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Artikel ; Online: Interferons in coronavirus pathogenesis: The good, the bad, and the ugly.

Channappanavar, Rudragouda

2022 Band 30, Heft 4, Seite(n) 427–430

Abstract: Interferons (IFNs) are a key component of the innate antiviral immunity and are generally implicated in protective host immune responses. Here, I discuss the central role of IFNs during different coronavirus (CoV) infections, the importance of timing of ... ...

Abstract	Interferons (IFNs) are a key component of the innate antiviral immunity and are generally implicated in protective host immune responses. Here, I discuss the central role of IFNs during different coronavirus (CoV) infections, the importance of timing of the IFN response, and how emerging human coronaviruses subvert antiviral IFN response to cause severe disease.
Mesh-Begriff(e)	Antiviral Agents/therapeutic use ; COVID-19 ; Cell Line ; Humans ; Immunity, Innate ; Interferons
Chemische Substanzen	Antiviral Agents ; Interferons (9008-11-1)
Sprache	Englisch
Erscheinungsdatum	2022-04-13
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2022.03.022
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Differential TLR-ERK1/2 activity promotes viral ssRNA and dsRNA mimic-induced dysregulated immunity in macrophages.

Shrestha, Rakshya / Johnson, Paige / Ghimire, Roshan / Whitley, Cody / Channappanavar, Rudragouda

bioRxiv : the preprint server for biology

2024

Abstract: RNA virus induced excessive inflammation and impaired antiviral interferon (IFN-I) responses are associated with severe disease. This innate immune response, also referred to as 'dysregulated immunity,' is caused by viral single-stranded RNA (ssRNA) and ... ...

Abstract	RNA virus induced excessive inflammation and impaired antiviral interferon (IFN-I) responses are associated with severe disease. This innate immune response, also referred to as 'dysregulated immunity,' is caused by viral single-stranded RNA (ssRNA) and double-stranded-RNA (dsRNA) mediated exuberant inflammation and viral protein-induced IFN antagonism. However, key host factors and the underlying mechanism driving viral RNA-mediated dysregulated immunity are poorly defined. Here, using viral ssRNA and dsRNA mimics, which activate toll-like receptor 7 (TLR7) and TLR3, respectively, we evaluated the role of viral RNAs in causing dysregulated immunity. We show that murine bone marrow-derived macrophages (BMDMs) stimulated with TLR3 and TLR7 agonists induce differential inflammatory and antiviral cytokine response. TLR7 activation triggered a robust inflammatory cytokine/chemokine induction compared to TLR3 activation, whereas TLR3 stimulation induced significantly increased IFN/IFN stimulated gene (ISG) response relative to TLR7 activation. To define the mechanistic basis for dysregulated immunity, we examined cell-surface and endosomal TLR levels and downstream mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-kB) activation. We identified a significantly higher cell-surface and endosomal TLR7 expression compared to TLR3, which further correlated with early and robust MAPK (pERK1/2 and p-P38) and NF-kB activation in TLR7-stimulated macrophages. Furthermore, blocking EKR1/2, p38, and NF-kB activity reduced TLR3/7-induced inflammatory cytokine/chemokine levels, whereas only ERK1/2 inhibition enhanced viral RNA-mimic-induced IFN/ISG responses. Collectively, our results illustrate that high cell surface and endosomal TLR7 expression and robust ERK1/2 activation drive viral ssRNA mimic-induced excessive inflammatory and reduced IFN/ISG responses, and blocking ERK1/2 activity would mitigate viral-RNA/TLR-induced dysregulated immunity.
Sprache	Englisch
Erscheinungsdatum	2024-05-25
Erscheinungsland	United States
Dokumenttyp	Preprint
DOI	10.1101/2024.05.24.595760
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Alveolar macrophages protect mice from MERS-CoV-induced pneumonia and severe disease

Channappanavar, Rudragouda / Selvaraj, Muneeswaran / More, Sunil / Perlman, Stanley

Veterinary pathology. 2022 July, v. 59, no. 4

2022

Abstract: Emerging and re-emerging human coronaviruses (hCoVs) cause severe respiratory illness in humans, but the basis for lethal pneumonia in these diseases is not well understood. Alveolar macrophages (AMs) are key orchestrators of host antiviral defense and ... ...

Abstract	Emerging and re-emerging human coronaviruses (hCoVs) cause severe respiratory illness in humans, but the basis for lethal pneumonia in these diseases is not well understood. Alveolar macrophages (AMs) are key orchestrators of host antiviral defense and tissue tolerance during a variety of respiratory infections, and AM dysfunction is associated with severe COVID-19. In this study, using a mouse model of Middle East respiratory syndrome coronavirus (MERS-CoV) infection, we examined the role of AMs in MERS pathogenesis. Our results show that depletion of AMs using clodronate (CL) liposomes significantly increased morbidity and mortality in human dipeptidyl peptidase 4 knock-in (hDPP4-KI) mice. Detailed examination of control and AM-depleted lungs at different days postinfection revealed increased neutrophil activity but a significantly reduced MERS-CoV-specific CD4 T-cell response in AM-deficient lungs during later stages of infection. Furthermore, enhanced MERS severity in AM-depleted mice correlated with lung inflammation and lesions. Collectively, these data demonstrate that AMs are critical for the development of an optimal virus-specific T-cell response and controlling excessive inflammation during MERS-CoV infection.
Schlagwörter	CD4-positive T-lymphocytes ; COVID-19 infection ; Middle East respiratory syndrome coronavirus ; animal pathology ; disease severity ; humans ; inflammation ; lungs ; macrophages ; mice ; morbidity ; mortality ; neutrophils ; pathogenesis ; pneumonia
Sprache	Englisch
Erscheinungsverlauf	2022-07
Umfang	p. 627-638.
Erscheinungsort	SAGE Publications
Dokumenttyp	Artikel
ZDB-ID	188012-3
ISSN	1544-2217 ; 0300-9858
ISSN (online)	1544-2217
ISSN	0300-9858
DOI	10.1177/03009858221095270
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Alveolar macrophages protect mice from MERS-CoV-induced pneumonia and severe disease.

Channappanavar, Rudragouda / Selvaraj, Muneeswaran / More, Sunil / Perlman, Stanley

Veterinary pathology

2022 Band 59, Heft 4, Seite(n) 627–638

Abstract	Emerging and re-emerging human coronaviruses (hCoVs) cause severe respiratory illness in humans, but the basis for lethal pneumonia in these diseases is not well understood. Alveolar macrophages (AMs) are key orchestrators of host antiviral defense and tissue tolerance during a variety of respiratory infections, and AM dysfunction is associated with severe COVID-19. In this study, using a mouse model of Middle East respiratory syndrome coronavirus (MERS-CoV) infection, we examined the role of AMs in MERS pathogenesis. Our results show that depletion of AMs using clodronate (CL) liposomes significantly increased morbidity and mortality in human dipeptidyl peptidase 4 knock-in (hDPP4-KI) mice. Detailed examination of control and AM-depleted lungs at different days postinfection revealed increased neutrophil activity but a significantly reduced MERS-CoV-specific CD4 T-cell response in AM-deficient lungs during later stages of infection. Furthermore, enhanced MERS severity in AM-depleted mice correlated with lung inflammation and lesions. Collectively, these data demonstrate that AMs are critical for the development of an optimal virus-specific T-cell response and controlling excessive inflammation during MERS-CoV infection.
Mesh-Begriff(e)	Animals ; Clodronic Acid ; Coronavirus Infections/immunology ; Macrophages, Alveolar/immunology ; Mice ; Mice, Transgenic ; Middle East Respiratory Syndrome Coronavirus ; Pneumonia/immunology ; Pneumonia/virology
Chemische Substanzen	Clodronic Acid (0813BZ6866)
Sprache	Englisch
Erscheinungsdatum	2022-05-02
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	188012-3
ISSN	1544-2217 ; 0300-9858
ISSN (online)	1544-2217
ISSN	0300-9858
DOI	10.1177/03009858221095270
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Age-related susceptibility to coronavirus infections: role of impaired and dysregulated host immunity.

Channappanavar, Rudragouda / Perlman, Stanley

The Journal of clinical investigation

2020 Band 130, Heft 12, Seite(n) 6204–6213

Abstract: Human coronaviruses (hCoVs) cause severe respiratory illness in the elderly. Age-related impairments in innate immunity and suboptimal virus-specific T cell and antibody responses are believed to cause severe disease upon respiratory virus infections. ... ...

Abstract	Human coronaviruses (hCoVs) cause severe respiratory illness in the elderly. Age-related impairments in innate immunity and suboptimal virus-specific T cell and antibody responses are believed to cause severe disease upon respiratory virus infections. This phenomenon has recently received increased attention, as elderly patients are at substantially elevated risk for severe COVID-19 disease and experience increased rates of mortality following SARS-CoV-2 infection compared with younger populations. However, the basis for age-related fatal pneumonia following pathogenic hCoVs is not well understood. In this Review, we provide an overview of our current understanding of hCoV-induced fatal pneumonia in the elderly. We describe host immune response to hCoV infections derived from studies of young and aged animal models and discuss the potential role of age-associated increases in sterile inflammation (inflammaging) and virus-induced dysregulated inflammation in causing age-related severe disease. We also highlight the existing gaps in our knowledge about virus replication and host immune responses to hCoV infection in young and aged individuals.
Mesh-Begriff(e)	Aging/immunology ; Animals ; COVID-19/immunology ; Disease Models, Animal ; Disease Susceptibility ; Humans ; Immunity, Innate ; Inflammation/immunology ; Inflammation/virology ; Risk Factors ; SARS-CoV-2/immunology ; Severity of Illness Index
Schlagwörter	covid19
Sprache	Englisch
Erscheinungsdatum	2020-10-21
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI144115
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Evaluation of Activation and Inflammatory Activity of Myeloid Cells During Pathogenic Human Coronavirus Infection.

Channappanavar, Rudragouda / Perlman, Stanley

Methods in molecular biology (Clifton, N.J.)

2020 Band 2099, Seite(n) 195–204

Abstract: Innate immune cells play a vital role in mounting an effective host response to a variety of pathogen challenges. Myeloid cells such as neutrophils and monocyte-macrophages are major innate leukocytes that orchestrate protective immunity to viral lung ... ...

Abstract	Innate immune cells play a vital role in mounting an effective host response to a variety of pathogen challenges. Myeloid cells such as neutrophils and monocyte-macrophages are major innate leukocytes that orchestrate protective immunity to viral lung infections. However, a dysregulated cytokine response can promote excessive infiltration and robust pro-inflammatory activity of neutrophils and monocyte-macrophages, leading to fatal disease. Following virus infection, the beneficial or deleterious role of infiltrating neutrophils and monocyte-macrophages is determined largely by their ability to secrete inflammatory cytokines and chemokines. A majority of studies use the total number of infiltrating cells and their activation status as measures to demonstrate their role during an infection. Consequently, the ability of neutrophils and Inflammatory Monocyte Macrophages (IMMs) to secrete inflammatory cytokines and chemokines, and its correlation with the disease severity, is not well defined. In this chapter, we report useful markers to identify lung infiltrating innate immune cells and define their activation status. We also describe a simple method to measure intracellular cytokine production to evaluate the inflammatory activity of neutrophils and IMMs in a mouse model of human coronavirus infection.
Mesh-Begriff(e)	Animals ; Chemokines/immunology ; Coronavirus Infections/immunology ; Coronavirus Infections/virology ; Cytokines/immunology ; Disease Models, Animal ; Humans ; Immunity, Innate ; Inflammation/immunology ; Leukocytes/immunology ; Lung/immunology ; Macrophages/immunology ; Mice ; Mice, Inbred BALB C ; Middle East Respiratory Syndrome Coronavirus/immunology ; Monocytes/immunology ; Myeloid Cells/immunology ; Neutrophils/immunology ; SARS Virus/immunology
Chemische Substanzen	Chemokines ; Cytokines
Schlagwörter	covid19
Sprache	Englisch
Erscheinungsdatum	2020-01-09
Erscheinungsland	United States
Dokumenttyp	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-0211-9_15
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Acellular Human Amniotic Fluid-Derived Extracellular Vesicles as Novel Anti-Inflammatory Therapeutics against SARS-CoV-2 Infection.

Chanda, Debarati / Del Rivero, Tania / Ghimire, Roshan / More, Sunil / Mitrani, Maria Ines / Bellio, Michael A / Channappanavar, Rudragouda

Viruses

2024 Band 16, Heft 2

Abstract: The ongoing COVID-19 pandemic caused by SARS-CoV-2 is associated with acute respiratory distress syndrome (ARDS) and fatal pneumonia. Excessive inflammation caused by SARS-CoV-2 is the key driver of ARDS and lethal disease. Several FDA-approved drugs ... ...

Abstract	The ongoing COVID-19 pandemic caused by SARS-CoV-2 is associated with acute respiratory distress syndrome (ARDS) and fatal pneumonia. Excessive inflammation caused by SARS-CoV-2 is the key driver of ARDS and lethal disease. Several FDA-approved drugs that suppress virus replication are in clinical use. However, despite strong evidence for the role of virus-induced inflammation in severe COVID-19, no effective anti-inflammatory drug is available to control fatal inflammation as well as efficiently clear the virus. Therefore, there is an urgent need to identify biologically derived immunomodulators that suppress inflammation and promote antiviral immunity. In this study, we evaluated acellular human amniotic fluid (acAF) containing extracellular vesicles (hAF-EVs) as a potential non-toxic and safe biologic for immunomodulation during COVID-19. Our in vitro results showed that acAF significantly reduced inflammatory cytokine production in TLR2/4/7 and SARS-CoV-2 structural protein-stimulated mouse macrophages. Importantly, an intraperitoneal administration of acAF reduced morbidity and mortality in SARS-CoV-2-infected mice. A detailed examination of SARS-CoV-2-infected lungs revealed that the increased protection in acAF-treated mice was associated with reduced viral titers and levels of inflammatory myeloid cell infiltration. Collectively, our results identify a novel biologic that has potential to suppress excessive inflammation and enhance survival following SARS-CoV-2 infection, highlighting the translational potential of acAF against COVID-19.
Mesh-Begriff(e)	Humans ; Animals ; Mice ; COVID-19 ; SARS-CoV-2 ; Amniotic Fluid ; Pandemics ; Inflammation ; Respiratory Distress Syndrome ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Extracellular Vesicles ; Biological Products
Chemische Substanzen	Anti-Inflammatory Agents ; Biological Products
Sprache	Englisch
Erscheinungsdatum	2024-02-09
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v16020273
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Age-related susceptibility to coronavirus infections: role of impaired and dysregulated host immunity

Channappanavar, Rudragouda / Perlman, Stanley

J. clin. invest

Abstract	Human coronaviruses (hCoVs) cause severe respiratory illness in the elderly. Age-related impairments in innate immunity and suboptimal virus-specific T cell and antibody responses are believed to cause severe disease upon respiratory virus infections. This phenomenon has recently received increased attention, as elderly patients are at substantially elevated risk for severe COVID-19 disease and experience increased rates of mortality following SARS-CoV-2 infection compared with younger populations. However, the basis for age-related fatal pneumonia following pathogenic hCoVs is not well understood. In this Review, we provide an overview of our current understanding of hCoV-induced fatal pneumonia in the elderly. We describe host immune response to hCoV infections derived from studies of young and aged animal models and discuss the potential role of age-associated increases in sterile inflammation (inflammaging) and virus-induced dysregulated inflammation in causing age-related severe disease. We also highlight the existing gaps in our knowledge about virus replication and host immune responses to hCoV infection in young and aged individuals.
Schlagwörter	covid19
Verlag	WHO
Dokumenttyp	Artikel
Anmerkung	WHO #Covidence: #883460
Datenquelle	COVID19

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Artikel: Evaluation of Activation and Inflammatory Activity of Myeloid Cells During Pathogenic Human Coronavirus Infection

Channappanavar, Rudragouda / Perlman, Stanley

Methods Mol Biol

Abstract	Innate immune cells play a vital role in mounting an effective host response to a variety of pathogen challenges. Myeloid cells such as neutrophils and monocyte-macrophages are major innate leukocytes that orchestrate protective immunity to viral lung infections. However, a dysregulated cytokine response can promote excessive infiltration and robust pro-inflammatory activity of neutrophils and monocyte-macrophages, leading to fatal disease. Following virus infection, the beneficial or deleterious role of infiltrating neutrophils and monocyte-macrophages is determined largely by their ability to secrete inflammatory cytokines and chemokines. A majority of studies use the total number of infiltrating cells and their activation status as measures to demonstrate their role during an infection. Consequently, the ability of neutrophils and Inflammatory Monocyte Macrophages (IMMs) to secrete inflammatory cytokines and chemokines, and its correlation with the disease severity, is not well defined. In this chapter, we report useful markers to identify lung infiltrating innate immune cells and define their activation status. We also describe a simple method to measure intracellular cytokine production to evaluate the inflammatory activity of neutrophils and IMMs in a mouse model of human coronavirus infection.
Schlagwörter	covid19
Verlag	WHO
Dokumenttyp	Artikel
Anmerkung	WHO #Covidence: #710769
Datenquelle	COVID19

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Artikel ; Online: Coronaviruses: Innate Immunity, Inflammasome Activation, Inflammatory Cell Death, and Cytokines.

Lee, SangJoon / Channappanavar, Rudragouda / Kanneganti, Thirumala-Devi

Trends in immunology

2020 Band 41, Heft 12, Seite(n) 1083–1099

Abstract: The innate immune system acts as the first line of defense against pathogens, including coronaviruses (CoVs). Severe acute respiratory syndrome (SARS)-CoV and Middle East respiratory syndrome (MERS)-CoV are epidemic zoonotic CoVs that emerged at the ... ...

Abstract	The innate immune system acts as the first line of defense against pathogens, including coronaviruses (CoVs). Severe acute respiratory syndrome (SARS)-CoV and Middle East respiratory syndrome (MERS)-CoV are epidemic zoonotic CoVs that emerged at the beginning of the 21st century. The recently emerged virus SARS-CoV-2 is a novel strain of CoV that has caused the coronavirus 2019 (COVID-19) pandemic. Scientific advancements made by studying the SARS-CoV and MERS-CoV outbreaks have provided a foundation for understanding pathogenesis and innate immunity against SARS-CoV-2. In this review, we focus on our present understanding of innate immune responses, inflammasome activation, inflammatory cell death pathways, and cytokine secretion during SARS-CoV, MERS-CoV, and SARS-CoV-2 infection. We also discuss how the pathogenesis of these viruses influences these biological processes.
Mesh-Begriff(e)	Animals ; COVID-19/immunology ; Cell Death/immunology ; Cytokines/immunology ; Humans ; Immunity, Innate/immunology ; Inflammasomes/immunology ; SARS-CoV-2/immunology
Chemische Substanzen	Cytokines ; Inflammasomes
Schlagwörter	covid19
Sprache	Englisch
Erscheinungsdatum	2020-10-15
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2020.10.005
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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