We are analyzing https://link.springer.com/article/10.1007/s00441-017-2776-8.

Title:
Neutrophil chemotaxis | Cell and Tissue Research
Description:
Neutrophils are the primary cells recruited to inflamed sites during an innate immune response to tissue damage and/or infection. They are finely sensitive to inciting stimuli to reach in great numbers and within minutes areas of inflammation and tissue insult. For this effective response, they can detect extracellular chemical gradients and move towards higher concentrations, the so-called chemotaxis process or guided cell migration. This directed neutrophil recruitment is orchestrated by chemoattractants, a chemically diverse group of molecular guidance cues (e.g., lipids, N-formylated peptides, complement, anaphylotoxins and chemokines). Neutrophils respond to these guidance signals in a hierarchical manner and, based on this concept, they can be further subdivided into two groups: “end target” and “intermediary” chemoattractants, the signals of the former dominant over the latter. Neutrophil chemoattractants exert their effects through interaction with heptahelical G protein-coupled receptors (GPCRs) expressed on cell surfaces and the chemotactic response is mainly regulated by the Rho family of GTPases. Additionally, neutrophil behavior might differ and be affected in different complex scenarios such as disease conditions and type of vascular bed in specific organs. Finally, there are different mechanisms to disrupt neutrophil chemotaxis either associated to the resolution of inflammation or to bacterial escape and systemic infection. Therefore, in the present review, we will discuss the different molecular players involved in neutrophil chemotaxis, paying special attention to the different chemoattractants described and the way that they interact intra- and extravascularly for neutrophils to properly reach the target tissue.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

Education
Telecommunications
Business & Finance

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We see no obvious way the site makes money.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {🔍}

pubmed, article, google, scholar, cas, neutrophil, central, cell, immunol, chemotaxis, migration, neutrophils, inflammation, biol, nat, kubes, protein, leukocyte, nourshargh, petri, med, vivo, recruitment, chemokines, regulation, sanz, disease, wang, crawling, res, molecular, receptors, chemotactic, mechanisms, receptor, blood, liu, voisin, research, tissue, mariajesús, immune, type, access, immunity, rev, van, zhang, signaling, mol,

Topics {✒️}

plc/pkc/pkd signaling axis hypoxia-inducible factor-dependent induction mice lacking glucose-6-phosphatase-beta mitogen-activated protein kinases maria-jesús sanz month download article/chapter protein-coupled receptor-mediated chemotaxis cytokine-induced neutrophil chemoattractant beta gamma-mediated pak1 phosphoinositide-transfer protein tipe2 chemotactic gradient sequestered fmlp-induced neutrophil chemotaxis platelet-activating factor g-protein-coupled receptor chemokine-mediated neutrophil trafficking p38 protein kinases chemoattractant-mediated signal transduction glucose-6-phosphate transport system venular basement membranes pix alpha-dependent activation anti-tumor monoclonal antibody pro-resolution lipid mediators full article pdf dipeptidyl peptidase iv vascular cell-cell interactions extracellular matrix degradation opposing chemotactic gradients induces neutrophil migration monocyte chemoattractant protein-1 chemokine-induced emigration related subjects protein-coupled receptors leukotriene b4 privacy choices/manage cookies murine neutrophil chemorepellent regulates rear retraction tissue research aims ridley aj facultad de medicina vascular basement membrane interleukin-33 attenuates sepsis article petri noninflammatory biosynthetic pathway annexin a1 pathway neutrophil chemoattractant receptors article cell signal-relay molecule small molecule disruption morote-garcia jc �prioritize’ chemotactic cues

Questions {❓}

Gallin JI (1984) Human neutrophil heterogeneity exists, but is it meaningful?
Serhan CN (2010) Novel lipid mediators and resolution mechanisms in acute inflammation: to resolve or not?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Neutrophil chemotaxis
         description:Neutrophils are the primary cells recruited to inflamed sites during an innate immune response to tissue damage and/or infection. They are finely sensitive to inciting stimuli to reach in great numbers and within minutes areas of inflammation and tissue insult. For this effective response, they can detect extracellular chemical gradients and move towards higher concentrations, the so-called chemotaxis process or guided cell migration. This directed neutrophil recruitment is orchestrated by chemoattractants, a chemically diverse group of molecular guidance cues (e.g., lipids, N-formylated peptides, complement, anaphylotoxins and chemokines). Neutrophils respond to these guidance signals in a hierarchical manner and, based on this concept, they can be further subdivided into two groups: “end target” and “intermediary” chemoattractants, the signals of the former dominant over the latter. Neutrophil chemoattractants exert their effects through interaction with heptahelical G protein-coupled receptors (GPCRs) expressed on cell surfaces and the chemotactic response is mainly regulated by the Rho family of GTPases. Additionally, neutrophil behavior might differ and be affected in different complex scenarios such as disease conditions and type of vascular bed in specific organs. Finally, there are different mechanisms to disrupt neutrophil chemotaxis either associated to the resolution of inflammation or to bacterial escape and systemic infection. Therefore, in the present review, we will discuss the different molecular players involved in neutrophil chemotaxis, paying special attention to the different chemoattractants described and the way that they interact intra- and extravascularly for neutrophils to properly reach the target tissue.
         datePublished:2018-01-19T00:00:00Z
         dateModified:2018-01-19T00:00:00Z
         pageStart:425
         pageEnd:436
         sameAs:https://doi.org/10.1007/s00441-017-2776-8
         keywords:
            Neutrophils
            Chemotaxis
            Migration
            Signaling
            Chemotactic gradient
            Human Genetics
            Proteomics
            Molecular Medicine
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00441-017-2776-8/MediaObjects/441_2017_2776_Fig1_HTML.gif
         isPartOf:
            name:Cell and Tissue Research
            issn:
               1432-0878
               0302-766X
            volumeNumber:371
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer Berlin Heidelberg
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Björn Petri
               affiliation:
                     name:University of Calgary
                     address:
                        name:Snyder Institute for Chronic Diseases Mouse Phenomics Resource Laboratory, University of Calgary, Calgary, Canada
                        type:PostalAddress
                     type:Organization
                     name:University of Calgary
                     address:
                        name:Department of Microbiology, Immunology and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Canada
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Maria-Jesús Sanz
               affiliation:
                     name:University Clinic Hospital of Valencia
                     address:
                        name:Institute of Health Research INCLIVA, University Clinic Hospital of Valencia, Valencia, Spain
                        type:PostalAddress
                     type:Organization
                     name:Universidad de Valencia
                     address:
                        name:Departamento de Farmacología, Facultad de Medicina, Universidad de Valencia, Valencia, Spain
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
         isAccessibleForFree:
         hasPart:
            isAccessibleForFree:
            cssSelector:.main-content
            type:WebPageElement
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Neutrophil chemotaxis
      description:Neutrophils are the primary cells recruited to inflamed sites during an innate immune response to tissue damage and/or infection. They are finely sensitive to inciting stimuli to reach in great numbers and within minutes areas of inflammation and tissue insult. For this effective response, they can detect extracellular chemical gradients and move towards higher concentrations, the so-called chemotaxis process or guided cell migration. This directed neutrophil recruitment is orchestrated by chemoattractants, a chemically diverse group of molecular guidance cues (e.g., lipids, N-formylated peptides, complement, anaphylotoxins and chemokines). Neutrophils respond to these guidance signals in a hierarchical manner and, based on this concept, they can be further subdivided into two groups: “end target” and “intermediary” chemoattractants, the signals of the former dominant over the latter. Neutrophil chemoattractants exert their effects through interaction with heptahelical G protein-coupled receptors (GPCRs) expressed on cell surfaces and the chemotactic response is mainly regulated by the Rho family of GTPases. Additionally, neutrophil behavior might differ and be affected in different complex scenarios such as disease conditions and type of vascular bed in specific organs. Finally, there are different mechanisms to disrupt neutrophil chemotaxis either associated to the resolution of inflammation or to bacterial escape and systemic infection. Therefore, in the present review, we will discuss the different molecular players involved in neutrophil chemotaxis, paying special attention to the different chemoattractants described and the way that they interact intra- and extravascularly for neutrophils to properly reach the target tissue.
      datePublished:2018-01-19T00:00:00Z
      dateModified:2018-01-19T00:00:00Z
      pageStart:425
      pageEnd:436
      sameAs:https://doi.org/10.1007/s00441-017-2776-8
      keywords:
         Neutrophils
         Chemotaxis
         Migration
         Signaling
         Chemotactic gradient
         Human Genetics
         Proteomics
         Molecular Medicine
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs00441-017-2776-8/MediaObjects/441_2017_2776_Fig1_HTML.gif
      isPartOf:
         name:Cell and Tissue Research
         issn:
            1432-0878
            0302-766X
         volumeNumber:371
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer Berlin Heidelberg
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Björn Petri
            affiliation:
                  name:University of Calgary
                  address:
                     name:Snyder Institute for Chronic Diseases Mouse Phenomics Resource Laboratory, University of Calgary, Calgary, Canada
                     type:PostalAddress
                  type:Organization
                  name:University of Calgary
                  address:
                     name:Department of Microbiology, Immunology and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Canada
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Maria-Jesús Sanz
            affiliation:
                  name:University Clinic Hospital of Valencia
                  address:
                     name:Institute of Health Research INCLIVA, University Clinic Hospital of Valencia, Valencia, Spain
                     type:PostalAddress
                  type:Organization
                  name:Universidad de Valencia
                  address:
                     name:Departamento de Farmacología, Facultad de Medicina, Universidad de Valencia, Valencia, Spain
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
      isAccessibleForFree:
      hasPart:
         isAccessibleForFree:
         cssSelector:.main-content
         type:WebPageElement
["Periodical","PublicationVolume"]:
      name:Cell and Tissue Research
      issn:
         1432-0878
         0302-766X
      volumeNumber:371
Organization:
      name:Springer Berlin Heidelberg
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:University of Calgary
      address:
         name:Snyder Institute for Chronic Diseases Mouse Phenomics Resource Laboratory, University of Calgary, Calgary, Canada
         type:PostalAddress
      name:University of Calgary
      address:
         name:Department of Microbiology, Immunology and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Canada
         type:PostalAddress
      name:University Clinic Hospital of Valencia
      address:
         name:Institute of Health Research INCLIVA, University Clinic Hospital of Valencia, Valencia, Spain
         type:PostalAddress
      name:Universidad de Valencia
      address:
         name:Departamento de Farmacología, Facultad de Medicina, Universidad de Valencia, Valencia, Spain
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Björn Petri
      affiliation:
            name:University of Calgary
            address:
               name:Snyder Institute for Chronic Diseases Mouse Phenomics Resource Laboratory, University of Calgary, Calgary, Canada
               type:PostalAddress
            type:Organization
            name:University of Calgary
            address:
               name:Department of Microbiology, Immunology and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Canada
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Maria-Jesús Sanz
      affiliation:
            name:University Clinic Hospital of Valencia
            address:
               name:Institute of Health Research INCLIVA, University Clinic Hospital of Valencia, Valencia, Spain
               type:PostalAddress
            type:Organization
            name:Universidad de Valencia
            address:
               name:Departamento de Farmacología, Facultad de Medicina, Universidad de Valencia, Valencia, Spain
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Snyder Institute for Chronic Diseases Mouse Phenomics Resource Laboratory, University of Calgary, Calgary, Canada
      name:Department of Microbiology, Immunology and Infectious Diseases, Cumming School of Medicine, University of Calgary, Calgary, Canada
      name:Institute of Health Research INCLIVA, University Clinic Hospital of Valencia, Valencia, Spain
      name:Departamento de Farmacología, Facultad de Medicina, Universidad de Valencia, Valencia, Spain
WebPageElement:
      isAccessibleForFree:
      cssSelector:.main-content

External Links {🔗}(435)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Clipboard.js
Prism.js

CDN Services {📦}

Crossref

4.68s.

LINK . SPRINGER . COM {}