interleukin-8 and sodium-sulfite

We investigated the effects of sodium sulfite (Na(2)SO(3)) on rhinovirus (RV)-induced chemokine production in A549 airway epithelial cells. Our results demonstrated that the treatment of A549 cells with 2,500 μM Na(2)SO(3) enhanced the mRNA expression of RV-induced interleukin (IL)-8 1.8 fold (p = 0.025); and regulated on activation, normal T cell expressed and secreted (RANTES), 2.9 fold (p = 0.025). Moreover, the secretion of IL-8, RANTES, and interferon-γ-inducible protein (IP)-10 was increased in a statistically significant manner without affecting cell viability and RV replication. Our results suggest that Na(2)SO(3) may potentiate RV infection by enhancing chemokine production.

Topics: Air Pollutants; Cell Line; Chemokines; Epithelial Cells; Humans; Interleukin-8; Rhinovirus; Sulfites

Clinical manifestations suggest that air pollution may induce deterioration of respiratory health. Some air pollutants, including sulfite, may play a role in the exacerbation of asthma. Sulfites are formed at bronchial mucosa from inhaled sulfur dioxide. It has been previously reported that sodium sulfite (Na(2)SO(3)) has pro-inflammatory properties and enhances neutrophil adhesion to A549 cells. Interleukin-8 (IL-8) plays a critical role in attracting inflammatory cells and is an excellent marker of pulmonary cell activation. To date, there have not been any reports on the effect of asthma drugs on the suppression of IL-8 production induced by sulfite in A549 cells or the involvement of specific signal transduction pathways. Thus, our study assessed the effects of salmeterol, fluticasone, and montelukast on human epithelial lung cell inflammation as well as the inhibitors in different signal transduction pathways.. A549 human lung epithelial cells were cultured under the following conditions: (1) treated with sodium sulfite (0, 100, 500, 1000, 2500 uM) for 16 hours; (2) cultured for 1 hour in the presence of SB203580, PD98059, SP600125, or wedeloactone, then co-incubated with sodium sulfite for another 16 hours; (3) cultured for 4 hours in the presence of salmeterol, fluticasone, or montelukast, then stimulated with sodium sulfite at a concentration of 1000 uM for 16 hours. We collected the supernatants from the above conditions and performed enzyme-linked immunosorbent assay (ELISA) to measure the IL-8 concentration.. IL-8 production increased after treatment with sodium sulfite at 1000 to 2500 uM (p

Topics: Acetates; Air Pollutants; Albuterol; Androstadienes; Anti-Asthmatic Agents; Cell Line; Cell Survival; Cyclopropanes; Dose-Response Relationship, Drug; Epithelial Cells; Fluticasone; Humans; Inflammation; Interleukin-8; Lung; Quinolines; Salmeterol Xinafoate; Signal Transduction; Sulfides; Sulfites

Air pollutant exposure may induce deterioration of respiratory health. Concentrations of air particles, ozone, nitrogen dioxide, sulfur dioxide, and sulfate are among the players involved in the initiation and/or exacerbation of lung diseases. We have previously documented that the pollutant sodium sulfite (Na(2)SO(3)) is a human neutrophil agonist. To date, there is no evidence in the literature that Na(2)SO(3) can activate epithelial lung cells. In the present study, we found that Na(2)SO(3) (0.01-10 mM) induces tyrosine phosphorylation events and interleukin-8 production in human epithelial lung A549 cells. In addition, we found that Na(2)SO(3) did not promote A549 cell apoptosis as assessed by the degradation of the cytoskeletal gelsolin protein and by FITC-annexin-V binding. Human neutrophil adhesion to Na(2)SO(3)-induced A549 cells was increased when compared with untreated A549 cells. As assessed by flow cytometry, cell surface expression of intercellular adhesion molecule (ICAM)-1, ICAM-3, and vascular cell adhesion molecule-1 (VCAM-1) on A549 cells was not affected by Na(2)SO(3). We conclude that Na(2)SO(3) can activate A549 cells. In addition, we conclude that neutrophil adhesion to Na(2)SO(3)-induced A549 cells is increased via an ICAM-1-, ICAM-3-, and VCAM-1-independent mechanism.

Topics: Air Pollutants; Antigens, Surface; Apoptosis; Cell Adhesion; Cell Line; Cell Separation; Cells, Cultured; Epithelial Cells; Humans; Intercellular Adhesion Molecule-1; Interleukin-8; Lung; Neutrophils; Phosphorylation; Sulfites; Tyrosine; Vascular Cell Adhesion Molecule-1

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.

Topics: Air Pollutants; CD11a Antigen; CD11b Antigen; CD11c Antigen; CD18 Antigens; Cell Adhesion Molecules; Cell Membrane; Chemotaxis, Leukocyte; Cytokines; Humans; In Vitro Techniques; Intercellular Adhesion Molecule-1; Interleukin 1 Receptor Antagonist Protein; Interleukin-12; Interleukin-4; Interleukin-8; Neutrophils; Sialoglycoproteins; Sulfites; Tumor Necrosis Factor-alpha

Sulfite exposure can induce inflammatory responses characterized by an influx of neutrophils into the airways leading to lung malfunctions. Studies focusing on sodium sulfite (Na(2)SO(3))/neutrophil interactions have shown that this chemical possesses proinflammatory properties based on its ability to induce a respiratory burst. Information regarding how this chemical could alter other neutrophil responses/functions as well as its role on immature promyelocytic cells is currently lacking in the literature. In this study, we report that Na(2)SO(3) can induce tyrosine phosphorylation events in human neutrophils but not in both HL-60 and HL-60 + DMSO. As a positive control, GM-CSF was found to induce tyrosine phosphorylation of a particular protein of 120-130 kDa in both HL-60 and HL-60 + DMSO cells testifying that these cells were responsive. In addition, we report that Na(2)SO(3) does not alter neutrophil phagocytosis and that this chemical increases the release of the proinflammatory cytokine IL-8 but not TNF-alpha. Paradoxically, we found that Na(2)SO(3) acts as a potent inhibitor of de novo neutrophil protein synthesis in a concentration-dependent fashion (0.1, 1, or 10 mM) as assessed by SDS-PAGE from metabolically [(35)S]-labeled cells. In contrast to mature neutrophils, we found that Na(2)SO(3) does not modulate de novo protein synthesis in HL-60 cells treated with low concentrations (0. 1 or 1 mM) and that this pollutant was toxic at 10 mM as judged by a drastic decrease of total protein content stained with Coomassie blue. We conclude that Na(2)SO(3) can activate human neutrophils and that its proinflammatory potential is further supported by its ability to increase IL-8 production. In addition, our results clearly indicate that HL-60 and HL-60 + DMSO respond differently than mature human neutrophils to the inflammatory pollutant Na(2)SO(3). Extrapolation of data obtained with HL-60 (and/or HL-60 + DMSO) to neutrophils should be taken with caution. Our data obtained with Na(2)SO(3) are an example.

Topics: Air Pollutants; Cell Death; Dimethyl Sulfoxide; HL-60 Cells; Humans; Interleukin-8; Neutrophil Activation; Neutrophils; Phagocytosis; Phosphorylation; Protein Biosynthesis; Sulfites; Tyrosine