title: Activation of human neutrophils by the pollutant sodium sulfite: effect on cytokine production, chemotaxis, and cell surface expression of cell adhesion molecules.
abstract: We have previously demonstrated that the pollutant sodium sulfite (Na(2)SO(3)) possesses some proinflammatory properties. This study was conducted in order to elucidate how this environmentally significant chemical can alter human neutrophil cell physiology. Using sensitive ELISAs, we found that Na(2)SO(3) induces the total (intra- and extracellular fractions) production of interleukin-12 (IL-12) and IL-8 but not TNF-alpha, IL-1alpha, or IL-4. IL-8 levels were significantly increased in both fractions while the levels of IL-12 were significantly increased only in the extracellular milieu. In contrast, IL-1Ra levels were significantly decreased in both fractions when cells were treated at the highest Na(2)SO(3) concentration (10 mM). Despite the fact that Na(2)SO(3) was found to increase IL-8 production, it does not induce neutrophil chemotaxis in vitro. Cell surface expression of CD18, CD11a, CD11b, CD11c, CD50, and CD54 was not affected by Na(2)SO(3) treatment. We conclude that Na(2)SO(3) is a modulator of cytokine production but that it does not alter either chemotaxis or cell surface expression of the tested molecules. Our results attest to the importance of systematically monitoring cytokine production from both intracellular and extracellular fractions in pollutant-induced neutrophils, since this could lead to different interpretations.
authors.affiliation: INRS-Institut Armand-Frappier, Université du Québec, Canada.
authors.forename: Claude
authors.initials: C
authors.lastname: Ratthé
authors.forename: Martin
authors.initials: M
authors.lastname: Pelletier
authors.forename: Charles J
authors.initials: CJ
authors.lastname: Roberge
authors.forename: Denis
authors.initials: D
authors.lastname: Girard
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D040881:CD11a Antigen / Q000378:metabolism; D039481:CD11b Antigen / Q000378:metabolism; D039521:CD11c Antigen / Q000378:metabolism; D018821:CD18 Antigens / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002462:Cell Membrane / Q000187:drug effects / Q000276:immunology; D002634:Chemotaxis, Leukocyte / Q000187:drug effects*; D016207:Cytokines / Q000096:biosynthesis*; D006801:Humans; D066298:In Vitro Techniques; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D053590:Interleukin 1 Receptor Antagonist Protein; D018664:Interleukin-12 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D016209:Interleukin-8 / Q000096:biosynthesis; D009504:Neutrophils / Q000187:drug effects* / Q000276:immunology*; D012795:Sialoglycoproteins / Q000096:biosynthesis; D013447:Sulfites / Q000633:toxicity*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D000393:Air Pollutants; D040881:CD11a Antigen; D039481:CD11b Antigen; D039521:CD11c Antigen; D018821:CD18 Antigens; D015815:Cell Adhesion Molecules; D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D016209:Interleukin-8; D012795:Sialoglycoproteins; D013447:Sulfites; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D018664:Interleukin-12; D015847:Interleukin-4; C025026:sodium sulfite