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  1. Article ; Online: Innate immune response of human alveolar macrophages during influenza A infection.

    Wang, Jieru / Nikrad, Mrinalini P / Travanty, Emily A / Zhou, Bin / Phang, Tzulip / Gao, Bifeng / Alford, Taylor / Ito, Yoko / Nahreini, Piruz / Hartshorn, Kevan / Wentworth, David / Dinarello, Charles A / Mason, Robert J

    PloS one

    2012  Volume 7, Issue 3, Page(s) e29879

    Abstract: ... Targeting local components of innate immune response might provide a strategy for controlling influenza ... of zymosan. In conclusion, influenza infection induced an extensive proinflammatory response in human AM ... immune responses to influenza virus in the lung. However, the genome-wide changes in response to influenza ...

    Abstract Alveolar macrophages (AM) are one of the key cell types for initiating inflammatory and immune responses to influenza virus in the lung. However, the genome-wide changes in response to influenza infection in AM have not been defined. We performed gene profiling of human AM in response to H1N1 influenza A virus PR/8 using Affymetrix HG-U133 Plus 2.0 chips and verified the changes at both mRNA and protein levels by real-time RT-PCR and ELISA. We confirmed the response with a contemporary H3N2 influenza virus A/New York/238/2005 (NY/238). To understand the local cellular response, we also evaluated the impact of paracrine factors on virus-induced chemokine and cytokine secretion. In addition, we investigated the changes in the expression of macrophage receptors and uptake of pathogens after PR/8 infection. Although macrophages fail to release a large amount of infectious virus, we observed a robust induction of type I and type III interferons and several cytokines and chemokines following influenza infection. CXCL9, 10, and 11 were the most highly induced chemokines by influenza infection. UV-inactivation abolished virus-induced cytokine and chemokine response, with the exception of CXCL10. The contemporary influenza virus NY/238 infection of AM induced a similar response as PR/8. Inhibition of TNF and/or IL-1β activity significantly decreased the secretion of the proinflammatory chemokines CCL5 and CXCL8 by over 50%. PR/8 infection also significantly decreased mRNA levels of macrophage receptors including C-type lectin domain family 7 member A (CLEC7A), macrophage scavenger receptor 1 (MSR1), and CD36, and reduced uptake of zymosan. In conclusion, influenza infection induced an extensive proinflammatory response in human AM. Targeting local components of innate immune response might provide a strategy for controlling influenza A infection-induced proinflammatory response in vivo.
    MeSH term(s) Chemokines/metabolism ; Cytokines/metabolism ; Enzyme-Linked Immunosorbent Assay/methods ; Gene Expression Regulation ; Humans ; Immunity, Innate ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza, Human/immunology ; Kinetics ; Lectins, C-Type/biosynthesis ; Macrophages/immunology ; Macrophages/virology ; Oligonucleotide Array Sequence Analysis ; Phagocytosis ; Pulmonary Alveoli/immunology ; Pulmonary Alveoli/virology ; Real-Time Polymerase Chain Reaction/methods
    Chemical Substances Chemokines ; Cytokines ; Lectins, C-Type ; dectin 1
    Keywords covid19
    Language English
    Publishing date 2012-03-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0029879
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Innate immune response of human alveolar macrophages during influenza A infection.

    Jieru Wang / Mrinalini P Nikrad / Emily A Travanty / Bin Zhou / Tzulip Phang / Bifeng Gao / Taylor Alford / Yoko Ito / Piruz Nahreini / Kevan Hartshorn / David Wentworth / Charles A Dinarello / Robert J Mason

    PLoS ONE, Vol 7, Iss 3, p e

    2012  Volume 29879

    Abstract: ... Targeting local components of innate immune response might provide a strategy for controlling influenza ... of zymosan. In conclusion, influenza infection induced an extensive proinflammatory response in human AM ... immune responses to influenza virus in the lung. However, the genome-wide changes in response to influenza ...

    Abstract Alveolar macrophages (AM) are one of the key cell types for initiating inflammatory and immune responses to influenza virus in the lung. However, the genome-wide changes in response to influenza infection in AM have not been defined. We performed gene profiling of human AM in response to H1N1 influenza A virus PR/8 using Affymetrix HG-U133 Plus 2.0 chips and verified the changes at both mRNA and protein levels by real-time RT-PCR and ELISA. We confirmed the response with a contemporary H3N2 influenza virus A/New York/238/2005 (NY/238). To understand the local cellular response, we also evaluated the impact of paracrine factors on virus-induced chemokine and cytokine secretion. In addition, we investigated the changes in the expression of macrophage receptors and uptake of pathogens after PR/8 infection. Although macrophages fail to release a large amount of infectious virus, we observed a robust induction of type I and type III interferons and several cytokines and chemokines following influenza infection. CXCL9, 10, and 11 were the most highly induced chemokines by influenza infection. UV-inactivation abolished virus-induced cytokine and chemokine response, with the exception of CXCL10. The contemporary influenza virus NY/238 infection of AM induced a similar response as PR/8. Inhibition of TNF and/or IL-1β activity significantly decreased the secretion of the proinflammatory chemokines CCL5 and CXCL8 by over 50%. PR/8 infection also significantly decreased mRNA levels of macrophage receptors including C-type lectin domain family 7 member A (CLEC7A), macrophage scavenger receptor 1 (MSR1), and CD36, and reduced uptake of zymosan. In conclusion, influenza infection induced an extensive proinflammatory response in human AM. Targeting local components of innate immune response might provide a strategy for controlling influenza A infection-induced proinflammatory response in vivo.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: In Vivo and In Vitro Studies of Cigarette Smoke Effects on Innate Responses to Influenza Virus: A Matter of Models?

    Wu, Wenxin / Alexander, Jeremy S / Metcalf, Jordan P

    Viruses

    2022  Volume 14, Issue 8

    Abstract: ... both immunosuppressive and proinflammatory effects on innate immune responses during IAV infection. Some of the results ... lung macrophages and dendritic cells. To achieve a successful infection, IAV must overcome ... chemokines to maximize the innate and adaptive antiviral response, as well as limiting the immunopathology ...

    Abstract Cigarette smoke (CS) is a significant public health problem and a leading risk factor for the development of chronic obstructive pulmonary disease (COPD) in the developed world. Respiratory viral infections, such as the influenza A virus (IAV), are associated with acute exacerbations of COPD and are more severe in cigarette smokers. To fight against viral infection, the host has developed an innate immune system, which has complicated mechanisms regulating the expression and activation of cytokines and chemokines to maximize the innate and adaptive antiviral response, as well as limiting the immunopathology that leads to exaggerated lung damage. In the case of IAV, responders include airway and alveolar epithelia, lung macrophages and dendritic cells. To achieve a successful infection, IAV must overcome these defenses. In this review, we summarize the detrimental role of CS in influenza infections. This includes both immunosuppressive and proinflammatory effects on innate immune responses during IAV infection. Some of the results, with respect to CS effects in mouse models, appear to have discordant results, which could be at least partially addressed by standardization of animal viral infection models to evaluate the effect of CS exposure in this context.
    MeSH term(s) Animals ; Cigarette Smoking/adverse effects ; Humans ; Immunity, Innate ; Influenza A virus/physiology ; Influenza, Human ; Mice ; Orthomyxoviridae Infections ; Pulmonary Disease, Chronic Obstructive ; Nicotiana
    Language English
    Publishing date 2022-08-20
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v14081824
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: H1N1 influenza virus dose dependent induction of dysregulated innate immune responses and STAT1/3 activation are associated with pulmonary immunopathological damage.

    Yao, Duoduo / Bao, Linlin / Li, Fengdi / Liu, Bo / Wu, Xu / Hu, Ziqi / Xu, Jiangnan / Wang, Wei / Zhang, Xulong

    Virulence

    2022  Volume 13, Issue 1, Page(s) 1558–1572

    Abstract: ... The severe innate immune responses may be the threshold at which protective functions give way ... to immunopathology, and assessing the magnitude of host innate immune responses is necessary in adjunctive ... mortality. Exacerbated pulmonary inflammatory responses are the major causes of extensive diffuse alveolar ...

    Abstract Influenza A virus (IAV) infection poses a substantial challenge and causes high morbidity and mortality. Exacerbated pulmonary inflammatory responses are the major causes of extensive diffuse alveolar immunopathological damage. However, the relationship between the extent of cytokine storm, neutrophils/macrophages infiltration, and different IAV infection dose and time still needs to be further elucidated, and it is still unclear whether the signal transduction and transcriptional activator 1/3 (STAT1/3) signalling pathway plays a beneficial or detrimental role. Here, we established a mouse model of high- and low-dose pH1N1 infection. We found that pH1N1 infection induced robust and early pathological damage and cytokine storm in an infection dose- and time-dependent manner. High-dose pH1N1 infection induced massive and sustained recruitment of neutrophils as well as a higher ratio of M1:M2, which may contribute to severe lung immunopathological damage. pH1N1 infection activated dose- and time-dependent STAT1 and STAT3. Inhibition of STAT1 and/or STAT3 aggravated low-dose pH1N1 infection, induced lung damage, and decreased survival rate. Appropriate activation of STAT1/3 provided survival benefits and pathological improvement during low-dose pH1N1 infection. These results demonstrate that high-dose pH1N1 infection induces robust and sustained neutrophil infiltration, imbalanced macrophage polarization, excessive and earlier cytokine storm, and STAT1/3 activation, which are associated with pulmonary dysregulated proinflammatory responses and progress of acute lung injury. The severe innate immune responses may be the threshold at which protective functions give way to immunopathology, and assessing the magnitude of host innate immune responses is necessary in adjunctive immunomodulatory therapy for alleviating influenza-induced pneumonia.
    MeSH term(s) Animals ; Cytokine Release Syndrome ; Humans ; Immunity, Innate ; Influenza A Virus, H1N1 Subtype/immunology ; Influenza, Human/immunology ; Lung/immunology ; Lung/pathology ; Lung Injury/etiology ; Lung Injury/pathology ; Mice ; Orthomyxoviridae Infections ; STAT1 Transcription Factor/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction
    Chemical Substances STAT1 Transcription Factor ; STAT3 Transcription Factor ; Stat1 protein, mouse
    Language English
    Publishing date 2022-09-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2657572-3
    ISSN 2150-5608 ; 2150-5594
    ISSN (online) 2150-5608
    ISSN 2150-5594
    DOI 10.1080/21505594.2022.2120951
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Inosine-containing RNA is a novel innate immune recognition element and reduces RSV infection.

    Liao, Jie-ying / Thakur, Sheetal A / Zalinger, Zachary B / Gerrish, Kevin E / Imani, Farhad

    PloS one

    2011  Volume 6, Issue 10, Page(s) e26463

    Abstract: ... by the host and induce innate immune responses. The cellular enzyme ADAR-1 (adenosine deaminase acting on RNA ... that ss-Ino-RNA is an as yet undescribed virus-associated innate immune stimulus. ... During viral infections, single- and double-stranded RNA (ssRNA and dsRNA) are recognized ...

    Abstract During viral infections, single- and double-stranded RNA (ssRNA and dsRNA) are recognized by the host and induce innate immune responses. The cellular enzyme ADAR-1 (adenosine deaminase acting on RNA-1) activation in virally infected cells leads to presence of inosine-containing RNA (Ino-RNA). Here we report that ss-Ino-RNA is a novel viral recognition element. We synthesized unmodified ssRNA and ssRNA that had 6% to16% inosine residues. The results showed that in primary human cells, or in mice, 10% ss-Ino-RNA rapidly and potently induced a significant increase in inflammatory cytokines, such as interferon (IFN)-β (35 fold), tumor necrosis factor (TNF)-α (9.7 fold), and interleukin (IL)-6 (11.3 fold) (p<0.01). Flow cytometry data revealed a corresponding 4-fold increase in influx of neutrophils into the lungs by ss-Ino-RNA treatment. In our in vitro experiments, treatment of epithelial cells with ss-Ino-RNA reduced replication of respiratory syncytial virus (RSV). Interestingly, RNA structural analysis showed that ss-Ino-RNA had increased formation of secondary structures. Our data further revealed that extracellular ss-Ino-RNA was taken up by scavenger receptor class-A (SR-A) which activated downstream MAP Kinase pathways through Toll-like receptor 3 (TLR3) and dsRNA-activated protein kinase (PKR). Our data suggests that ss-Ino-RNA is an as yet undescribed virus-associated innate immune stimulus.
    MeSH term(s) Animals ; Antiviral Agents/chemistry ; Antiviral Agents/metabolism ; Antiviral Agents/pharmacology ; Base Sequence ; Cell Line ; Chemokines/biosynthesis ; Chemokines/metabolism ; Endocytosis ; Epithelial Cells/drug effects ; Epithelial Cells/immunology ; Epithelial Cells/metabolism ; Epithelial Cells/virology ; Extracellular Space/drug effects ; Extracellular Space/immunology ; Extracellular Space/metabolism ; Extracellular Space/virology ; Humans ; Immunity, Innate/drug effects ; Inosine ; Interferon-beta/biosynthesis ; Interleukin-6/biosynthesis ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/immunology ; Macrophages, Alveolar/drug effects ; Macrophages, Alveolar/immunology ; Macrophages, Alveolar/metabolism ; Macrophages, Alveolar/virology ; Mice ; Nucleic Acid Conformation ; Protein Kinases/metabolism ; RNA/chemistry ; RNA/metabolism ; RNA/pharmacology ; Respiratory Syncytial Viruses/drug effects ; Respiratory Syncytial Viruses/immunology ; Respiratory Syncytial Viruses/physiology ; Scavenger Receptors, Class A/metabolism ; Toll-Like Receptor 3/metabolism ; Transcriptome/drug effects ; Transcriptome/immunology ; Tumor Necrosis Factor-alpha/biosynthesis ; Virus Replication/drug effects ; Virus Replication/immunology
    Chemical Substances Antiviral Agents ; Chemokines ; Interleukin-6 ; Scavenger Receptors, Class A ; TLR3 protein, human ; Toll-Like Receptor 3 ; Tumor Necrosis Factor-alpha ; Inosine (5A614L51CT) ; RNA (63231-63-0) ; Interferon-beta (77238-31-4) ; Protein Kinases (EC 2.7.-)
    Language English
    Publishing date 2011-10-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0026463
    Database MEDical Literature Analysis and Retrieval System OnLINE

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