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Modulating influence of chemotactic factor-induced cell adhesiveness on granulocyte function

J Fehr, C Dahinden

    The Journal of Clinical Investigation
    |July 1, 1979
    PubMed

    Insights

    High concentrations of N-formyl peptides decrease polymorphonuclear leukocyte (PMN) motility by increasing cell adhesion. This phenomenon explains PMN deactivation and may trap cells at inflammatory sites or impair emigration in conditions like septicemia.

    Area of Science:

    • Immunology
    • Cell Biology
    • Biochemistry

    Background:

    • The role of adhesion in regulating polymorphonuclear leukocyte (PMN) locomotion and accumulation is not fully understood.
    • N-formyl peptides are known chemoattractants for PMNs, but their effect at higher concentrations is complex.

    Purpose of the Study:

    • To investigate the impact of N-formyl-methionyl-leucyl-phenylalanine (f-Met-Leu-Phe) concentration on human PMN adhesion and motility.
    • To elucidate the mechanism behind high-dose inhibition of PMN chemotaxis.

    Main Methods:

    • Human PMNs were resuspended in heat-inactivated plasma and exposed to varying concentrations of f-Met-Leu-Phe.
    • Cell motility was assessed by measuring random and chemotactic movement.
    • Cell adherence to Petri dishes was quantified.
    • Phase-contrast microscopy was used to observe cell morphology.
    • Hexose monophosphate pathway activity and lysosomal enzyme release were measured.

    Main Results:

    • PMN chemotaxis was maximal at 1-10 nM f-Met-Leu-Phe but decreased significantly at concentrations above 100 nM.
    • Increased f-Met-Leu-Phe concentrations led to heightened PMN adherence, with maximal adhesion at >10 nM.
    • Cells exposed to high f-Met-Leu-Phe concentrations became flattened and immobilized, exhibiting reduced random and chemotactic motility.
    • This hyperadhesiveness correlated strongly with increased hexose monophosphate pathway activity and lysosomal enzyme release.
    • PMN ingestion rates were not depressed by high f-Met-Leu-Phe concentrations, indicating selective functional changes.

    Conclusions:

    • High-dose inhibition of PMN chemotaxis by N-formyl peptides is a result of increased cell adhesiveness, termed 'chemotactic deactivation'.
    • This increased adhesion mechanism can lead to PMN trapping at inflammatory sites.
    • Impaired PMN emigration due to this phenomenon may occur in conditions such as septicemia.

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