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Related Experiment Videos

Cytokine expression by inflammatory neutrophils

J A Quayle1, S Adams, R C Bucknall

  • 1Department of Biochemistry, University of Liverpool, UK.

FEMS Immunology and Medical Microbiology
|March 1, 1994
PubMed
Summary

Neutrophils can produce interleukin-1 beta (IL-1 beta) when stimulated. In rheumatoid arthritis, low IL-1 beta mRNA in synovial fluid neutrophils suggests a small, activated cell subset contributes to disease pathogenesis.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Neutrophils are key immune cells involved in inflammation.
  • Interleukin-1 beta (IL-1 beta) is a pro-inflammatory cytokine implicated in rheumatoid arthritis (RA).
  • The role of neutrophils in IL-1 beta production in RA is not fully understood.

Purpose of the Study:

  • To investigate the expression of IL-1 beta mRNA in neutrophils.
  • To determine the effect of granulocyte-macrophage colony-stimulating factor (rGM-CSF) on neutrophil cytokine mRNA.
  • To analyze cytokine mRNA levels in neutrophils from patients with rheumatoid arthritis.

Main Methods:

  • Neutrophils were isolated from blood and synovial fluid.
  • Cells were treated with rGM-CSF in vitro.

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  • Messenger RNA (mRNA) levels for IL-1 beta, IL-6, TNF-alpha, and TGF-beta were quantified using molecular techniques.

    • Main Results:

    • Blood neutrophils did not express IL-1 beta mRNA but rapidly induced it upon rGM-CSF stimulation.
    • rGM-CSF also induced IL-6 and TNF-alpha mRNA in blood neutrophils.
    • Synovial fluid neutrophils from RA patients showed low IL-1 beta mRNA but no detectable IL-6 or TNF-alpha mRNA.
    • Transforming growth factor-beta (TGF-beta) mRNA was constitutively expressed in all neutrophils.

    Conclusions:

    • Low IL-1 beta mRNA levels in synovial fluid neutrophils from RA patients may originate from a small subpopulation of activated cells.
    • This localized IL-1 beta production by neutrophils could contribute to the pathogenesis of rheumatoid disease.
    • Neutrophil activation and cytokine profiles differ between blood and inflamed joint environments.