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Chemotactic factor receptor modulation and cytoskeletal structures

I Spilberg, J Mehta

    Infection and Immunity
    |April 1, 1981
    PubMed
    Summary
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    Cytochalasins disrupt neutrophil chemotactic factor binding by reducing available receptor sites. This effect on formylmethionylleucylphenylalanine binding is independent of intact microfilaments, unlike microtubule agents.

    Area of Science:

    • Cellular Biology
    • Immunology
    • Pharmacology

    Background:

    • Neutrophils utilize chemotactic factors for directed migration.
    • Chemotactic factor receptors on neutrophils are crucial for immune responses.
    • Microfilaments and microtubules are key cytoskeletal components influencing cell function.

    Purpose of the Study:

    • To investigate the effect of microfilament-disrupting agents on chemotactic factor binding to neutrophil receptors.
    • To determine if cytoskeletal integrity is required for this binding process.

    Main Methods:

    • Treatment of neutrophils with cytochalasins A, B, and D.
    • Assay of [3H]formylmethionylleucylphenylalanine and 125I-labeled crystal-induced chemotactic factor binding.
    • Scatchard plot analysis to assess receptor binding sites.

    Related Experiment Videos

  • Comparison of effects on intact cells versus membrane preparations.
  • Testing microtubule modifiers colchicine and vinblastine.

    • Main Results:

    • Cytochalasins A, B, and D impaired chemotactic factor binding.
    • Cytochalasin B reduced available neutrophil receptor binding sites.
    • The inhibitory effect of cytochalasin B was observed in both intact cells and membrane preparations.
    • Colchicine and vinblastine had no impact on chemotactic factor binding.

    Conclusions:

    • Microfilament-disrupting agents, like cytochalasins, interfere with neutrophil chemotactic factor receptor binding.
    • The mechanism of inhibition by cytochalasin B does not necessitate an intact microfilament system.
    • Microtubule integrity is not essential for chemotactic factor receptor binding.