article
(This article belongs to the Special Issue The Role of the Complement System in Chronic Inflammation)
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Other

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6 pages, 486 KiB  
Perspective
Complement Activation on Endothelial Cell-Derived Microparticles—A Key Determinant for Cardiovascular Risk in Patients with Systemic Lupus Erythematosus?
by Naomi Martin, Xiaodie Tu, Alicia J. Egan and Cordula Stover
Medicina 2020, 56(10), 533; https://doi.org/10.3390/medicina56100533 - 13 Oct 2020
Cited by 5 | Viewed by 2401
Abstract
Systemic lupus erythematosus is a classical systemic autoimmune disease that overactivates complement and can affect all organs. Early diagnosis and effective management are important in this immune-complex-mediated chronic inflammatory disease, which has a strong component of vasculitis and carries an increased risk of [...] Read more.
Systemic lupus erythematosus is a classical systemic autoimmune disease that overactivates complement and can affect all organs. Early diagnosis and effective management are important in this immune-complex-mediated chronic inflammatory disease, which has a strong component of vasculitis and carries an increased risk of thrombosis, even in the absence of antiphospholipid antibodies. Development of lupus nephritis can be life limiting but is managed with dialysis and renal transplantation. Therefore, data have become available that cardiovascular risk poses a serious feature of systemic lupus erythematosus that requires monitoring and prospective treatment. Cell-derived microparticles circulate in plasma and thereby intersect the humoral and cellular component of inflammation. They are involved in disease pathophysiology, particularly thrombosis, and represent a known cardiovascular risk. This viewpoint argues that a focus on characteristics of circulating microparticles measured in patients with systemic lupus erythematosus may help to classify certain ethnic groups who are especially at additional risk of experiencing cardiovascular complications. Full article
(This article belongs to the Special Issue The Role of the Complement System in Chronic Inflammation)
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5 pages, 257 KiB  
Perspective
The Value of Targeting Complement Components in Asthma
by Marwa M. E. Mohamed, Alicia D. Nicklin and Cordula M. Stover
Medicina 2020, 56(8), 405; https://doi.org/10.3390/medicina56080405 - 12 Aug 2020
Cited by 1 | Viewed by 2587
Abstract
Asthma is an important respiratory illness. Though pharmacological and biological treatment is well established and is staged according to endotypes and their responses to treatment, novel avenues are being explored. Our focus is complement. In this viewpoint, we evaluate the approach to target [...] Read more.
Asthma is an important respiratory illness. Though pharmacological and biological treatment is well established and is staged according to endotypes and their responses to treatment, novel avenues are being explored. Our focus is complement. In this viewpoint, we evaluate the approach to target complement in this complex hypersensitivity reaction that develops chronicity and has a personal—as well as a societal—cost. Full article
(This article belongs to the Special Issue The Role of the Complement System in Chronic Inflammation)
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