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Article ; Online: Overview: Systemic Inflammatory Response Derived From Lung Injury Caused by SARS-CoV-2 Infection Explains Severe Outcomes in COVID-19.

Polidoro, Rafael B / Hagan, Robert S / de Santis Santiago, Roberta / Schmidt, Nathan W

2020 Volume 11, Page(s) 1626

Abstract: Most SARS-CoV2 infections will not develop into severe COVID-19. However, in some patients, lung infection leads to the activation of alveolar macrophages and lung epithelial cells that will release proinflammatory cytokines. IL-6, TNF, and IL-1β ... ...

Abstract	Most SARS-CoV2 infections will not develop into severe COVID-19. However, in some patients, lung infection leads to the activation of alveolar macrophages and lung epithelial cells that will release proinflammatory cytokines. IL-6, TNF, and IL-1β increase expression of cell adhesion molecules (CAMs) and VEGF, thereby increasing permeability of the lung endothelium and reducing barrier protection, allowing viral dissemination and infiltration of neutrophils and inflammatory monocytes. In the blood, these cytokines will stimulate the bone marrow to produce and release immature granulocytes, that return to the lung and further increase inflammation, leading to acute respiratory distress syndrome (ARDS). This lung-systemic loop leads to cytokine storm syndrome (CSS). Concurrently, the acute phase response increases the production of platelets, fibrinogen and other pro-thrombotic factors. Systemic decrease in ACE2 function impacts the Renin-Angiotensin-Kallikrein-Kinin systems (RAS-KKS) increasing clotting. The combination of acute lung injury with RAS-KKS unbalance is herein called COVID-19 Associated Lung Injury (CALI). This conservative two-hit model of systemic inflammation due to the lung injury allows new intervention windows and is more consistent with the current knowledge.
MeSH term(s)	Acute Lung Injury/immunology ; Acute Lung Injury/pathology ; Acute Lung Injury/therapy ; Betacoronavirus/immunology ; COVID-19 ; Coronavirus Infections/immunology ; Coronavirus Infections/pathology ; Coronavirus Infections/therapy ; Humans ; Lung/immunology ; Lung/pathology ; Pandemics ; Pneumonia, Viral/immunology ; Pneumonia, Viral/pathology ; Pneumonia, Viral/therapy ; SARS-CoV-2 ; Severe Acute Respiratory Syndrome/immunology ; Severe Acute Respiratory Syndrome/pathology ; Severe Acute Respiratory Syndrome/therapy ; Systemic Inflammatory Response Syndrome/immunology ; Systemic Inflammatory Response Syndrome/pathology ; Systemic Inflammatory Response Syndrome/therapy
Keywords	covid19
Language	English
Publishing date	2020-06-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01626
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Overview

Rafael B. Polidoro / Robert S. Hagan / Roberta de Santis Santiago / Nathan W. Schmidt

Frontiers in Immunology, Vol

Systemic Inflammatory Response Derived From Lung Injury Caused by SARS-CoV-2 Infection Explains Severe Outcomes in COVID-19

2020 Volume 11

Abstract	Most SARS-CoV2 infections will not develop into severe COVID-19. However, in some patients, lung infection leads to the activation of alveolar macrophages and lung epithelial cells that will release proinflammatory cytokines. IL-6, TNF, and IL-1β increase expression of cell adhesion molecules (CAMs) and VEGF, thereby increasing permeability of the lung endothelium and reducing barrier protection, allowing viral dissemination and infiltration of neutrophils and inflammatory monocytes. In the blood, these cytokines will stimulate the bone marrow to produce and release immature granulocytes, that return to the lung and further increase inflammation, leading to acute respiratory distress syndrome (ARDS). This lung-systemic loop leads to cytokine storm syndrome (CSS). Concurrently, the acute phase response increases the production of platelets, fibrinogen and other pro-thrombotic factors. Systemic decrease in ACE2 function impacts the Renin-Angiotensin-Kallikrein-Kinin systems (RAS-KKS) increasing clotting. The combination of acute lung injury with RAS-KKS unbalance is herein called COVID-19 Associated Lung Injury (CALI). This conservative two-hit model of systemic inflammation due to the lung injury allows new intervention windows and is more consistent with the current knowledge.
Keywords	SARS-CoV2 ; COVID-19 ; severe COVID-19 ; bisphosphonates ; inflammatory monocytes ; ARDS ; Immunologic diseases. Allergy ; RC581-607 ; covid19
Subject code	610
Language	English
Publishing date	2020-06-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Overview

Polidoro, Rafael B. / Hagan, Robert S. / de Santis Santiago, Roberta / Schmidt, Nathan W.

Frontiers in Immunology

Systemic Inflammatory Response Derived From Lung Injury Caused by SARS-CoV-2 Infection Explains Severe Outcomes in COVID-19

2020 Volume 11

Keywords	covid19
Publisher	Frontiers Media SA
Publishing country	ch
Document type	Article ; Online
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01626
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Innate immune activation restricts priming and protective efficacy of the radiation-attenuated PfSPZ malaria vaccine.

Senkpeil, Leetah / Bhardwaj, Jyoti / Little, Morgan R / Holla, Prasida / Upadhye, Aditi / Fusco, Elizabeth M / Swanson Ii, Phillip A / Wiegand, Ryan E / Macklin, Michael D / Bi, Kevin / Flynn, Barbara J / Yamamoto, Ayako / Gaskin, Erik L / Sather, D Noah / Oblak, Adrian L / Simpson, Edward / Gao, Hongyu / Haining, W Nicholas / Yates, Kathleen B /

Liu, Xiaowen / Murshedkar, Tooba / Richie, Thomas L / Sim, B Kim Lee / Otieno, Kephas / Kariuki, Simon / Xuei, Xiaoling / Liu, Yunlong / Polidoro, Rafael B / Hoffman, Stephen L / Oneko, Martina / Steinhardt, Laura C / Schmidt, Nathan W / Seder, Robert A / Tran, Tuan M

JCI insight

2024

Abstract: A systems analysis was conducted to determine the potential molecular mechanisms underlying differential immunogenicity and protective efficacy results of a clinical trial of the radiation-attenuated whole sporozoite PfSPZ Vaccine in African infants. ... ...

Abstract	A systems analysis was conducted to determine the potential molecular mechanisms underlying differential immunogenicity and protective efficacy results of a clinical trial of the radiation-attenuated whole sporozoite PfSPZ Vaccine in African infants. Innate immune activation and myeloid signatures at pre-vaccination baseline correlated with protection from Pf parasitemia in placebo controls. These same signatures were associated with susceptibility to parasitemia among infants who received the highest and most protective PfSPZ Vaccine dose. Machine learning identified spliceosome, proteosome, and resting dendritic cell signatures as pre-vaccination features predictive of protection after highest-dose PfSPZ vaccination, whereas baseline CSP-specific IgG predicted non-protection. Pre-vaccination innate inflammatory and myeloid signatures were associated with higher sporozoite-specific IgG Ab response but undetectable PfSPZ-specific CD8+ T-cell responses post-vaccination. Consistent with these human data, innate stimulation in vivo conferred protection against infection by sporozoite injection in malaria-naïve mice while diminishing the CD8+ T-cell response to radiation-attenuated sporozoites. These data suggest a dichotomous role of innate stimulation for malaria protection and induction of protective immunity of whole-sporozoite malaria vaccines. The uncoupling of vaccine-induced protective immunity achieved by Abs from more protective CD8+ T cell responses suggest that PfSPZ Vaccine efficacy in malaria-endemic settings may be constrained by opposing antigen presentation pathways.
Language	English
Publishing date	2024-04-30
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.167408
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Article ; Online: SARS-CoV-2 selectively induces the expression of unproductive splicing isoforms of interferon, class I MHC and splicing machinery genes

Lüscher Dias, Thomaz / Mamede Costa Andrade da Conceição, Izabela / Toledo, Nayara E. / Queiroz, Lucio Rezende / de Castro, Ícaro Maia Santos / Polidoro, Rafael B / Del-Bem, Luiz-Eduardo / Nakaya, Helder / Franco, Glória Regina

bioRxiv

Abstract: ... suppresses interferon (IFN) expression, leading to B cell and CD8+ T cell leukopenia, while simultaneously ... genes, and splicing machinery genes, including IRF7, OAS3, HLA-B, and HNRNPH1. In stark contrast ...

Abstract	Splicing is a highly conserved, intricate mechanism intimately linked to transcription elongation, serving as a pivotal regulator of gene expression. Alternative splicing may generate specific transcripts incapable of undergoing translation into proteins, designated as unproductive. A plethora of respiratory viruses, including Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), strategically manipulate the host9s splicing machinery to circumvent antiviral responses. During the infection, SARS-CoV-2 effectively suppresses interferon (IFN) expression, leading to B cell and CD8+ T cell leukopenia, while simultaneously increasing the presence of macrophages and neutrophils in patients with severe COVID-19. In this study, we integrated publicly available omics datasets to systematically analyze transcripts at the isoform level and delineate the nascent-peptide translatome landscapes of SARS-CoV-2-infected human cells. Our findings reveal a hitherto uncharacterized mechanism whereby SARS-CoV-2 infection induces the predominant expression of unproductive splicing isoforms in key IFN signaling genes, interferon-stimulated genes (ISGs), class I MHC genes, and splicing machinery genes, including IRF7, OAS3, HLA-B, and HNRNPH1. In stark contrast, cytokine and chemokine genes, such as IL6, CXCL8, and TNF, predominantly express productive (protein-coding) splicing isoforms in response to SARS-CoV-2 infection. We postulate that SARS-CoV-2 employs a previously unreported tactic of exploiting the host splicing machinery to bolster viral replication and subvert the immune response by selectively upregulating unproductive splicing isoforms from antigen presentation and antiviral response genes. Our study sheds new light on the molecular interplay between SARS-CoV-2 and the host immune system, offering a foundation for the development of novel therapeutic strategies to combat COVID-19.
Keywords	covid19
Language	English
Publishing date	2023-04-13
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2023.04.12.536671
Database	COVID19

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Article ; Online: γδ T cells suppress Plasmodium falciparum blood-stage infection by direct killing and phagocytosis.

Junqueira, Caroline / Polidoro, Rafael B / Castro, Guilherme / Absalon, Sabrina / Liang, Zhitao / Sen Santara, Sumit / Crespo, Ângela / Pereira, Dhelio B / Gazzinelli, Ricardo T / Dvorin, Jeffrey D / Lieberman, Judy

Nature immunology

2021 Volume 22, Issue 3, Page(s) 347–357

Abstract: Activated Vγ9Vδ2 (γδ2) T lymphocytes that sense parasite-produced phosphoantigens are expanded in Plasmodium falciparum-infected patients. Although previous studies suggested that γδ2 T cells help control erythrocytic malaria, whether γδ2 T cells ... ...

Abstract	Activated Vγ9Vδ2 (γδ2) T lymphocytes that sense parasite-produced phosphoantigens are expanded in Plasmodium falciparum-infected patients. Although previous studies suggested that γδ2 T cells help control erythrocytic malaria, whether γδ2 T cells recognize infected red blood cells (iRBCs) was uncertain. Here we show that iRBCs stained for the phosphoantigen sensor butyrophilin 3A1 (BTN3A1). γδ2 T cells formed immune synapses and lysed iRBCs in a contact, phosphoantigen, BTN3A1 and degranulation-dependent manner, killing intracellular parasites. Granulysin released into the synapse lysed iRBCs and delivered death-inducing granzymes to the parasite. All intra-erythrocytic parasites were susceptible, but schizonts were most sensitive. A second protective γδ2 T cell mechanism was identified. In the presence of patient serum, γδ2 T cells phagocytosed and degraded opsonized iRBCs in a CD16-dependent manner, decreasing parasite multiplication. Thus, γδ2 T cells have two ways to control blood-stage malaria-γδ T cell antigen receptor (TCR)-mediated degranulation and phagocytosis of antibody-coated iRBCs.
MeSH term(s)	Antigens, CD/metabolism ; Antigens, Differentiation, T-Lymphocyte/metabolism ; Antigens, Protozoan/blood ; Antigens, Protozoan/immunology ; Boston ; Brazil ; Butyrophilins/metabolism ; Cells, Cultured ; Cytotoxicity, Immunologic ; Erythrocytes/immunology ; Erythrocytes/metabolism ; Erythrocytes/parasitology ; Female ; Granzymes/metabolism ; Host-Parasite Interactions ; Humans ; Immunological Synapses/metabolism ; Immunological Synapses/parasitology ; Intraepithelial Lymphocytes/immunology ; Intraepithelial Lymphocytes/metabolism ; Intraepithelial Lymphocytes/parasitology ; Lymphocyte Activation ; Malaria, Falciparum/blood ; Malaria, Falciparum/immunology ; Malaria, Falciparum/parasitology ; Male ; Phagocytosis ; Plasmodium falciparum/growth & development ; Plasmodium falciparum/microbiology
Chemical Substances	Antigens, CD ; Antigens, Differentiation, T-Lymphocyte ; Antigens, Protozoan ; BTN2A1 protein, human ; BTN3A1 protein, human ; Butyrophilins ; GNLY protein, human ; GZMB protein, human (EC 3.4.21.-) ; Granzymes (EC 3.4.21.-)
Language	English
Publishing date	2021-01-11
Publishing country	United States
Document type	Journal Article ; Multicenter Study ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/s41590-020-00847-4
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Article ; Online: Overview

Polidoro, Rafael B. / Hagan, Robert S. / de Santis Santiago, Roberta / Schmidt, Nathan W.

Publisher

Systemic Inflammatory Response Derived From Lung Injury Caused by SARS-CoV-2 Infection Explains Severe Outcomes in COVID-19

2020

Abstract	Most SARS-CoV2 infections will not develop into severe COVID-19. However, in some patients, lung infection leads to the activation of alveolar macrophages and lung epithelial cells that will release proinflammatory cytokines. IL-6, TNF and IL-1β increase expression of cell adhesion molecules (CAMs) and VEGF, thereby increasing permeability of the lung endothelium and reducing barrier protection, allowing viral dissemination and infiltration of neutrophils and inflammatory monocytes. In the blood, these cytokines will stimulate the bone marrow to produce and release immature granulocytes, that return to the lung and further increase inflammation, leading to acute respiratory distress syndrome (ARDS). This lung-systemic loop leads to cytokine release syndrome (CRS). Concurrently, the acute phase response increases the production of platelets, fibrinogen and other pro-thrombotic factors. Systemic decrease in ACE2 function impacts the Renin-Angiotensin-Kallikrein-Kinin systems (RAS-KKS) increasing clotting. The combination of acute lung injury with RAS-KKS unbalance is herein called COVID-19 Associated Lung Injury (CALI). This conservative two-hit model of systemic inflammation due to the lung injury allows new intervention windows and is more consistent with the current knowledge. Indiana University Health—Indiana University School of Medicine Strategic Research Initiative
Keywords	COVID-19 ; Lung Inflammation ; Acute Respiratory Distress Syndrome ; Immunology ; covid19
Subject code	610
Language	English
Publishing date	2020-06-26
Publisher	Frontiers Media
Publishing country	us
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Lymphocyte innateness defined by transcriptional states reflects a balance between proliferation and effector functions.

Gutierrez-Arcelus, Maria / Teslovich, Nikola / Mola, Alex R / Polidoro, Rafael B / Nathan, Aparna / Kim, Hyun / Hannes, Susan / Slowikowski, Kamil / Watts, Gerald F M / Korsunsky, Ilya / Brenner, Michael B / Raychaudhuri, Soumya / Brennan, Patrick J

Nature communications

2019 Volume 10, Issue 1, Page(s) 687

Abstract: How innate T cells (ITC), including invariant natural killer T (iNKT) cells, mucosal-associated invariant T (MAIT) cells, and γδ T cells, maintain a poised effector state has been unclear. Here we address this question using low-input and single-cell RNA- ...

Abstract	How innate T cells (ITC), including invariant natural killer T (iNKT) cells, mucosal-associated invariant T (MAIT) cells, and γδ T cells, maintain a poised effector state has been unclear. Here we address this question using low-input and single-cell RNA-seq of human lymphocyte populations. Unbiased transcriptomic analyses uncover a continuous 'innateness gradient', with adaptive T cells at one end, followed by MAIT, iNKT, γδ T and natural killer cells at the other end. Single-cell RNA-seq reveals four broad states of innateness, and heterogeneity within canonical innate and adaptive populations. Transcriptional and functional data show that innateness is characterized by pre-formed mRNA encoding effector functions, but impaired proliferation marked by decreased baseline expression of ribosomal genes. Together, our data shed new light on the poised state of ITC, in which innateness is defined by a transcriptionally-orchestrated trade-off between rapid cell growth and rapid effector function.
MeSH term(s)	Cell Proliferation/physiology ; Female ; Gene Ontology ; Humans ; Immunity, Innate/physiology ; Immunophenotyping ; Leukocytes, Mononuclear/metabolism ; Lymphocyte Activation/physiology ; Lymphocytes/metabolism ; Male ; Natural Killer T-Cells/metabolism ; T-Lymphocyte Subsets/metabolism
Language	English
Publishing date	2019-02-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-08604-4
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Article ; Online: Transient transfection and expression of foreign and endogenous genes in the intracellular stages of Trypanosoma cruzi.

Padmanabhan, Prasad K / Polidoro, Rafael B / Barteneva, Natasha S / Gazzinelli, Ricardo T / Burleigh, Barbara A

Molecular and biochemical parasitology

2014 Volume 198, Issue 2, Page(s) 100–103

Abstract: The capacity for rapid localization of epitope-tagged or fluorescent fusion proteins in cells is an important tool for biological discovery and functional analysis. For Trypanosoma cruzi, the protozoan parasite that causes human Chagas disease, ... ...

Abstract	The capacity for rapid localization of epitope-tagged or fluorescent fusion proteins in cells is an important tool for biological discovery and functional analysis. For Trypanosoma cruzi, the protozoan parasite that causes human Chagas disease, visualization of ectopically-expressed proteins in the clinically-relevant mammalian stages is hindered by the necessity to first perform transfection and lengthy selection procedures in the insect vector form of the parasite. Here, we demonstrate the ability to by-pass the insect stage with the delivery of plasmid DNA to non-dividing, tissue culture trypomastigotes such that upon host cell infection, transgenes are expressed and rapidly localized in intracellular T. cruzi amastigotes. The inclusion of a sorting step prior to host cell infection by trypomastigotes greatly enriches (>90%) the number of transgene-expressing amastigotes observed in mammalian host cells. This is a significant methodological advance that has the potential to accelerate the pace of discovery in the Chagas disease field.
MeSH term(s)	Animals ; Cell Line ; Gene Expression ; Mammals ; Molecular Biology/methods ; Parasitology/methods ; Protozoan Proteins/biosynthesis ; Protozoan Proteins/genetics ; Recombinant Proteins/biosynthesis ; Recombinant Proteins/genetics ; Transfection ; Trypanosoma cruzi/genetics
Chemical Substances	Protozoan Proteins ; Recombinant Proteins
Language	English
Publishing date	2014-12
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	756166-0
ISSN	1872-9428 ; 0166-6851
ISSN (online)	1872-9428
ISSN	0166-6851
DOI	10.1016/j.molbiopara.2015.02.001
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Article ; Online: Killer lymphocytes use granulysin, perforin and granzymes to kill intracellular parasites.

Dotiwala, Farokh / Mulik, Sachin / Polidoro, Rafael B / Ansara, James A / Burleigh, Barbara A / Walch, Michael / Gazzinelli, Ricardo T / Lieberman, Judy

Nature medicine

2016 Volume 22, Issue 2, Page(s) 210–216

Abstract: Protozoan infections are a serious global health problem. Natural killer (NK) cells and cytolytic T lymphocytes (CTLs) eliminate pathogen-infected cells by releasing cytolytic granule contents--granzyme (Gzm) proteases and the pore-forming perforin (PFN)- ...

Abstract	Protozoan infections are a serious global health problem. Natural killer (NK) cells and cytolytic T lymphocytes (CTLs) eliminate pathogen-infected cells by releasing cytolytic granule contents--granzyme (Gzm) proteases and the pore-forming perforin (PFN)--into the infected cell. However, these cytotoxic molecules do not kill intracellular parasites. CD8(+) CTLs protect against parasite infections in mice primarily by secreting interferon (IFN)-γ. However, human, but not rodent, cytotoxic granules contain the antimicrobial peptide granulysin (GNLY), which selectively destroys cholesterol-poor microbial membranes, and GNLY, PFN and Gzms rapidly kill intracellular bacteria. Here we show that GNLY delivers Gzms into three protozoan parasites (Trypanosoma cruzi, Toxoplasma gondii and Leishmania major), in which the Gzms generate superoxide and inactivate oxidative defense enzymes to kill the parasite. PFN delivers GNLY and Gzms into infected cells, and GNLY then delivers Gzms to the intracellular parasites. Killer cell-mediated parasite death, which we term 'microbe-programmed cell death' or 'microptosis', is caspase independent but resembles mammalian apoptosis, causing mitochondrial swelling, transmembrane potential dissipation, membrane blebbing, phosphatidylserine exposure, DNA damage and chromatin condensation. GNLY-transgenic mice are protected against infection by T. cruzi and T. gondii, and survive infections that are lethal to wild-type mice. Thus, GNLY-, PFN- and Gzm-mediated elimination of intracellular protozoan parasites is an unappreciated immune defense mechanism.
MeSH term(s)	Animals ; Antigens, Differentiation, T-Lymphocyte/genetics ; Antigens, Differentiation, T-Lymphocyte/immunology ; Chagas Disease/immunology ; Granzymes/immunology ; Humans ; Killer Cells, Natural/immunology ; Leishmania major ; Leishmaniasis, Cutaneous/immunology ; Mice ; Mice, Transgenic ; Perforin/immunology ; T-Lymphocytes, Cytotoxic/immunology ; Toxoplasma ; Toxoplasmosis/immunology ; Trypanosoma cruzi
Chemical Substances	Antigens, Differentiation, T-Lymphocyte ; GNLY protein, human ; Perforin (126465-35-8) ; GZMB protein, human (EC 3.4.21.-) ; Granzymes (EC 3.4.21.-) ; GZMA protein, human (EC 3.4.21.78)
Language	English
Publishing date	2016-01-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1220066-9
ISSN	1546-170X ; 1078-8956
ISSN (online)	1546-170X
ISSN	1078-8956
DOI	10.1038/nm.4023
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