Sulfite induces adherence of polymorphonuclear neutrophils to immobilized fibrinogen through activation of Mac-1

Tetsuya Shigehara1, Hideki Mitsuhashi, Fumie Ota

  • 1Third Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.

Life Sciences
|May 15, 2002
PubMed

Insights

Sulfite, an air pollutant, activates human immune cells called polymorphonuclear neutrophils (PMN). This process involves cell adhesion via Mac-1, suggesting sulfite

Area of Science:

  • Environmental Science
  • Immunology
  • Cell Biology

Background:

  • Sulfite is a significant air pollutant linked to respiratory inflammation.
  • Polymorphonuclear neutrophils (PMN) are key immune cells involved in inflammation.
  • Previous research indicated human PMN can produce sulfite.

Purpose of the Study:

  • To investigate the role of sulfite in PMN activation and adhesion.
  • To elucidate the molecular mechanisms underlying sulfite-induced PMN responses.

Main Methods:

  • Human PMN were treated with sulfite.
  • Cell adhesion assays were performed using immobilized fibrinogen.
  • Flow cytometry was used to assess Mac-1 expression.
  • The effect of sulfhydryl reagents (DTNB) and pertussis toxin on PMN adhesion was evaluated.

Main Results:

  • Sulfite activates PMN to adhere to fibrinogen.
  • Adhesion is mediated by the beta2-integrin Mac-1 (CD11b/CD18).
  • Sulfite does not alter Mac-1 expression levels.
  • Sulfite-induced adhesion is dependent on cell surface thiol modification and unaffected by pertussis toxin.

Conclusions:

  • Sulfite triggers PMN adhesion through a mechanism involving surface thiol modification.
  • Sulfite may function as an endogenous mediator in host defense and inflammation.
  • Understanding sulfite's role in PMN activation is crucial for respiratory health research.

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