Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

The microvasculature in inflammation

M G Tonnesen, L Smedly, A Goins

    Agents and Actions. Supplements
    |January 1, 1982
    PubMed
    Summary
    This summary is machine-generated.

    Related Concept Videos

    You might also read

    Related Articles

    Articles linked to this work by shared authors, journal, and citation graph.

    Sort by
    Same author

    Ly6C(+) monocyte efferocytosis and cross-presentation of cell-associated antigens.

    Cell death and differentiation·2016
    Same author

    Mammary epithelial cell phagocytosis downstream of TGF-β3 is characterized by adherens junction reorganization.

    Cell death and differentiation·2015
    Same author

    Biochemical characteristics of ATP-induced secretion of lysosomal enzymes from rabbit polymorphonuclear leukocytes.

    Inflammation·2013
    Same author

    Ultrastructural alterations during ATP-induced secretion of lysosomal enzymes from rabbit polymorphonuclear leukocytes.

    Inflammation·2013
    Same author

    Isolation and characterization of a noncytotoxic mast-cell activator from cobra venom.

    Inflammation·2013
    Same author

    Interaction of cells with immune complexes: adherence, release of constituents, and tissue injury.

    The Journal of experimental medicine·2009

    Complement C5 fragments promote neutrophil migration into blood vessels during inflammation. This study validates in vitro models for examining neutrophil-endothelial cell interactions, crucial for understanding inflammatory responses.

    Area of Science:

    • Immunology
    • Cell Biology
    • Vascular Biology

    Background:

    • Neutrophil emigration from blood vessels into tissues is a key inflammatory process.
    • Chemotactic factors, especially complement C5 fragments, are known to mediate neutrophil emigration in vivo.
    • Understanding neutrophil-endothelial interactions is vital for controlling inflammation.

    Purpose of the Study:

    • To investigate the in vivo role of C5 fragments in inducing neutrophil migration through rabbit carotid artery walls.
    • To establish and validate an in vitro assay for assessing neutrophil adherence to endothelial cells.
    • To explore the influence of prostaglandin E2 (PGE2) on neutrophil adherence and transmigration.

    Main Methods:

    • In vivo experiments using rabbit carotid arteries treated with C5 fragments, mechanical trauma, or PGE2.

    Related Experiment Videos

  • Development of a sensitive in vitro assay using human umbilical vein endothelial cell monolayers.
  • Dose-response assessment of neutrophil adherence stimulated by fMetLeuPhe or C5 fragments.

    • Main Results:

    • C5 fragments induced neutrophil adherence and migration into the rabbit carotid artery wall when combined with trauma or PGE2.
    • An in vitro assay successfully quantified neutrophil adherence to endothelial cells.
    • Chemotactic factors stimulated adherence in a dose-dependent manner, but PGE2's synergistic effect seen in vivo was absent in vitro.
    • Endothelial cell pretreatment did not enhance adherence, suggesting the effect is neutrophil-mediated.

    Conclusions:

    • Neutrophil interaction with large artery endothelium is demonstrable in vivo and supports in vitro models.
    • C5 fragments are potent stimulators of neutrophil adherence to endothelial cells.
    • PGE2 may not play a role in the initial neutrophil-endothelial adhesive interaction during emigration.