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Updated: Oct 1, 2026

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions
Published on: August 23, 2013
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.
Abstract:
Sulfite is a major air pollutant which can cause respiratory tract inflammation characterized by an influx of polymorphonuclear neutrophils (PMN). We have previously shown that human PMN can produce sulfite either spontaneously or in response to stimulation with lipopolysaccharide. We now demonstrate that sulfite activates PMN to adhere to immobilized fibrinogen via the beta2-integrin Mac-1 (CD11b/CD18). Mac-1 expression is not altered by treatment with this agent. Although unaffected by pertussis toxin, sulfite-triggered PMN adhesion was abrogated by pretreating cells with the membrane-impermeant sulfhydryl reagent 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB), a modifier of thiol groups on the cell surface. These results suggest that sulfite-induced PMN adhesion is dependent on a modification of thiols at the cell surface. Given its potent antioxidant and antimicrobial activities, sulfite may act as an endogenous mediator in host defense and/or inflammation.
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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