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  1. Article ; Online: CLEC5A is critical in Pseudomonas aeruginosa-induced NET formation and acute lung injury.

    Sung, Pei-Shan / Peng, Yu-Chun / Yang, Shao-Ping / Chiu, Cheng-Hsun / Hsieh, Shie-Liang

    JCI insight

    2022  Volume 7, Issue 18

    Abstract: Pseudomonas aeruginosa is one of the most common nosocomial infections worldwide, and it frequently causes ventilator-associated acute pneumonia in immunocompromised patients. Abundant neutrophil extracellular traps (NETs) contribute to acute lung injury, ...

    Abstract Pseudomonas aeruginosa is one of the most common nosocomial infections worldwide, and it frequently causes ventilator-associated acute pneumonia in immunocompromised patients. Abundant neutrophil extracellular traps (NETs) contribute to acute lung injury, thereby aggravating ventilator-induced lung damage. While pattern recognition receptors (PRRs) TLR4 and TLR5 are required for host defense against P. aeruginosa invasion, the PRR responsible for P. aeruginosa-induced NET formation, proinflammatory cytokine release, and acute lung injury remains unclear. We found that myeloid C-type lectin domain family 5 member A (CLEC5A) interacts with LPS of P. aeruginosa and is responsible for P. aeruginosa-induced NET formation and lung inflammation. P. aeruginosa activates CLEC5A to induce caspase-1-dependent NET formation, but it neither causes gasdermin D (GSDMD) cleavage nor contributes to P. aeruginosa-induced neutrophil death. Blockade of CLEC5A attenuates P. aeruginosa-induced NETosis and lung injury, and simultaneous administration of anti-CLEC5A mAb with ciprofloxacin increases survival rate and decreases collagen deposition in the lungs of mice challenged with a lethal dose of P. aeruginosa. Thus, CLEC5A is a promising therapeutic target to reduce ventilator-associated lung injury and fibrosis in P. aeruginosa-induced pneumonia.
    MeSH term(s) Acute Lung Injury/metabolism ; Acute Lung Injury/pathology ; Animals ; Caspases ; Ciprofloxacin ; Cytokines ; Lectins, C-Type/metabolism ; Lipopolysaccharides/toxicity ; Mice ; Pneumonia/metabolism ; Pneumonia/pathology ; Pseudomonas aeruginosa ; Receptors, Cell Surface ; Toll-Like Receptor 4 ; Toll-Like Receptor 5
    Chemical Substances Clec5a protein, mouse ; Cytokines ; Lectins, C-Type ; Lipopolysaccharides ; Receptors, Cell Surface ; Toll-Like Receptor 4 ; Toll-Like Receptor 5 ; Ciprofloxacin (5E8K9I0O4U) ; Caspases (EC 3.4.22.-)
    Language English
    Publishing date 2022-09-01
    Publishing country United States
    Document type Journal Article
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.156613
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: CLEC5A and TLR2 are critical in SARS-CoV-2-induced NET formation and lung inflammation.

    Sung, Pei-Shan / Yang, Shao-Ping / Peng, Yu-Chun / Sun, Cheng-Pu / Tao, Mi-Hwa / Hsieh, Shie-Liang

    Journal of biomedical science

    2022  Volume 29, Issue 1, Page(s) 52

    Abstract: Background: Coronavirus-induced disease 19 (COVID-19) infects more than three hundred and sixty million patients worldwide, and people with severe symptoms frequently die of acute respiratory distress syndrome (ARDS). Recent studies indicated that ... ...

    Abstract Background: Coronavirus-induced disease 19 (COVID-19) infects more than three hundred and sixty million patients worldwide, and people with severe symptoms frequently die of acute respiratory distress syndrome (ARDS). Recent studies indicated that excessive neutrophil extracellular traps (NETs) contributed to immunothrombosis, thereby leading to extensive intravascular coagulopathy and multiple organ dysfunction. Thus, understanding the mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced NET formation would be helpful to reduce thrombosis and prevent ARDS in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.
    Methods: We incubated SARS-CoV-2 with neutrophils in the presence or absence of platelets to observe NET formation. We further isolated extracellular vesicles from COVID-19 patients' sera (COVID-19-EVs) to examine their ability to induce NET formation.
    Results: We demonstrated that antagonistic mAbs against anti-CLEC5A mAb and anti-TLR2 mAb can inhibit COVID-19-EVs-induced NET formation, and generated clec5a
    Conclusions: This study demonstrates that SARS-CoV-2-activated platelets produce EVs to enhance thromboinflammation via CLEC5A and TLR2, and highlight the importance of CLEC5A and TLR2 as therapeutic targets to reduce the risk of ARDS in COVID-19 patients.
    MeSH term(s) Animals ; Blood Platelets/immunology ; Blood Platelets/pathology ; Blood Platelets/virology ; COVID-19/blood ; COVID-19/immunology ; Humans ; Lectins, C-Type/immunology ; Mice ; Neutrophils/immunology ; Neutrophils/pathology ; Neutrophils/virology ; Pneumonia/immunology ; Pneumonia/pathology ; Pneumonia/virology ; Receptors, Cell Surface ; Respiratory Distress Syndrome/immunology ; Respiratory Distress Syndrome/virology ; SARS-CoV-2/immunology ; Thrombosis/blood ; Thrombosis/immunology ; Thrombosis/virology ; Toll-Like Receptor 2/immunology
    Chemical Substances CLEC5A protein, human ; Clec5a protein, mouse ; Lectins, C-Type ; Receptors, Cell Surface ; TLR2 protein, human ; Tlr2 protein, mouse ; Toll-Like Receptor 2
    Language English
    Publishing date 2022-07-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 1193378-1
    ISSN 1423-0127 ; 1021-7770
    ISSN (online) 1423-0127
    ISSN 1021-7770
    DOI 10.1186/s12929-022-00832-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: CLEC5A and TLR2 are critical in SARS-CoV-2-induced NET formation and lung inflammation

    Sung, Pei-Shan / Yang, Shao-Ping / Peng, Yu-Chun / Sun, Cheng-Pu / Tao, Mi-Hwa / Hsieh, Shie-Liang

    bioRxiv

    Abstract: Coronavirus-induced disease 19 (COVID-19) infects more than three hundred and sixty million patients worldwide, and people with severe symptoms frequently die of acute respiratory distress syndrome (ARDS). Autopsy demonstrates the presence of thrombosis ... ...

    Abstract Coronavirus-induced disease 19 (COVID-19) infects more than three hundred and sixty million patients worldwide, and people with severe symptoms frequently die of acute respiratory distress syndrome (ARDS). Autopsy demonstrates the presence of thrombosis and microangiopathy in the small vessels and capillaries. Recent studies indicated that excessive neutrophil extracellular traps (NETs) contributed to immunothrombosis, thereby leading to extensive intravascular coagulopathy and multiple organ dysfunction. Thus, understanding the mechanism of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced NET formation would be helpful to reduce thrombosis and prevent ARDS. It has been shown that sera from individuals with COVID-19 triggered NET release in vitro, and spleen tyrosine kinase (Syk) inhibitor R406 inhibited NETosis caused by COVID-19 plasma. However, the serum components responsible for NET formation are still unknown. In this study, we found that virus-free extracellular vesicles (EVs) from COVID-19 patients (COVID-19 EVs) induced robust NET formation via Syk-coupled C-type lectin member 5A (CLEC5A). Blockade of CLEC5A inhibited COVID-19 EVs-induced NETosis, and simultaneous blockade of CLEC5A and TLR2 further suppressed SARS-CoV-2-induced NETosis in vitro. Moreover, thromboinflammation and lung fibrosis were attenuated dramatically in clec5a<sup>-/-</sup>/tlr2<sup>-/-</sup> mice. These results suggest that COVID-19 EVs play critical roles in SARS-CoV-2-induced immunothrombosis, and blockade of CLEC5A and TLR2 is a promising strategy to inhibit SARS-CoV-2-induced intravascular coagulopathy and reduce the risk of ARDS in COVID-19 patients.
    Keywords covid19
    Language English
    Publishing date 2022-02-02
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2022.02.01.478701
    Database COVID19

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  4. Article: Neutrophil Extracellular Traps Impair Intestinal Barrier Function during Experimental Colitis.

    Lin, Elliot Yi-Hsin / Lai, Hsuan-Ju / Cheng, Yuan-Kai / Leong, Kai-Quan / Cheng, Li-Chieh / Chou, Yi-Chun / Peng, Yu-Chun / Hsu, Yi-Hsuan / Chiang, Hao-Sen

    Biomedicines

    2020  Volume 8, Issue 8

    Abstract: Aberrant neutrophil extracellular trap (NET) formation and the loss of barrier integrity in inflamed intestinal tissues have long been associated with inflammatory bowel disease (IBD). However, whether NETs alter intestinal epithelium permeability during ...

    Abstract Aberrant neutrophil extracellular trap (NET) formation and the loss of barrier integrity in inflamed intestinal tissues have long been associated with inflammatory bowel disease (IBD). However, whether NETs alter intestinal epithelium permeability during colitis remains elusive. Here, we demonstrated that NETs promote the breakdown in intestinal barrier function for the pathogenesis of intestinal inflammation in mouse models of colitis. NETs were abundant in the colon of mice with colitis experimentally induced by dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Analysis of the intestinal barrier integrity revealed that NETs impaired gut permeability, enabling the initiation of luminal bacterial translocation and inflammation. Furthermore, NETs induced the apoptosis of epithelial cells and disrupted the integrity of tight junctions and adherens junctions. Intravenous administration of DNase I, an enzyme that dissolves the web-like DNA filaments of NETs, during colitis restored the mucosal barrier integrity which reduced the dissemination of luminal bacteria and attenuated intestinal inflammation in both DSS and TNBS models. We conclude that NETs serve a detrimental factor in the gut epithelial barrier function leading to the pathogenesis of mucosal inflammation during acute colitis.
    Language English
    Publishing date 2020-08-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines8080275
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Effect of temperature on the physico-chemical properties of a room temperature ionic liquid (1-Methyl-3-pentylimidazolium hexafluorophosphate) with polyethylene glycol oligomer.

    Wu, Tzi-Yi / Chen, Bor-Kuan / Hao, Lin / Peng, Yu-Chun / Sun, I-Wen

    International journal of molecular sciences

    2011  Volume 12, Issue 4, Page(s) 2598–2617

    Abstract: A systematic study of the effect of composition on the thermo-physical properties of the binary mixtures of 1-methyl-3-pentyl imidazolium hexafluorophosphate [MPI][PF(6)] with poly(ethylene glycol) (PEG) [M(w) = 400] is presented. The excess molar volume, ...

    Abstract A systematic study of the effect of composition on the thermo-physical properties of the binary mixtures of 1-methyl-3-pentyl imidazolium hexafluorophosphate [MPI][PF(6)] with poly(ethylene glycol) (PEG) [M(w) = 400] is presented. The excess molar volume, refractive index deviation, viscosity deviation, and surface tension deviation values were calculated from these experimental density, ρ, refractive index, n, viscosity, η, and surface tension, γ, over the whole concentration range, respectively. The excess molar volumes are negative and continue to become increasingly negative with increasing temperature; whereas the viscosity and surface tension deviation are negative and become less negative with increasing temperature. The surface thermodynamic functions, such as surface entropy, enthalpy, as well as standard molar entropy, Parachor, and molar enthalpy of vaporization for pure ionic liquid, have been derived from the temperature dependence of the surface tension values.
    MeSH term(s) Entropy ; Imidazoles/chemistry ; Ionic Liquids/chemistry ; Polyethylene Glycols/chemistry ; Refractometry ; Surface Tension ; Temperature ; Thermodynamics ; Viscosity
    Chemical Substances Imidazoles ; Ionic Liquids ; Polyethylene Glycols (3WJQ0SDW1A)
    Language English
    Publishing date 2011-04-18
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms12042598
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