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  1. Article ; Online: An 82-Year-Old Male with Syncope.

    Byer, Stefano Henry / Simonson, Tanner J / Stewart, Colten / Mansour, Shareef / Grewal, Udhayvir Singh

    The American journal of medicine

    2024  Volume 137, Issue 5, Page(s) e94–e95

    MeSH term(s) Humans ; Male ; Syncope/etiology ; Aged, 80 and over ; Electrocardiography
    Language English
    Publishing date 2024-02-17
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 80015-6
    ISSN 1555-7162 ; 1873-2178 ; 0002-9343 ; 1548-2766
    ISSN (online) 1555-7162 ; 1873-2178
    ISSN 0002-9343 ; 1548-2766
    DOI 10.1016/j.amjmed.2024.02.014
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Mincle-Mediated Neutrophil Extracellular Trap Formation by Regulation of Autophagy.

    Sharma, Atul / Simonson, Tanner J / Jondle, Christopher N / Mishra, Bibhuti B / Sharma, Jyotika

    The Journal of infectious diseases

    2017  Volume 215, Issue 7, Page(s) 1040–1048

    Abstract: Background: Neutrophil extracellular traps (NETs) constitute antimicrobial function of neutrophils but have also been linked to perpetuation of inflammation. Despite this evident physiological relevance, mechanistic understanding of NET formation is ... ...

    Abstract Background: Neutrophil extracellular traps (NETs) constitute antimicrobial function of neutrophils but have also been linked to perpetuation of inflammation. Despite this evident physiological relevance, mechanistic understanding of NET formation is poor. In this study, we examined the mechanism by which Mincle, a C-type lectin receptor, regulates NET formation.
    Methods: NET formation, reactive oxygen species, autophagy activation and intracellular signaling pathways were analyzed in Mincle-sufficient and -deficient neutrophils stimulated in vitro with various stimuli and in vivo during Klebsiella infection.
    Results: We found that Mincle mediates NET formation in response to several activation stimuli in vitro and in vivo during pneumoseptic infection with Klebsiella pneumoniae, indicating its regulatory role in NET formation. Mechanistically, we show that attenuated NET formation in Mincle-/- neutrophils correlates with an impaired autophagy activation in vitro and in vivo, whereas reactive oxygen species (ROS) formation in these neutrophils remained intact. The requirement of autophagy in Mincle-mediated NET formation was further supported by exogenous treatment with autophagy inducer tamoxifen, which rescued the NET formation defect in Mincle-/- neutrophils.
    Conclusions: Our findings identify a previously unrecognized role of Mincle as a regulator of autophagy, which mediates NET formation without affecting ROS generation. Our study addresses a major challenge in the field by positing this pathway to be targeted for modulation of NETs while preserving ROS production, an important innate immune defense.
    MeSH term(s) Animals ; Autophagy/drug effects ; Extracellular Traps/metabolism ; Immunity, Innate ; Klebsiella Infections/immunology ; Klebsiella pneumoniae/isolation & purification ; Lectins, C-Type/metabolism ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Neutrophils/immunology ; Reactive Oxygen Species/metabolism ; Signal Transduction ; Tamoxifen/pharmacology
    Chemical Substances Clecsf8 protein, mouse ; Lectins, C-Type ; Membrane Proteins ; Reactive Oxygen Species ; Tamoxifen (094ZI81Y45)
    Language English
    Publishing date 2017-02-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1093/infdis/jix072
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 445: Show issues

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  3. Article ; Online: Macrophage Galactose-Type Lectin-1 Deficiency Is Associated with Increased Neutrophilia and Hyperinflammation in Gram-Negative Pneumonia.

    Jondle, Christopher N / Sharma, Atul / Simonson, Tanner J / Larson, Benjamin / Mishra, Bibhuti B / Sharma, Jyotika

    Journal of immunology (Baltimore, Md. : 1950)

    2016  Volume 196, Issue 7, Page(s) 3088–3096

    Abstract: C-type lectin receptors (CLRs), the carbohydrate-recognizing molecules, orchestrate host immune response in homeostasis and in inflammation. In the present study we examined the function of macrophage galactose-type lectin-1 (MGL1), a mammalian CLR, in ... ...

    Abstract C-type lectin receptors (CLRs), the carbohydrate-recognizing molecules, orchestrate host immune response in homeostasis and in inflammation. In the present study we examined the function of macrophage galactose-type lectin-1 (MGL1), a mammalian CLR, in pneumonic sepsis, a deadly immune disorder frequently associated with a nonresolving hyperinflammation. In a murine model of pneumonic sepsis using pulmonary infection with Klebsiella pneumoniae, the expression of MGL1 was upregulated in the lungs of K. pneumoniae-infected mice, and the deficiency of this CLR in MGL1(-/-) mice resulted in significantly increased mortality to infection than in the MGL1-sufficient wild-type mice, despite a similar bacterial burden. The phagocytic cells from MGL1(-/-) mice did not exhibit any defects in bacterial uptake and intracellular killing and were fully competent in neutrophil extracellular trap formation, a recently identified extracellular killing modality of neutrophils. Instead, the increased susceptibility of MGL1(-/-) mice seemed to correlate with severe lung pathology, indicating that MGL1 is required for resolution of pulmonary inflammation. Indeed, the MGL1(-/-) mice exhibited a hyperinflammatory response, massive pulmonary neutrophilia, and an increase in neutrophil-associated immune mediators. Concomitantly, MGL1-deficient neutrophils exhibited an increased influx in pneumonic lungs of K. pneumoniae-infected mice. Taken together, these results show a previously undetermined role of MGL1 in controlling neutrophilia during pneumonic infection, thus playing an important role in resolution of inflammation. To our knowledge, this is the first study depicting a protective function of MGL1 in an acute pneumonic bacterial infection.
    MeSH term(s) Adoptive Transfer ; Animals ; Asialoglycoproteins/deficiency ; Disease Models, Animal ; Extracellular Traps/immunology ; Gene Expression ; Genetic Predisposition to Disease ; Gram-Negative Bacterial Infections/genetics ; Gram-Negative Bacterial Infections/immunology ; Gram-Negative Bacterial Infections/microbiology ; Gram-Negative Bacterial Infections/mortality ; Gram-Negative Bacterial Infections/pathology ; Inflammation Mediators/metabolism ; Klebsiella pneumoniae ; Lectins, C-Type/deficiency ; Leukocytosis/immunology ; Macrophages/immunology ; Macrophages/metabolism ; Membrane Proteins/deficiency ; Mice ; Mice, Knockout ; Neutrophil Infiltration/genetics ; Neutrophil Infiltration/immunology ; Neutrophils/immunology ; Neutrophils/pathology ; Phagocytosis/genetics ; Phagocytosis/immunology ; Pneumonia, Bacterial/genetics ; Pneumonia, Bacterial/immunology ; Pneumonia, Bacterial/microbiology ; Pneumonia, Bacterial/mortality ; Pneumonia, Bacterial/pathology
    Chemical Substances Asialoglycoproteins ; Clec10a protein, mouse ; Inflammation Mediators ; Lectins, C-Type ; Membrane Proteins
    Language English
    Publishing date 2016-02-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1501790
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 28: Show issues

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  4. Article ; Online: Alarmin function of galectin-9 in murine respiratory tularemia.

    Steichen, Anthony L / Simonson, Tanner J / Salmon, Sharon L / Metzger, Dennis W / Mishra, Bibhuti B / Sharma, Jyotika

    PloS one

    2015  Volume 10, Issue 4, Page(s) e0123573

    Abstract: Sepsis is a complex immune disorder that is characterized by systemic hyperinflammation. Alarmins, which are multifunctional endogenous factors, have been implicated in exacerbation of inflammation in many immune disorders including sepsis. Here we show ... ...

    Abstract Sepsis is a complex immune disorder that is characterized by systemic hyperinflammation. Alarmins, which are multifunctional endogenous factors, have been implicated in exacerbation of inflammation in many immune disorders including sepsis. Here we show that Galectin-9, a host endogenous β-galactoside binding lectin, functions as an alarmin capable of mediating inflammatory response during sepsis resulting from pulmonary infection with Francisella novicida, a Gram negative bacterial pathogen. Our results show that this galectin is upregulated and is likely released during tissue damage in the lungs of F. novicida infected septic mice. In vitro, purified recombinant galectin-9 exacerbated F. novicida-induced production of the inflammatory mediators by macrophages and neutrophils. Concomitantly, Galectin-9 deficient (Gal-9-/-) mice exhibited improved lung pathology, reduced cell death and reduced leukocyte infiltration, particularly neutrophils, in their lungs. This positively correlated with overall improved survival of F. novicida infected Gal-9-/- mice as compared to their wild-type counterparts. Collectively, these findings suggest that galectin-9 functions as a novel alarmin by augmenting the inflammatory response in sepsis development during pulmonary F. novicida infection.
    MeSH term(s) Alarmins/physiology ; Animals ; Bronchopneumonia/immunology ; Bronchopneumonia/metabolism ; Bronchopneumonia/microbiology ; Female ; Francisella/immunology ; Galectins/physiology ; Inflammation Mediators/metabolism ; Lung/immunology ; Lung/microbiology ; Lung/pathology ; Mice, Inbred C57BL ; Mice, Knockout ; Neutrophils/immunology ; Pneumonia, Bacterial/immunology ; Pneumonia, Bacterial/metabolism ; Pneumonia, Bacterial/microbiology ; Tularemia/immunology ; Tularemia/metabolism ; Tularemia/microbiology
    Chemical Substances Alarmins ; Galectins ; Inflammation Mediators ; galectin 9, mouse
    Language English
    Publishing date 2015-04-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0123573
    Database MEDical Literature Analysis and Retrieval System OnLINE

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