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  1. Article ; Online: Interleukin-1 Receptor-Like 2: One Receptor, Three Agonists, and Many Implications.

    Manzanares-Meza, Laura D / Valle-Rios, Ricardo / Medina-Contreras, Oscar

    Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research

    2022  Volume 42, Issue 2, Page(s) 49–61

    Abstract: The interleukin (IL)-1 superfamily of cytokines comprises 11 pro- and anti-inflammatory cytokines, which play essential roles during the immune response. Several pathogenic pathways are initiated by IL-1RL2 (interleukin 1 receptor-like 2) signaling, also ...

    Abstract The interleukin (IL)-1 superfamily of cytokines comprises 11 pro- and anti-inflammatory cytokines, which play essential roles during the immune response. Several pathogenic pathways are initiated by IL-1RL2 (interleukin 1 receptor-like 2) signaling, also known as IL-36R, in the skin, lungs, and gut. IL-36 cytokines promote the secretion of proinflammatory cytokines and chemokines, upregulation of antimicrobial peptides, proliferation mediators, and adhesion molecules on endothelial cells. In addition, the IL-36-IL-1RL2 axis has an essential role against viral infections, including a potential role in COVID-19 pathology. The evidence presented in this review highlights the importance of the axis IL-36-IL-1RL2 in the development of several inflammation-related diseases and the healing process. It suggests that IL-1RL2 ligands have specific roles depending on the tissue or cell source. However, there is still much to discover about this cytokine family, their functions in other organs, and how they accomplish a dual effect in inflammation and healing.
    MeSH term(s) Animals ; COVID-19/physiopathology ; Cytokine Release Syndrome/physiopathology ; Cytokines/physiology ; Host-Pathogen Interactions ; Humans ; Inflammation/physiopathology ; Interleukin-1/physiology ; Interleukins/classification ; Intestines/metabolism ; Intestines/pathology ; Ligands ; Lung/metabolism ; Lung/pathology ; MAP Kinase Signaling System ; Mice ; NF-kappa B/metabolism ; Protein Domains ; Receptors, Interleukin/classification ; Receptors, Interleukin-1/agonists ; Receptors, Interleukin-1/antagonists & inhibitors ; Receptors, Interleukin-1/chemistry ; Receptors, Interleukin-1/physiology ; SARS-CoV-2 ; Signal Transduction ; Skin/metabolism ; Skin/pathology
    Chemical Substances Cytokines ; IL1RL2 protein, human ; Interleukin-1 ; Interleukins ; Ligands ; NF-kappa B ; Receptors, Interleukin ; Receptors, Interleukin-1 ; interleukin 36, human
    Language English
    Publishing date 2022-02-16
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1226675-9
    ISSN 1557-7465 ; 1079-9907
    ISSN (online) 1557-7465
    ISSN 1079-9907
    DOI 10.1089/jir.2021.0173
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: SARS-CoV-2 and influenza: a comparative overview and treatment implications.

    Manzanares-Meza, Laura D / Medina-Contreras, Oscar

    Boletin medico del Hospital Infantil de Mexico

    2020  Volume 77, Issue 5, Page(s) 262–273

    Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Alphainfluenzavirus are RNA viruses that cause coronavirus disease-19 and influenza, respectively. Both viruses infect the respiratory tract, show similar symptoms, and use surface proteins ...

    Title translation SARS-CoV-2 e influenza: revisión comparativa e implicaciones del tratamiento.
    Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Alphainfluenzavirus are RNA viruses that cause coronavirus disease-19 and influenza, respectively. Both viruses infect the respiratory tract, show similar symptoms, and use surface proteins to infect the host. Influenza requires hemagglutinin and neuraminidase to infect, whereas SARS-CoV-2 uses protein S. Both viruses depend on a viral RNA polymerase to express their proteins, but only SARS-CoV-2 has a proofreading mechanism, which results in a low mutation rate compared to influenza. E1KC4 and camostat mesylate are potential inhibitors of SARS-CoV-2 S protein, achieving an effect similar to oseltamivir. Due to the SARS-CoV-2 low mutation rate, nucleoside analogs have been developed (such as EIDD-2801), which insert lethal mutations in the viral RNA. Furthermore, the SARS-CoV-2 low mutation rate suggests that a vaccine, as well as the immunity developed in recovered patients, could provide long-lasting protection compared to vaccines against influenza, which are rendered obsolete as the virus mutates.
    MeSH term(s) Animals ; Antiviral Agents/administration & dosage ; Antiviral Agents/pharmacology ; Betacoronavirus/immunology ; Betacoronavirus/isolation & purification ; Coronavirus Infections/drug therapy ; Coronavirus Infections/immunology ; Coronavirus Infections/prevention & control ; Coronavirus Infections/virology ; Humans ; Influenza A virus/immunology ; Influenza A virus/isolation & purification ; Influenza, Human/immunology ; Influenza, Human/virology ; Mutation ; Pandemics/prevention & control ; Pneumonia, Viral/immunology ; Pneumonia, Viral/prevention & control ; Pneumonia, Viral/virology ; Viral Vaccines
    Chemical Substances Antiviral Agents ; COVID-19 vaccine ; Viral Vaccines
    Keywords covid19
    Language English
    Publishing date 2020-10-16
    Publishing country Mexico
    Document type Journal Article ; Review
    ZDB-ID 730519-9
    ISSN 1665-1146 ; 1665-1146 ; 0539-6115 ; 0539-6123
    ISSN (online) 1665-1146
    ISSN 1665-1146 ; 0539-6115 ; 0539-6123
    DOI 10.24875/BMHIM.20000183
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: SARS-CoV-2 e influenza: revisión comparativa e implicaciones del tratamiento./ SARS-CoV-2 and influenza: a comparative overview and treatment implications

    Manzanares-Meza, Laura D / Medina-Contreras, Oscar

    Bol Med Hosp Infant Mex

    Abstract: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Alphainfluenzavirus are RNA viruses that cause coronavirus disease-19 and influenza, respectively. Both viruses infect the respiratory tract, show similar symptoms, and use surface proteins ...

    Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and Alphainfluenzavirus are RNA viruses that cause coronavirus disease-19 and influenza, respectively. Both viruses infect the respiratory tract, show similar symptoms, and use surface proteins to infect the host. Influenza requires hemagglutinin and neuraminidase to infect, whereas SARS-CoV-2 uses protein S. Both viruses depend on a viral RNA polymerase to express their proteins, but only SARS-CoV-2 has a proofreading mechanism, which results in a low mutation rate compared to influenza. E1KC4 and camostat mesylate are potential inhibitors of SARS-CoV-2 S protein, achieving an effect similar to oseltamivir. Due to the SARS-CoV-2 low mutation rate, nucleoside analogs have been developed (such as EIDD-2801), which insert lethal mutations in the viral RNA. Furthermore, the SARS-CoV-2 low mutation rate suggests that a vaccine, as well as the immunity developed in recovered patients, could provide long-lasting protection compared to vaccines against influenza, which are rendered obsolete as the virus mutates.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #869463
    Database COVID19

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  4. Article ; Online: IL-36γ is secreted through an unconventional pathway using the Gasdermin D and P2X7R membrane pores.

    Manzanares-Meza, Laura D / Gutiérrez-Román, Claudia I / Jiménez-Pineda, Albertana / Castro-Martínez, Felipe / Patiño-López, Genaro / Rodríguez-Arellano, Eunice / Valle-Rios, Ricardo / Ortíz-Navarrete, Vianney F / Medina-Contreras, Oscar

    Frontiers in immunology

    2022  Volume 13, Page(s) 979749

    Abstract: Mucosal innate immunity functions as the first line of defense against invading pathogens. Members of the IL-1 family are key cytokines upregulated in the inflamed mucosa. Inflammatory cytokines are regulated by limiting their function and availability ... ...

    Abstract Mucosal innate immunity functions as the first line of defense against invading pathogens. Members of the IL-1 family are key cytokines upregulated in the inflamed mucosa. Inflammatory cytokines are regulated by limiting their function and availability through their activation and secretion mechanisms. IL-1 cytokines secretion is affected by the lack of a signal peptide on their sequence, which prevents them from accessing the conventional protein secretion pathway; thus, they use unconventional protein secretion pathways. Here we show in mouse macrophages that LPS/ATP stimulation induces cytokine relocalization to the plasma membrane, and conventional secretion blockade using monensin or Brefeldin A triggers no IL-36γ accumulation within the cell.
    MeSH term(s) Animals ; Biological Transport ; Cytokines/metabolism ; Immunity, Mucosal ; Interleukin-1 ; Mice ; Phosphate-Binding Proteins/metabolism ; Pore Forming Cytotoxic Proteins/metabolism ; Receptors, Purinergic P2X7/metabolism
    Chemical Substances Cytokines ; Gsdmd protein, mouse ; IL1F9 protein, mouse ; Interleukin-1 ; P2rx7 protein, mouse ; Phosphate-Binding Proteins ; Pore Forming Cytotoxic Proteins ; Receptors, Purinergic P2X7
    Language English
    Publishing date 2022-08-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.979749
    Database MEDical Literature Analysis and Retrieval System OnLINE

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