Sulfite induces adherence of polymorphonuclear neutrophils to immobilized fibrinogen through activation of Mac-1 beta2-integrin (CD11b/CD18).
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.
Shigehara
Tetsuya
T
Third Department of Internal Medicine, Gunma University School of Medicine, Maebashi, Japan.
Mitsuhashi
Hideki
H
Ota
Fumie
F
Kuroiwa
Takashi
T
Kaneko
Yoriaki
Y
Ueki
Kazue
K
Tsukada
Yoshito
Y
Maezawa
Akira
A
Nojima
Yoshihisa
Y
D018821:CD18 Antigens / Q000502:physiology*; D002448:Cell Adhesion / Q000187:drug effects; D004228:Dithionitrobenzoic Acid / Q000494:pharmacology; D005340:Fibrinogen / Q000502:physiology*; D006801:Humans; D016177:Macrophage-1 Antigen / Q000502:physiology*; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects* / Q000502:physiology; D013447:Sulfites / Q000494:pharmacology*
D018821:CD18 Antigens; D016177:Macrophage-1 Antigen; D013447:Sulfites; D009240:N-Formylmethionine Leucyl-Phenylalanine; D005340:Fibrinogen; D004228:Dithionitrobenzoic Acid