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Imaging Cell Interaction in Tracheal Mucosa During Influenza Virus Infection Using Two-photon Intravital Microscopy
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Published on: August 17, 2018

Characterization of the chemotactic defect in polymorphonuclear leukocytes exposed to influenza virus in vitro

D L Moore, E L Mills

    Blood
    |August 1, 1987
    PubMed

    Insights

    Influenza virus impairs polymorphonuclear leukocyte (PMN) migration by limiting their movement extent, not by affecting chemoattractant recognition or initial shape change. This impacts immune cell function during infection.

    Area of Science:

    • Immunology
    • Virology
    • Cell Biology

    Background:

    • Influenza virus infection can compromise the host immune response.
    • Polymorphonuclear leukocytes (PMNs) are crucial for innate immunity, particularly in combating viral infections.
    • Understanding how influenza virus affects PMN function is vital for comprehending host-pathogen interactions.

    Purpose of the Study:

    • To investigate the mechanism by which influenza A virus interferes with polymorphonuclear leukocyte (PMN) chemotaxis.
    • To determine if influenza virus affects PMN chemoattractant recognition, shape change, or migration capacity.

    Main Methods:

    • Human PMNs were incubated with influenza A virus in vitro.
    • PMN migration was assessed using under-agarose and filter assays in response to chemoattractants like FMLP and zymosan-activated serum.
    • PMN aggregation and bipolar shape change were also evaluated.

    Main Results:

    • Influenza virus significantly decreased PMN migration in response to chemoattractants.
    • Virus-treated PMNs showed a tendency to aggregate, which was mitigated in filter assays.
    • PMN migration through thicker filters was reduced, but migration through thinner filters and initial shape change remained unaffected.
    • Influenza virus was not chemotactic and did not induce PMN shape change.

    Conclusions:

    • Influenza virus interferes with PMN chemotaxis by limiting the extent of migration, rather than impairing chemoattractant recognition or initial motility.
    • The observed inhibition of PMN migration is not due to chemotactic deactivation by the virus.
    • These findings highlight a specific mechanism by which influenza virus can modulate the innate immune cell response.

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