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  1. Article ; Online: Neutrophil migration under normal and sepsis conditions.

    Lerman, Yelena V / Kim, Minsoo

    Cardiovascular & hematological disorders drug targets

    2015  Volume 15, Issue 1, Page(s) 19–28

    Abstract: Neutrophil migration is critical for pathogen clearance and host survival during severe sepsis. Interaction of neutrophil adhesion receptors with ligands on endothelial cells results in firm adhesion of the circulating neutrophils, followed by neutrophil ...

    Abstract Neutrophil migration is critical for pathogen clearance and host survival during severe sepsis. Interaction of neutrophil adhesion receptors with ligands on endothelial cells results in firm adhesion of the circulating neutrophils, followed by neutrophil activation and directed migration to sites of infection through the basement membrane and interstitial extracellular matrix. Proteolytic enzymes and reactive oxygen species are produced and released by neutrophils in response to a variety of inflammatory stimuli. Although these mediators are important for host defense, they also promote tissue damage. Excessive neutrophil migration during the early stages of sepsis may lead to an exaggerated inflammatory response with associated tissue damage and subsequent organ dysfunction. On the other hand, dysregulation of migration and insufficient migratory response that occurs during the latter stages of severe sepsis contributes to neutrophils' inability to contain and control infection and impaired wound healing. This review discusses the major steps and associated molecules involved in the balance of neutrophil trafficking, the precise regulation of which during sepsis spells life or death for the host.
    MeSH term(s) Animals ; Cell Movement/physiology ; Humans ; Multiple Organ Failure/etiology ; Neutrophils/metabolism ; Reactive Oxygen Species/metabolism ; Sepsis/complications ; Sepsis/physiopathology ; Severity of Illness Index ; Survival
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2015-02-02
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2244164-5
    ISSN 2212-4063 ; 1871-529X
    ISSN (online) 2212-4063
    ISSN 1871-529X
    DOI 10.2174/1871529x15666150108113236
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Long-Term Microgliosis Driven by Acute Systemic Inflammation.

    Trzeciak, Alissa / Lerman, Yelena V / Kim, Tae-Hyoun / Kim, Ma Rie / Mai, Nguyen / Halterman, Marc W / Kim, Minsoo

    Journal of immunology (Baltimore, Md. : 1950)

    2019  Volume 203, Issue 11, Page(s) 2979–2989

    Abstract: Severe sepsis, a systemic inflammatory response to infection, is an increasing cause of morbidity in intensive care units. During sepsis, the vasculature is profoundly altered, leading to release of microbial virulence factors and proinflammatory ... ...

    Abstract Severe sepsis, a systemic inflammatory response to infection, is an increasing cause of morbidity in intensive care units. During sepsis, the vasculature is profoundly altered, leading to release of microbial virulence factors and proinflammatory mediators to surrounding tissue, causing severe systemic inflammatory responses and hypoxic injury of multiple organs. To date, multiple studies have explored pathologic conditions in many vital organs, including lungs, liver, and kidneys. Although data suggest that sepsis is emerging as a key driver of chronic brain dysfunction, the immunological consequence of severe inflammatory responses in the brain remain poorly understood. In this study, we used C57BL/6 sepsis mouse models to establish a disease phenotype in which septic mice with various degrees of severity recover. In the early phases of sepsis, monocytes infiltrate the brain with significantly elevated proinflammatory cytokine levels. In recovered animals, monocytes return to vehicle levels, but the number of brain-resident microglia is significantly increased in the cortex, the majority of which remain activated. The increase in microglia number is mainly due to self-proliferation, which is completely abolished in CCR2 knockout mice. Collectively our data suggest that early monocyte infiltration causes permanent changes to microglia during sepsis, which may ultimately dictate the outcome of future infections and neuropathological diseases.
    MeSH term(s) Acute Disease ; Animals ; Disease Models, Animal ; Female ; Inflammation/immunology ; Inflammation/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microglia/immunology ; Microglia/pathology ; Sepsis/immunology ; Sepsis/pathology
    Language English
    Publishing date 2019-10-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    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.1900317
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Activated Protein C Attenuates Severe Inflammation by Targeting VLA-3

    Sarangi, Pranita P / Lee, Hyun-Wook / Lerman, Yelena V / Trzeciak, Alissa / Harrower, Eric J / Rezaie, Alireza R / Kim, Minsoo

    Journal of immunology (Baltimore, Md. : 1950)

    2017  Volume 199, Issue 8, Page(s) 2930–2936

    Abstract: The host injury involved in multiorgan system failure during severe inflammation is mediated, in part, by massive infiltration and sequestration of hyperactive neutrophils in the visceral organ. A recombinant form of human activated protein C (rhAPC) has ...

    Abstract The host injury involved in multiorgan system failure during severe inflammation is mediated, in part, by massive infiltration and sequestration of hyperactive neutrophils in the visceral organ. A recombinant form of human activated protein C (rhAPC) has shown cytoprotective and anti-inflammatory functions in some clinical and animal studies, but the direct mechanism is not fully understood. Recently, we reported that, during endotoxemia and severe polymicrobial peritonitis, integrin VLA-3 (CD49c/CD29) is specifically upregulated on hyperinflammatory neutrophils and that targeting the VLA-3
    MeSH term(s) Animals ; Biological Therapy ; Cells, Cultured ; Humans ; Inflammation/immunology ; Integrin alpha3beta1/metabolism ; Lung/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Multiple Organ Failure/immunology ; Mutation/genetics ; Neutrophil Activation ; Neutrophils/immunology ; Peritonitis/immunology ; Protein Binding ; Protein C/genetics ; Protein C/metabolism ; Recombinant Proteins/genetics
    Chemical Substances Integrin alpha3beta1 ; Protein C ; Recombinant Proteins
    Language English
    Publishing date 2017-09-06
    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.1700541
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Role of β1 integrin in tissue homing of neutrophils during sepsis.

    Sarangi, Pranita P / Hyun, Young-Min / Lerman, Yelena V / Pietropaoli, Anthony P / Kim, Minsoo

    Shock (Augusta, Ga.)

    2012  Volume 38, Issue 3, Page(s) 281–287

    Abstract: Aberrant activation of neutrophils during sepsis results in the widespread release of proinflammatory mediators, leading to multiorgan system failure and death. However, aberrant activation of neutrophils during sepsis results in the widespread release ... ...

    Abstract Aberrant activation of neutrophils during sepsis results in the widespread release of proinflammatory mediators, leading to multiorgan system failure and death. However, aberrant activation of neutrophils during sepsis results in the widespread release of harmful inflammatory mediators causing host tissue injuries that can lead to multiorgan system failure and death. One of the pivotal components of neutrophil migration during inflammation is the expression of surface integrins. In this study, we show that administration of a cyclic analog of RGD peptide (Arg-Gly-Asp) significantly reduced the number of tissue-invading neutrophils and the degree of sepsis-induced lethality in mice as compared with control peptide. Second, β1 integrin (CD29) was highly upregulated on the neutrophils isolated from both septic patients and animals. Finally, conditional genetic ablation of β1 integrin from granulocytes also improved survival and bacterial clearance in septic animals Thus, our results indicate that expression of β1 integrin is important for modulating neutrophil trafficking during sepsis and that therapeutics designed against β1 integrins may be beneficial.
    MeSH term(s) Animals ; Anti-Infective Agents/administration & dosage ; Anti-Infective Agents/pharmacology ; CD18 Antigens/physiology ; Cell Movement/physiology ; Humans ; Integrin beta1/physiology ; Ligation ; Lipopolysaccharides/toxicity ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Multiple Organ Failure/etiology ; Neutrophil Infiltration/physiology ; Neutrophils/physiology ; Oligopeptides/administration & dosage ; Oligopeptides/pharmacology ; Sepsis/etiology ; Up-Regulation
    Chemical Substances Anti-Infective Agents ; CD18 Antigens ; Integrin beta1 ; Lipopolysaccharides ; Oligopeptides ; arginyl-glycyl-aspartic acid (78VO7F77PN)
    Language English
    Publishing date 2012-06-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1185432-7
    ISSN 1540-0514 ; 1073-2322
    ISSN (online) 1540-0514
    ISSN 1073-2322
    DOI 10.1097/SHK.0b013e31826136f8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3985: Show issues Location:
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  5. Article ; Online: NMR structure of a 4 x 4 nucleotide RNA internal loop from an R2 retrotransposon: identification of a three purine-purine sheared pair motif and comparison to MC-SYM predictions.

    Lerman, Yelena V / Kennedy, Scott D / Shankar, Neelaabh / Parisien, Marc / Major, Francois / Turner, Douglas H

    RNA (New York, N.Y.)

    2011  Volume 17, Issue 9, Page(s) 1664–1677

    Abstract: The NMR solution structure is reported of a duplex, 5'GUGAAGCCCGU/3'UCACAGGAGGC, containing a 4 × 4 nucleotide internal loop from an R2 retrotransposon RNA. The loop contains three sheared purine-purine pairs and reveals a structural element found in ... ...

    Abstract The NMR solution structure is reported of a duplex, 5'GUGAAGCCCGU/3'UCACAGGAGGC, containing a 4 × 4 nucleotide internal loop from an R2 retrotransposon RNA. The loop contains three sheared purine-purine pairs and reveals a structural element found in other RNAs, which we refer to as the 3RRs motif. Optical melting measurements of the thermodynamics of the duplex indicate that the internal loop is 1.6 kcal/mol more stable at 37°C than predicted. The results identify the 3RRs motif as a common structural element that can facilitate prediction of 3D structure. Known examples include internal loops having the pairings: 5'GAA/3'AGG, 5'GAG/3'AGG, 5'GAA/3'AAG, and 5'AAG/3'AGG. The structural information is compared with predictions made with the MC-Sym program.
    MeSH term(s) Adenine/chemistry ; Amino Acid Motifs ; Base Pairing ; Nuclear Magnetic Resonance, Biomolecular/methods ; Nucleic Acid Conformation ; Protein Interaction Domains and Motifs ; Purine Nucleotides/chemistry ; RNA/chemistry ; RNA/genetics ; Retroelements ; Sequence Analysis, RNA ; Thermodynamics
    Chemical Substances Purine Nucleotides ; Retroelements ; RNA (63231-63-0) ; Adenine (JAC85A2161)
    Language English
    Publishing date 2011-07-21
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1241540-6
    ISSN 1469-9001 ; 1355-8382
    ISSN (online) 1469-9001
    ISSN 1355-8382
    DOI 10.1261/rna.2641911
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4777: Show issues Location:
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  6. Article ; Online: Sepsis lethality via exacerbated tissue infiltration and TLR-induced cytokine production by neutrophils is integrin α3β1-dependent.

    Lerman, Yelena V / Lim, Kihong / Hyun, Young-Min / Falkner, Kathleen L / Yang, Hongmei / Pietropaoli, Anthony P / Sonnenberg, Arnoud / Sarangi, Pranita P / Kim, Minsoo

    Blood

    2014  Volume 124, Issue 24, Page(s) 3515–3523

    Abstract: Integrin-mediated migration of neutrophils to infected tissue sites is vital for pathogen clearance and therefore host survival. Although β2 integrins have been shown to mediate neutrophil transendothelial migration during systemic and local inflammation, ...

    Abstract Integrin-mediated migration of neutrophils to infected tissue sites is vital for pathogen clearance and therefore host survival. Although β2 integrins have been shown to mediate neutrophil transendothelial migration during systemic and local inflammation, relatively little information is available regarding neutrophil migration in sepsis beyond the endothelial cell layer. In this study, we report that integrin α3β1 (VLA-3; CD49c/CD29) is dramatically upregulated on neutrophils isolated from both human septic patients and in mouse models of sepsis. Compared with the α3β1 (low) granulocytes, α3β1 (high) cells from septic animals displayed hyperinflammatory phenotypes. Administration of a α3β1 blocking peptide and conditional deletion of α3 in granulocytes significantly reduced the number of extravasating neutrophils and improved survival in septic mice. In addition, expression of α3β1 on neutrophils was associated with Toll-like receptor-induced inflammatory responses and cytokine productions. Thus, our results show that α3β1 is a novel marker of tissue homing and hyperresponsive neutrophil subtypes in sepsis, and blocking of α3β1 may represent a new therapeutic approach in sepsis treatment.
    MeSH term(s) Animals ; Cytokines/genetics ; Cytokines/immunology ; Disease Models, Animal ; Humans ; Integrin alpha3beta1/antagonists & inhibitors ; Integrin alpha3beta1/genetics ; Integrin alpha3beta1/immunology ; Male ; Mice ; Mice, Knockout ; Neutrophil Infiltration/drug effects ; Neutrophil Infiltration/genetics ; Neutrophil Infiltration/immunology ; Neutrophils/immunology ; Neutrophils/pathology ; Peptides/pharmacology ; Sepsis/chemically induced ; Sepsis/drug therapy ; Sepsis/genetics ; Sepsis/immunology ; Sepsis/pathology ; Toll-Like Receptors/genetics ; Toll-Like Receptors/immunology
    Chemical Substances Cytokines ; Integrin alpha3beta1 ; Peptides ; Toll-Like Receptors
    Language English
    Publishing date 2014-10-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2014-01-552943
    Database MEDical Literature Analysis and Retrieval System OnLINE

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