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

Complement-induced granulocyte aggregation in vivo

D E Hammerschmidt, P D Harris, J H Wayland

    The American Journal of Pathology
    |February 1, 1981
    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

    Bank voles (Myodes glareolus) and house mice (Mus musculus musculus; M. m. domesticus) in Europe are each parasitized by their own distinct species of Aspiculuris (Nematoda, Oxyurida).

    Parasitology·2015
    Same author

    The Status of Heligmosomoides americanus, Representative of an American Clade of Vole-Infecting Nematodes.

    The Journal of parasitology·2015
    Same author

    Identification of a new species of digenean Notocotylus malhamensis n. sp. (Digenea: Notocotylidae) from the bank vole (Myodes glareolus) and the field vole (Microtus agrestis).

    Parasitology·2012
    Same author

    Differences in the ecology of Bartonella infections of Apodemus flavicollis and Myodes glareolus in a boreal forest.

    Parasitology·2012
    Same author

    Freshwater charr (Salvelinus alpinus) as hosts for Gyrodactylus salaris: implications for management.

    The Veterinary record·2011
    Same author

    Multi-centre testing and validation of current protocols for the identification of Gyrodactylus salaris (Monogenea).

    International journal for parasitology·2010
    Same journal

    Lxrα Deficiency Primes Retinal Degeneration, but Aging Drives Disease Severity.

    The American journal of pathology·2026
    Same journal

    MYC is functionally required in both normal and neoplastic Meibomian glands.

    The American journal of pathology·2026
    Same journal

    Fumaric Acid Esters as Modulators of Ocular Inflammation and Angiogenesis.

    The American journal of pathology·2026
    Same journal

    Krüppel-like factor 5 inhibition rescues cavernous nerve-injured erectile dysfunction by preventing phenotypic switch and mitochondrial dysfunction-dependent apoptosis in corpus cavernosum smooth muscle cells.

    The American journal of pathology·2026
    Same journal

    APOE4 as a Modifier of Chemotherapy Response.

    The American journal of pathology·2026
    Same journal

    Spatial Pathobiology in the Omics Era: Transforming Modern Pathology.

    The American journal of pathology·2026
    See all related articles

    Activated complement (C), specifically C5a, causes neutrophil (PMN) aggregation and endothelial damage in vivo. This immune response may contribute to tissue damage in various disease states.

    Area of Science:

    • Immunology
    • Microcirculation
    • Pathophysiology

    Background:

    • Previous studies showed neutrophils (PMNs) damage endothelial cells in vitro when exposed to activated complement (C), specifically C5a.
    • It was hypothesized that this immune response could also occur in vivo, indicating a novel mechanism for immune-mediated tissue damage.

    Purpose of the Study:

    • To investigate whether PMN aggregation and endothelial damage, triggered by complement activation, occur in vivo.
    • To confirm the role of C5a in mediating these microvascular events.

    Main Methods:

    • Intravital microscopy was used to observe microvascular events in live animals.
    • Complement (C) was activated, or C5a was infused, to study its effects on PMNs and microvasculature.

    Related Experiment Videos

    Main Results:

    • Intravital microscopy confirmed PMN aggregation and leukoembolization in live animals following complement activation or C5a infusion.
    • These microvascular events were associated with plasma protein extravasation, indicating endothelial damage.

    Conclusions:

    • Activated complement (C) and C5a induce PMN aggregation and leukoembolization in vivo.
    • The observed microvascular changes suggest a role for PMN behavior in complement-mediated endothelial damage and immune tissue injury.
    • Altered PMN microvascular behavior is a potential pathogenetic mechanism in diseases associated with complement activation.