Activation of human epithelial lung A549 cells by the pollutant sodium sulfite: Enhancement of neutrophil adhesion

被引:26
作者
Pelletier, M [1 ]
Lavastre, V [1 ]
Girard, D [1 ]
机构
[1] Univ Quebec, INRS, Inst Armand Frappier, Pointe Claire, PQ H9R 1G6, Canada
关键词
inflammation; sodium sulfite; Na2SO3; lung cells; neutrophils; cell adhesion;
D O I
10.1093/toxsci/69.1.210
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
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 (Na2SO3) is a human neutrophil agonist. To date, there is no evidence in the literature that Na2SO3 can activate epithelial lung cells. In the present study, we found that Na2SO3 (0.01-10 mM) induces tyrosine phosphorylation events and interleukin-8 production in human epithelial lung A549 cells. In addition, we found that Na2SO3 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 Na2SO3-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 Na2SO3. We conclude that Na2SO3 can activate A549 cells. In addition, we conclude that neutrophil adhesion to Na2SO3-induced A549 cells is increased via an ICAM-1-, ICAM-3-, and VCAM-1-independent mechanism.
引用
收藏
页码:210 / 216
页数:7
相关论文
共 49 条
[1]   Asbestos causes apoptosis in alveolar epithelial cells: Role of iron-induced free radicals [J].
Aljandali, A ;
Pollack, H ;
Yeldandi, A ;
Li, YY ;
Weitzman, SA ;
Kamp, DW .
JOURNAL OF LABORATORY AND CLINICAL MEDICINE, 2001, 137 (05) :330-339
[2]   Short-term associations between emergency hospital admissions for respiratory and cardiovascular disease and outdoor air pollution in London [J].
Atkinson, RW ;
Bremner, SA ;
Anderson, HR ;
Strachan, DP ;
Bland, JM ;
de Leon, AP .
ARCHIVES OF ENVIRONMENTAL HEALTH, 1999, 54 (06) :398-411
[3]  
BALMES JR, 1989, ENVIRON HEALTH PERSP, V79, P163
[4]   SULFITE STIMULATES NADPH OXIDASE OF HUMAN NEUTROPHILS TO PRODUCE ACTIVE OXYGEN RADICALS VIA PROTEIN-KINASE-C AND CA2+/CALMODULIN PATHWAYS [J].
BECKSPEIER, I ;
LIESE, JG ;
BELOHRADSKY, BH ;
GODLESKI, JJ .
FREE RADICAL BIOLOGY AND MEDICINE, 1993, 14 (06) :661-668
[5]   RESPONSES OF HUMAN NEUTROPHILS TO SULFITE [J].
BECKSPEIER, I ;
LENZ, AG ;
GODLESKI, JJ .
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH, 1994, 41 (03) :285-297
[6]   Persistent airway inflammation but accommodated antioxidant and lung function responses after repeated daily exposure to nitrogen dioxide [J].
Blomberg, A ;
Krishna, MT ;
Helleday, R ;
Söderberg, M ;
Ledin, MC ;
Kelly, FJ ;
Frew, AJ ;
Holgate, ST ;
Sandström, T .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1999, 159 (02) :536-543
[7]  
BRACH MA, 1992, BLOOD, V80, P2920
[8]   The α4β1 (very late antigen (VLA)-4, CD49d/CD29) and α5β1 (VLA-5, CD49e/CD29) integrins mediate β2 (CD11/CD18) integrin-independent neutrophil recruitment to endotoxin-induced lung inflammation [J].
Burns, JA ;
Issekutz, TB ;
Yagita, H ;
Issekutz, AC .
JOURNAL OF IMMUNOLOGY, 2001, 166 (07) :4644-4649
[9]   The β2, α4, α5 integrins and selectins mediate chemotactic factor and endotoxin-enhanced neutrophil sequestration in the lung [J].
Burns, JA ;
Issekutz, TB ;
Yagita, H ;
Issekutz, AC .
AMERICAN JOURNAL OF PATHOLOGY, 2001, 158 (05) :1809-1819
[10]   ICAM-1-independent adhesion of neutrophils to phorbol ester-stimulated human airway epithelial cells [J].
Celi, A ;
Cianchetti, S ;
Petruzzelli, S ;
Carnevali, S ;
Baliva, F ;
Giuntini, C .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1999, 277 (03) :L465-L471