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  1. Article: Chlamydia pneumoniae

    Porritt, Rebecca A / Crother, Timothy R

    Forum on immunopathological diseases and therapeutics

    2018  Volume 7, Issue 3-4, Page(s) 237–254

    Abstract: Chlamydia ... ...

    Abstract Chlamydia pneumoniae
    Language English
    Publishing date 2018-12-18
    Publishing country United States
    Document type Journal Article
    ISSN 2151-8017
    ISSN 2151-8017
    DOI 10.1615/ForumImmunDisTher.2017020161
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Multisystem Inflammatory Syndrome in Children and Long COVID: The SARS-CoV-2 Viral Superantigen Hypothesis.

    Noval Rivas, Magali / Porritt, Rebecca A / Cheng, Mary Hongying / Bahar, Ivet / Arditi, Moshe

    Frontiers in immunology

    2022  Volume 13, Page(s) 941009

    Abstract: Multisystem inflammatory syndrome in children (MIS-C) is a febrile pediatric inflammatory disease that may develop weeks after initial SARS-CoV-2 infection or exposure. MIS-C involves systemic hyperinflammation and multiorgan involvement, including ... ...

    Abstract Multisystem inflammatory syndrome in children (MIS-C) is a febrile pediatric inflammatory disease that may develop weeks after initial SARS-CoV-2 infection or exposure. MIS-C involves systemic hyperinflammation and multiorgan involvement, including severe cardiovascular, gastrointestinal (GI) and neurological symptoms. Some clinical attributes of MIS-C-such as persistent fever, rashes, conjunctivitis and oral mucosa changes (red fissured lips and strawberry tongue)-overlap with features of Kawasaki disease (KD). In addition, MIS-C shares striking clinical similarities with toxic shock syndrome (TSS), which is triggered by bacterial superantigens (SAgs). The remarkable similarities between MIS-C and TSS prompted a search for SAg-like structures in the SARS-CoV-2 virus and the discovery of a unique SAg-like motif highly similar to a Staphylococcal enterotoxin B (SEB) fragment in the SARS-CoV-2 spike 1 (S1) glycoprotein. Computational studies suggest that the SAg-like motif has a high affinity for binding T-cell receptors (TCRs) and MHC Class II proteins. Immunosequencing of peripheral blood samples from MIS-C patients revealed a profound expansion of TCR β variable gene 11-2 (TRBV11-2), which correlates with MIS-C severity and serum cytokine levels, consistent with a SAg-triggered immune response. Computational sequence analysis of SARS-CoV-2 spike further identified conserved neurotoxin-like motifs which may alter neuronal cell function and contribute to neurological symptoms in COVID-19 and MIS-C patients. Additionally, autoantibodies are detected during MIS-C, which may indicate development of post-SARS-CoV-2 autoreactive and autoimmune responses. Finally, prolonged persistence of SARS-CoV-2 RNA in the gut, increased gut permeability and elevated levels of circulating S1 have been observed in children with MIS-C. Accordingly, we hypothesize that continuous and prolonged exposure to the viral SAg-like and neurotoxin-like motifs in SARS-CoV-2 spike may promote autoimmunity leading to the development of post-acute COVID-19 syndromes, including MIS-C and long COVID, as well as the neurological complications resulting from SARS-CoV-2 infection.
    MeSH term(s) COVID-19/complications ; Child ; Connective Tissue Diseases ; Humans ; Neurotoxins ; RNA, Viral ; SARS-CoV-2 ; Superantigens ; Systemic Inflammatory Response Syndrome ; Post-Acute COVID-19 Syndrome
    Chemical Substances Neurotoxins ; RNA, Viral ; Superantigens
    Language English
    Publishing date 2022-07-07
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; 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.2022.941009
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  3. Article ; Online: COVID-19-associated multisystem inflammatory syndrome in children (MIS-C): A novel disease that mimics toxic shock syndrome-the superantigen hypothesis.

    Noval Rivas, Magali / Porritt, Rebecca A / Cheng, Mary Hongying / Bahar, Ivet / Arditi, Moshe

    The Journal of allergy and clinical immunology

    2020  Volume 147, Issue 1, Page(s) 57–59

    MeSH term(s) COVID-19/metabolism ; COVID-19/pathology ; Child ; Child, Preschool ; Female ; Humans ; Male ; SARS-CoV-2/metabolism ; Shock, Septic/metabolism ; Shock, Septic/pathology ; Superantigens/metabolism ; Systemic Inflammatory Response Syndrome/metabolism ; Systemic Inflammatory Response Syndrome/pathology
    Chemical Substances Superantigens
    Keywords covid19
    Language English
    Publishing date 2020-10-16
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 121011-7
    ISSN 1097-6825 ; 1085-8725 ; 0091-6749
    ISSN (online) 1097-6825 ; 1085-8725
    ISSN 0091-6749
    DOI 10.1016/j.jaci.2020.10.008
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  4. Article ; Online: Dynamic control of type I IFN signalling by an integrated network of negative regulators.

    Porritt, Rebecca A / Hertzog, Paul J

    Trends in immunology

    2015  Volume 36, Issue 3, Page(s) 150–160

    Abstract: Whereas type I interferons (IFNs) have critical roles in protection from pathogens, excessive IFN responses contribute to pathology in both acute and chronic settings, pointing to the importance of balancing activating signals with regulatory mechanisms ... ...

    Abstract Whereas type I interferons (IFNs) have critical roles in protection from pathogens, excessive IFN responses contribute to pathology in both acute and chronic settings, pointing to the importance of balancing activating signals with regulatory mechanisms that appropriately tune the response. Here we review evidence for an integrated network of negative regulators of IFN production and action, which function at all levels of the activating and effector signalling pathways. We propose that the aim of this extensive network is to limit tissue damage while enabling an IFN response that is temporally appropriate and of sufficient magnitude. Understanding the architecture and dynamics of this network, and how it differs in distinct tissues, will provide new insights into IFN biology and aid the design of more effective therapeutics.
    MeSH term(s) Dendritic Cells/immunology ; Feedback, Physiological ; Gene Expression Regulation/immunology ; Gene Regulatory Networks/immunology ; Humans ; Immunity, Innate ; Interferon Type I/genetics ; Interferon Type I/immunology ; Interleukins/genetics ; Interleukins/immunology ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/immunology ; MicroRNAs/genetics ; MicroRNAs/immunology ; Receptors, Cytokine/genetics ; Receptors, Cytokine/immunology ; Signal Transduction ; Smad Proteins/genetics ; Smad Proteins/immunology ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/immunology ; Viruses/immunology
    Chemical Substances Interferon Type I ; Interleukins ; Intracellular Signaling Peptides and Proteins ; MicroRNAs ; Receptors, Cytokine ; Smad Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2015-03
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2015.02.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 2: Show issues

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  5. Article ; Online: Platelets exacerbate cardiovascular inflammation in a murine model of Kawasaki disease vasculitis.

    Kocatürk, Begüm / Lee, Youngho / Nosaka, Nobuyuki / Abe, Masanori / Martinon, Daisy / Lane, Malcolm E / Moreira, Debbie / Chen, Shuang / Fishbein, Michael C / Porritt, Rebecca A / Franklin, Bernardo S / Noval Rivas, Magali / Arditi, Moshe

    JCI insight

    2023  Volume 8, Issue 14

    Abstract: Kawasaki disease (KD) is the leading cause of acquired heart disease among children. Increased platelet counts and activation are observed during the course of KD, and elevated platelet counts are associated with higher risks of developing intravenous ... ...

    Abstract Kawasaki disease (KD) is the leading cause of acquired heart disease among children. Increased platelet counts and activation are observed during the course of KD, and elevated platelet counts are associated with higher risks of developing intravenous immunoglobulin resistance and coronary artery aneurysms. However, the role of platelets in KD pathogenesis remains unclear. Here, we analyzed transcriptomics data generated from the whole blood of patients with KD and discovered changes in the expression of platelet-related genes during acute KD. In the Lactobacillus casei cell wall extract (LCWE) murine model of KD vasculitis, LCWE injection increased platelet counts and the formation of monocyte-platelet aggregates (MPAs), upregulated the concentration of soluble P-selectin, and increased circulating thrombopoietin and interleukin 6 (IL-6). Furthermore, platelet counts correlated with the severity of cardiovascular inflammation. Genetic depletion of platelets (Mpl-/- mice) or treatment with an anti-CD42b antibody significantly reduced LCWE-induced cardiovascular lesions. Furthermore, in the mouse model, platelets promoted vascular inflammation via the formation of MPAs, which likely amplified IL-1B production. Altogether, our results indicate that platelet activation exacerbates the development of cardiovascular lesions in a murine model of KD vasculitis. These findings enhance our understanding of KD vasculitis pathogenesis and highlight MPAs, which are known to enhance IL-1B production, as a potential therapeutic target for this disorder.
    MeSH term(s) Animals ; Mice ; Mucocutaneous Lymph Node Syndrome/genetics ; Mucocutaneous Lymph Node Syndrome/drug therapy ; Blood Platelets/metabolism ; Disease Models, Animal ; Vasculitis ; Inflammation
    Language English
    Publishing date 2023-07-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.169855
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  6. Article ; Online: Platelets exacerbate cardiovascular inflammation in a murine model of Kawasaki disease vasculitis

    Begüm Kocatürk / Youngho Lee / Nobuyuki Nosaka / Masanori Abe / Daisy Martinon / Malcolm E. Lane / Debbie Moreira / Shuang Chen / Michael C. Fishbein / Rebecca A. Porritt / Bernardo S. Franklin / Magali Noval Rivas / Moshe Arditi

    JCI Insight, Vol 8, Iss

    2023  Volume 17

    Keywords Medicine ; R
    Language English
    Publishing date 2023-09-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article: An insertion unique to SARS-CoV-2 exhibits superantigenic character strengthened by recent mutations.

    Cheng, Mary Hongying / Zhang, She / Porritt, Rebecca A / Arditi, Moshe / Bahar, Ivet

    bioRxiv : the preprint server for biology

    2020  

    Abstract: Multisystem Inflammatory Syndrome in Children (MIS-C) associated with Coronavirus Disease 2019 (COVID-19) is a newly recognized condition in which children with recent SARS-CoV-2 infection present with a constellation of symptoms including hypotension, ... ...

    Abstract Multisystem Inflammatory Syndrome in Children (MIS-C) associated with Coronavirus Disease 2019 (COVID-19) is a newly recognized condition in which children with recent SARS-CoV-2 infection present with a constellation of symptoms including hypotension, multiorgan involvement, and elevated inflammatory markers. These symptoms and the associated laboratory values strongly resemble toxic shock syndrome, an escalation of the cytotoxic adaptive immune response triggered upon the binding of pathogenic superantigens to MHCII molecules and T cell receptors (TCRs). Here, we used structure-based computational models to demonstrate that the SARS-CoV-2 spike (S) exhibits a high-affinity motif for binding TCR, interacting closely with both the α- and β-chains variable domains' complementarity-determining regions. The binding epitope on S harbors a sequence motif unique to SARS-CoV-2 (not present in any other SARS coronavirus), which is highly similar in both sequence and structure to bacterial superantigens. Further examination revealed that this interaction between the virus and human T cells is strengthened in the context of a recently reported rare mutation (D839Y/N/E) from a European strain of SARS-CoV-2. Furthermore, the interfacial region includes selected residues from a motif shared between the SARS viruses from the 2003 and 2019 pandemics, which has intracellular adhesion molecule (ICAM)-like character. These data suggest that the SARS-CoV-2 S may act as a superantigen to drive the development of MIS-C as well as cytokine storm in adult COVID-19 patients, with important implications for the development of therapeutic approaches.
    Keywords covid19
    Language English
    Publishing date 2020-05-21
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2020.05.21.109272
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  8. Article ; Online: Osteopontin depletion in macrophages perturbs proteostasis

    Rentsendorj, Altan / Raedschelders, Koen / Fuchs, Dieu-Trang / Sheyn, Julia / Vaibhav, Vineet / Porritt, Rebecca A / Shi, Haoshen / Dagvadorj, Jargalsaikhan / de Freitas Germano, Juliana / Koronyo, Yosef / Arditi, Moshe / Black, Keith L / Gaire, Bhakta Prasad / Van Eyk, Jennifer E / Koronyo-Hamaoui, Maya

    Frontiers in immunology

    2023  Volume 14, Page(s) 1155935

    Abstract: Introduction: Osteopontin (OPN; also known as SPP1), an immunomodulatory cytokine highly expressed in bone marrow-derived macrophages (BMMΦ), is known to regulate diverse cellular and molecular immune responses. We previously revealed that glatiramer ... ...

    Abstract Introduction: Osteopontin (OPN; also known as SPP1), an immunomodulatory cytokine highly expressed in bone marrow-derived macrophages (BMMΦ), is known to regulate diverse cellular and molecular immune responses. We previously revealed that glatiramer acetate (GA) stimulation of BMMΦ upregulates OPN expression, promoting an anti-inflammatory, pro-healing phenotype, whereas OPN inhibition triggers a pro-inflammatory phenotype. However, the precise role of OPN in macrophage activation state is unknown.
    Methods: Here, we applied global proteome profiling via mass spectrometry (MS) analysis to gain a mechanistic understanding of OPN suppression versus induction in primary macrophage cultures. We analyzed protein networks and immune-related functional pathways in BMMΦ either with OPN knockout (OPN
    Results and discussion: We identified 631 DEPs in OPN
    MeSH term(s) Osteopontin/genetics ; Osteopontin/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Proteostasis ; Proteome/metabolism ; Macrophages ; Mitochondria/metabolism ; Apoptosis
    Chemical Substances Osteopontin (106441-73-0) ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Proteome
    Language English
    Publishing date 2023-05-30
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; 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.2023.1155935
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Platelets exacerbate cardiovascular inflammation in a murine model of Kawasaki disease vasculitis

    Begüm Kocatürk / Youngho Lee / Nobuyuki Nosaka / Masanori Abe / Daisy Martinon / Malcolm E. Lane / Debbie Moreira / Shuang Chen / Michael C. Fishbein / Rebecca A. Porritt / Bernardo S. Franklin / Magali Noval Rivas / Moshe Arditi

    JCI Insight, Vol 8, Iss

    2023  Volume 14

    Abstract: Kawasaki disease (KD) is the leading cause of acquired heart disease among children. Increased platelet counts and activation are observed during the course of KD, and elevated platelet counts are associated with higher risks of developing intravenous ... ...

    Abstract Kawasaki disease (KD) is the leading cause of acquired heart disease among children. Increased platelet counts and activation are observed during the course of KD, and elevated platelet counts are associated with higher risks of developing intravenous immunoglobulin resistance and coronary artery aneurysms. However, the role of platelets in KD pathogenesis remains unclear. Here, we analyzed transcriptomics data generated from the whole blood of patients with KD and discovered changes in the expression of platelet-related genes during acute KD. In the Lactobacillus casei cell wall extract (LCWE) murine model of KD vasculitis, LCWE injection increased platelet counts and the formation of monocyte-platelet aggregates (MPAs), upregulated the concentration of soluble P-selectin, and increased circulating thrombopoietin and interleukin 6 (IL-6). Furthermore, platelet counts correlated with the severity of cardiovascular inflammation. Genetic depletion of platelets (Mpl–/– mice) or treatment with an anti-CD42b antibody significantly reduced LCWE-induced cardiovascular lesions. Furthermore, in the mouse model, platelets promoted vascular inflammation via the formation of MPAs, which likely amplified IL-1B production. Altogether, our results indicate that platelet activation exacerbates the development of cardiovascular lesions in a murine model of KD vasculitis. These findings enhance our understanding of KD vasculitis pathogenesis and highlight MPAs, which are known to enhance IL-1B production, as a potential therapeutic target for this disorder.
    Keywords Inflammation ; Vascular biology ; Medicine ; R
    Subject code 630
    Language English
    Publishing date 2023-08-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Author Correction: Apoptotic stress causes mtDNA release during senescence and drives the SASP.

    Victorelli, Stella / Salmonowicz, Hanna / Chapman, James / Martini, Helene / Vizioli, Maria Grazia / Riley, Joel S / Cloix, Catherine / Hall-Younger, Ella / Machado Espindola-Netto, Jair / Jurk, Diana / Lagnado, Anthony B / Sales Gomez, Lilian / Farr, Joshua N / Saul, Dominik / Reed, Rebecca / Kelly, George / Eppard, Madeline / Greaves, Laura C / Dou, Zhixun /
    Pirius, Nicholas / Szczepanowska, Karolina / Porritt, Rebecca A / Huang, Huijie / Huang, Timothy Y / Mann, Derek A / Masuda, Claudio Akio / Khosla, Sundeep / Dai, Haiming / Kaufmann, Scott H / Zacharioudakis, Emmanouil / Gavathiotis, Evripidis / LeBrasseur, Nathan K / Lei, Xue / Sainz, Alva G / Korolchuk, Viktor I / Adams, Peter D / Shadel, Gerald S / Tait, Stephen W G / Passos, João F

    Nature

    2024  Volume 625, Issue 7995, Page(s) E15

    Language English
    Publishing date 2024-01-02
    Publishing country England
    Document type Published Erratum
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-023-07002-7
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