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Article ; Online: Does the Lectin Complement Pathway Link Kawasaki Disease and SARS-CoV-2?

Polycarpou, Anastasia / Grigoriadou, Sofia / Klavinskis, Linda / Sacks, Steven

2021 Volume 11, Page(s) 604512

MeSH term(s)	COVID-19/complications ; COVID-19/immunology ; Child ; Child, Preschool ; Complement Pathway, Mannose-Binding Lectin/immunology ; Female ; Humans ; Male ; Mucocutaneous Lymph Node Syndrome/immunology ; SARS-CoV-2 ; Systemic Inflammatory Response Syndrome/immunology
Language	English
Publishing date	2021-01-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.604512
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: A Systematic Review of Immunological Studies of Erythema Nodosum Leprosum.

Polycarpou, Anastasia / Walker, Stephen L / Lockwood, Diana N J

Frontiers in immunology

2017 Volume 8, Page(s) 233

Abstract: Erythema nodosum leprosum (ENL) is a painful inflammatory complication of leprosy occurring in 50% of lepromatous leprosy patients and 5-10% of borderline lepromatous patients. It is a significant cause of economic hardship, morbidity and mortality in ... ...

Abstract	Erythema nodosum leprosum (ENL) is a painful inflammatory complication of leprosy occurring in 50% of lepromatous leprosy patients and 5-10% of borderline lepromatous patients. It is a significant cause of economic hardship, morbidity and mortality in leprosy patients. Our understanding of the causes of ENL is limited. We performed a systematic review of the published literature and critically evaluated the evidence for the role of neutrophils, immune complexes (ICs), T-cells, cytokines, and other immunological factors that could contribute to the development of ENL. Searches of the literature were performed in PubMed. Studies, independent of published date, using samples from patients with ENL were included. The search revealed more than 20,000 articles of which 146 eligible studies were included in this systematic review. The studies demonstrate that ENL may be associated with a neutrophilic infiltrate, but it is not clear whether it is an IC-mediated process or that the presence of ICs is an epiphenomenon. Increased levels of tumor necrosis factor-α and other pro-inflammatory cytokines support the role of this cytokine in the inflammatory phase of ENL but not necessarily the initiation. T-cell subsets appear to be important in ENL since multiple studies report an increased CD4
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2017.00233
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Article ; Online: Rationale for targeting complement in COVID-19.

Polycarpou, Anastasia / Howard, Mark / Farrar, Conrad A / Greenlaw, Roseanna / Fanelli, Giorgia / Wallis, Russell / Klavinskis, Linda S / Sacks, Steven

EMBO molecular medicine

2020 Volume 12, Issue 8, Page(s) e12642

Abstract: A novel coronavirus, SARS-CoV-2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID-19 caused by SARS-CoV-2 is associated with an acute respiratory illness that varies from mild to the life- ... ...

Abstract	A novel coronavirus, SARS-CoV-2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID-19 caused by SARS-CoV-2 is associated with an acute respiratory illness that varies from mild to the life-threatening acute respiratory distress syndrome (ARDS). The complement system is part of the innate immune arsenal against pathogens, in which many viruses can evade or employ to mediate cell entry. The immunopathology and acute lung injury orchestrated through the influx of pro-inflammatory macrophages and neutrophils can be directly activated by complement components to prime an overzealous cytokine storm. The manifestations of severe COVID-19 such as the ARDS, sepsis and multiorgan failure have an established relationship with activation of the complement cascade. We have collected evidence from all the current studies we are aware of on SARS-CoV-2 immunopathogenesis and the preceding literature on SARS-CoV-1 and MERS-CoV infection linking severe COVID-19 disease directly with dysfunction of the complement pathways. This information lends support for a therapeutic anti-inflammatory strategy against complement, where a number of clinically ready potential therapeutic agents are available.
MeSH term(s)	Adult ; Alveolar Epithelial Cells/immunology ; Alveolar Epithelial Cells/metabolism ; Alveolar Epithelial Cells/virology ; Angiotensin-Converting Enzyme 2 ; Animals ; Betacoronavirus/physiology ; COVID-19 ; Child ; Complement Activation/drug effects ; Complement C3b/antagonists & inhibitors ; Complement C3b/physiology ; Complement Inactivating Agents/pharmacology ; Complement Inactivating Agents/therapeutic use ; Coronavirus Infections/drug therapy ; Coronavirus Infections/immunology ; Cytokine Release Syndrome/drug therapy ; Cytokine Release Syndrome/etiology ; Cytokine Release Syndrome/immunology ; Glycosylation ; Humans ; Immunity, Innate ; Ligands ; Mice ; Models, Animal ; Models, Molecular ; Pandemics ; Pattern Recognition, Automated ; Peptidyl-Dipeptidase A/metabolism ; Pneumonia, Viral/drug therapy ; Pneumonia, Viral/immunology ; Protein Conformation ; Protein Processing, Post-Translational ; Receptors, Virus/metabolism ; Respiratory Distress Syndrome/etiology ; Respiratory Distress Syndrome/immunology ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/chemistry ; Spike Glycoprotein, Coronavirus/metabolism ; COVID-19 Drug Treatment
Chemical Substances	Complement Inactivating Agents ; Ligands ; Receptors, Virus ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2 ; Complement C3b (80295-43-8) ; Peptidyl-Dipeptidase A (EC 3.4.15.1) ; ACE2 protein, human (EC 3.4.17.23) ; Ace2 protein, mouse (EC 3.4.17.23) ; Angiotensin-Converting Enzyme 2 (EC 3.4.17.23)
Keywords	covid19
Language	English
Publishing date	2020-07-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2467145-9
ISSN	1757-4684 ; 1757-4676
ISSN (online)	1757-4684
ISSN	1757-4676
DOI	10.15252/emmm.202012642
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Article ; Online: The complement pattern recognition molecule CL-11 promotes invasion and injury of respiratory epithelial cells by SARS-CoV-2.

Polycarpou, Anastasia / Wagner-Gamble, Tara / Greenlaw, Roseanna / O'Neill, Lauren A. / Khan, Hataf / Malim, Michael M / Romano, Marco / Smolarek, Dorota / Doores, Katie J / Wallis, Russell / Klavinskis, Linda S / Sacks, Steven

bioRxiv

Abstract: Collectin-11 is a soluble C-type lectin produced at epithelial surfaces to initiate pathogen elimination by complement. Given the respiratory epithelium is a source of CL-11 and downstream complement-pathway components, we investigated the potential of ... ...

Abstract	Collectin-11 is a soluble C-type lectin produced at epithelial surfaces to initiate pathogen elimination by complement. Given the respiratory epithelium is a source of CL-11 and downstream complement-pathway components, we investigated the potential of CL-11 to impact the pathogenicity of SARS-CoV-2. While the SARS-CoV-2 spike trimer could bind CL-11 and trigger complement activation followed by MAC formation, the virus was resistant to lysis. Surprisingly, virus production by infected respiratory epithelial cells was enhanced by CL-11 opsonisation of virus but this effect was fully inhibited by sugar-blockade of CL-11. Moreover, SARS-CoV-2 spike protein expressed at the bronchial epithelial cell surface was associated with increased CL-11 binding and MAC formation. We propose that SARS-CoV-2 pathogenicity is exacerbated both by resistance to complement and CL-11 driven respiratory cell invasion and injury at the portal of entry. Contrary to expectation, CL-11 blockade could offer a novel approach to limit the pathogenicity of SARS-CoV-2.
Keywords	covid19
Language	English
Publishing date	2023-12-12
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2023.12.11.571109
Database	COVID19

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Article ; Online: Rationale for targeting complement in COVID‐19

Anastasia Polycarpou / Mark Howard / Conrad A Farrar / Roseanna Greenlaw / Giorgia Fanelli / Russell Wallis / Linda S Klavinskis / Steven Sacks

EMBO Molecular Medicine, Vol 12, Iss 8, Pp n/a-n/a (2020)

2020

Abstract: Abstract A novel coronavirus, SARS‐CoV‐2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID‐19 caused by SARS‐CoV‐2 is associated with an acute respiratory illness that varies from mild to ... ...

Abstract	Abstract A novel coronavirus, SARS‐CoV‐2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID‐19 caused by SARS‐CoV‐2 is associated with an acute respiratory illness that varies from mild to the life‐threatening acute respiratory distress syndrome (ARDS). The complement system is part of the innate immune arsenal against pathogens, in which many viruses can evade or employ to mediate cell entry. The immunopathology and acute lung injury orchestrated through the influx of pro‐inflammatory macrophages and neutrophils can be directly activated by complement components to prime an overzealous cytokine storm. The manifestations of severe COVID‐19 such as the ARDS, sepsis and multiorgan failure have an established relationship with activation of the complement cascade. We have collected evidence from all the current studies we are aware of on SARS‐CoV‐2 immunopathogenesis and the preceding literature on SARS‐CoV‐1 and MERS‐CoV infection linking severe COVID‐19 disease directly with dysfunction of the complement pathways. This information lends support for a therapeutic anti‐inflammatory strategy against complement, where a number of clinically ready potential therapeutic agents are available.
Keywords	complement proteins ; COVID‐19 ; lectin pathway ; SARS‐CoV‐2 ; therapeutics ; Medicine (General) ; R5-920 ; Genetics ; QH426-470 ; covid19
Language	English
Publishing date	2020-08-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: New findings in the pathogenesis of leprosy and implications for the management of leprosy.

Polycarpou, Anastasia / Walker, Stephen L / Lockwood, Diana N

Current opinion in infectious diseases

2013 Volume 26, Issue 5, Page(s) 413–419

Abstract: Purpose of review: This review focuses on recent work in leprosy pathogenesis. New research of both innate and adaptive immune responses to Mycobacterium leprae is described. The proposition that Mycobacterium lepromatosis is a new species causing ... ...

Abstract	Purpose of review: This review focuses on recent work in leprosy pathogenesis. New research of both innate and adaptive immune responses to Mycobacterium leprae is described. The proposition that Mycobacterium lepromatosis is a new species causing leprosy is discussed. Recent findings: Modulation of the lipid metabolism and reprogramming of adult Schwann cells have both been suggested as mechanisms used by M. leprae to disseminate the disease. New markers associated with localized, disseminated disease or the occurrences of leprosy reactions include the human interferons, CD163, microRNA-21, NOD2, galectin-3 and toll-like receptor 4. The role of keratinocytes instead of macrophages is underlined in the pathogenesis of leprosy. Adaptive immunity reports focus on the role of T regulatory cells and cytokines secreted by T helper cells in leprosy. Finally, a newly identified species named M. lepromatosis has been detected in patients with leprosy and severe erythema nodosum leprosum. Summary: Novel biological pathways have been identified to be associated with the clinical phenotype of leprosy or the occurrence of leprosy reactions. Future work should include larger numbers of clinical samples from across the leprosy spectrum in order to give new insights in the pathogenesis and management of the disease.
MeSH term(s)	Humans ; Leprosy/microbiology ; Leprosy/therapy ; Mycobacterium leprae/isolation & purification
Language	English
Publishing date	2013-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645085-4
ISSN	1473-6527 ; 1535-3877 ; 0951-7375 ; 1355-834X
ISSN (online)	1473-6527 ; 1535-3877
ISSN	0951-7375 ; 1355-834X
DOI	10.1097/QCO.0b013e3283638b04
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Article: Rationale for targeting complement in COVID-19

Polycarpou, Anastasia / Howard, Mark / Farrar, Conrad A / Greenlaw, Roseanna / Fanelli, Giorgia / Wallis, Russell / Klavinskis, Linda S / Sacks, Steven

EMBO Mol Med

Abstract	A novel coronavirus, SARS-CoV-2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID-19 caused by SARS-CoV-2 is associated with an acute respiratory illness that varies from mild to the life-threatening acute respiratory distress syndrome (ARDS). The complement system is part of the innate immune arsenal against pathogens, in which many viruses can evade or employ to mediate cell entry. The immunopathology and acute lung injury orchestrated through the influx of pro-inflammatory macrophages and neutrophils can be directly activated by complement components to prime an overzealous cytokine storm. The manifestations of severe COVID-19 such as the ARDS, sepsis and multiorgan failure have an established relationship with activation of the complement cascade. We have collected evidence from all the current studies we are aware of on SARS-CoV-2 immunopathogenesis and the preceding literature on SARS-CoV-1 and MERS-CoV infection linking severe COVID-19 disease directly with dysfunction of the complement pathways. This information lends support for a therapeutic anti-inflammatory strategy against complement, where a number of clinically ready potential therapeutic agents are available.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #607958
Database	COVID19

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Article: Association of the endothelial nitric oxide synthase (NOS3) Glu298Asp gene polymorphism with the risk of Alzheimer's disease-- a meta-analysis.

Ntais, Christos / Polycarpou, Anastasia

Journal of neurology

2005 Volume 252, Issue 10, Page(s) 1276–1278

MeSH term(s)	Alleles ; Alzheimer Disease/enzymology ; Alzheimer Disease/genetics ; Asian Continental Ancestry Group/genetics ; Asian Continental Ancestry Group/statistics & numerical data ; Aspartic Acid/genetics ; Case-Control Studies ; Confidence Intervals ; European Continental Ancestry Group/genetics ; European Continental Ancestry Group/statistics & numerical data ; Gene Frequency ; Genotype ; Glutamic Acid/genetics ; Homozygote ; Humans ; Models, Statistical ; Nitric Oxide Synthase Type III/genetics ; Odds Ratio ; Polymorphism, Genetic ; Risk Factors
Chemical Substances	Aspartic Acid (30KYC7MIAI) ; Glutamic Acid (3KX376GY7L) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2005-10
Publishing country	Germany
Document type	Comparative Study ; Letter ; Meta-Analysis
ZDB-ID	187050-6
ISSN	1432-1459 ; 0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
ISSN (online)	1432-1459
ISSN	0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
DOI	10.1007/s00415-005-0823-y
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Article ; Online: Mycobacterium leprae Activates Toll-Like Receptor-4 Signaling and Expression on Macrophages Depending on Previous Bacillus Calmette-Guerin Vaccination.

Polycarpou, Anastasia / Holland, Martin J / Karageorgiou, Ioannis / Eddaoudi, Ayad / Walker, Stephen L / Willcocks, Sam / Lockwood, Diana N J

Frontiers in cellular and infection microbiology

2016 Volume 6, Page(s) 72

Abstract: Toll-like receptor (TLR)-1 and TLR2 have been shown to be receptors for Mycobacterium leprae (M. leprae), yet it is unclear whether M. leprae can signal through alternative TLRs. Other mycobacterial species possess ligands for TLR4 and genetic ... ...

Abstract	Toll-like receptor (TLR)-1 and TLR2 have been shown to be receptors for Mycobacterium leprae (M. leprae), yet it is unclear whether M. leprae can signal through alternative TLRs. Other mycobacterial species possess ligands for TLR4 and genetic association studies in human populations suggest that people with TLR4 polymorphisms may be protected against leprosy. Using human embryonic kidney (HEK)-293 cells co-transfected with TLR4, we demonstrate that M. leprae activates TLR4. We used human macrophages to show that M. leprae stimulation of cytokine production is diminished if pre-treated with TLR4 neutralizing antibody. TLR4 protein expression was up-regulated on macrophages derived from non-bacillus Calmette-Guerin (BCG) vaccinated healthy volunteers after incubation with M. leprae, whereas it was down-regulated in macrophages derived from BCG-vaccinated donors. Finally, pre-treatment of macrophages derived from BCG-naive donors with BCG reversed the effect of M. leprae on TLR4 expression. This may be a newly described phenomenon by which BCG vaccination stimulates "non-specific" protection to the human immune system.
MeSH term(s)	Animals ; Antibodies, Monoclonal ; Antibodies, Neutralizing ; BCG Vaccine/immunology ; BCG Vaccine/pharmacology ; Cell Differentiation/immunology ; Cytokines/metabolism ; HEK293 Cells ; Humans ; Leprosy/immunology ; Leprosy/microbiology ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Monocytes/drug effects ; Monocytes/immunology ; Mycobacterium leprae/immunology ; Mycobacterium leprae/metabolism ; Signal Transduction ; Toll-Like Receptor 4/biosynthesis ; Toll-Like Receptor 4/immunology ; Toll-Like Receptor 4/metabolism
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Neutralizing ; BCG Vaccine ; Cytokines ; TLR4 protein, human ; Toll-Like Receptor 4
Language	English
Publishing date	2016
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2016.00072
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Targeting sustainable bioeconomy: A new development strategy for Southern European countries. The Manifesto of the European Mezzogiorno

Koukios, Emmanuel / Anastasia Zabaniotou / Anthi Charalambous / Eva López Hernández / Francisco Girio / Juan Carlos Parajó / Manuel Jose Texeira Carrondo / Massimo Monteleone / Polycarpos Polycarpou / Sofia Mannelli

Journal of cleaner production. 2018 Jan. 20, v. 172

2018

Abstract: This policy-oriented opinion paper, which has taken the form of a Manifesto, is co-authored by scientists and engineers from Southern European Union countries that are presently experiencing deep and complex systemic crises: Portugal, Spain, Italy, ... ...

Abstract	This policy-oriented opinion paper, which has taken the form of a Manifesto, is co-authored by scientists and engineers from Southern European Union countries that are presently experiencing deep and complex systemic crises: Portugal, Spain, Italy, Greece and Cyprus. With their Manifesto, the authors advocate the adoption of a new development model, focusing on the target of sustainable bioeconomy, around which other development themes and topics will crystallize. Implementing this model will act as a locomotive to get the economies and societies of these countries efficiently out of their crises, and smoothly into greener post-crisis pastures. The proposal is articulated in ten critical steps or theses for immediate action by the policy- and decision-makers, as well as industry, markets and other key actors within this troubled area of the European Mezzogiorno. Corroborating evidence of these theses comes in the form of short reports or “letters” on the key topics of this Manifesto from the countries and regions concerned.
Keywords	bioeconomics ; European Union ; industry ; markets ; models ; pastures ; reports ; sustainable development ; Cyprus ; Greece ; Italy ; Portugal ; Southern European region ; Spain
Language	English
Dates of publication	2018-0120
Size	p. 3931-3941.
Publishing place	Elsevier Ltd
Document type	Article
ISSN	0959-6526
DOI	10.1016/j.jclepro.2017.05.020
Database	NAL-Catalogue (AGRICOLA)

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