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Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus enterotoxin B in mice

Wouter Huvenne (UGent) , Ellen Lanckacker (UGent) , Olga Krysko (UGent) , Ken Bracke (UGent) , Tine Demoor (UGent) , Peter W Hellings, Guy Brusselle (UGent) , Guy Joos (UGent) , Claus Bachert (UGent) and Tania Maes (UGent)
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Abstract
Background: Cigarette smoke (CS) is a major risk factor for the development of COPD. CS exposure is associated with an increased risk of bacterial colonization and respiratory tract infection, because of suppressed antibacterial activities of the immune system and delayed clearance of microbial agents from the lungs. Colonization with Staphylococcus aureus results in release of virulent enterotoxins, with superantigen activity which causes T cell activation. Objective: To study the effect of Staphylococcus aureus enterotoxin B (SEB) on CS-induced inflammation, in a mouse model of COPD. Methods: C57/Bl6 mice were exposed to CS or air for 4 weeks (5 cigarettes/exposure, 4x/day, 5 days/week). Endonasal SEB (10 mu g/ml) or saline was concomitantly applied starting from week 3, on alternate days. 24 h after the last CS and SEB exposure, mice were sacrificed and bronchoalveolar lavage (BAL) fluid and lung tissue were collected. Results: Combined exposure to CS and SEB resulted in a raised number of lymphocytes and neutrophils in BAL, as well as increased numbers of CD8(+) T lymphocytes and granulocytes in lung tissue, compared to sole CS or SEB exposure. Moreover, concomitant CS/SEB exposure induced both IL-13 mRNA expression in lungs and goblet cell hyperplasia in the airway wall. In addition, combined CS/SEB exposure stimulated the formation of dense, organized aggregates of B-and T-lymphocytes in lungs, as well as significant higher CXCL-13 (protein, mRNA) and CCL19 (mRNA) levels in lungs. Conclusions: Combined CS and SEB exposure aggravates CS-induced inflammation in mice, suggesting that Staphylococcus aureus could influence the pathogenesis of COPD.
Keywords
AIRWAY INFLAMMATION, BACTERIAL SUPERANTIGEN, DEPENDENT AIRWAY, CELL-ACTIVATION, IGE-ANTIBODIES, TH17 CELLS, DISEASE, NASAL, SENSITIZATION, PATHOGENESIS

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MLA
Huvenne, Wouter, Ellen Lanckacker, Olga Krysko, et al. “Exacerbation of Cigarette Smoke-induced Pulmonary Inflammation by Staphylococcus Aureus Enterotoxin B in Mice.” RESPIRATORY RESEARCH 12 (2011): n. pag. Print.
APA
Huvenne, W., Lanckacker, E., Krysko, O., Bracke, K., Demoor, T., Hellings, P. W., Brusselle, G., et al. (2011). Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus enterotoxin B in mice. RESPIRATORY RESEARCH, 12.
Chicago author-date
Huvenne, Wouter, Ellen Lanckacker, Olga Krysko, Ken Bracke, Tine Demoor, Peter W Hellings, Guy Brusselle, Guy Joos, Claus Bachert, and Tania Maes. 2011. “Exacerbation of Cigarette Smoke-induced Pulmonary Inflammation by Staphylococcus Aureus Enterotoxin B in Mice.” Respiratory Research 12.
Chicago author-date (all authors)
Huvenne, Wouter, Ellen Lanckacker, Olga Krysko, Ken Bracke, Tine Demoor, Peter W Hellings, Guy Brusselle, Guy Joos, Claus Bachert, and Tania Maes. 2011. “Exacerbation of Cigarette Smoke-induced Pulmonary Inflammation by Staphylococcus Aureus Enterotoxin B in Mice.” Respiratory Research 12.
Vancouver
1.
Huvenne W, Lanckacker E, Krysko O, Bracke K, Demoor T, Hellings PW, et al. Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus enterotoxin B in mice. RESPIRATORY RESEARCH. 2011;12.
IEEE
[1]
W. Huvenne et al., “Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus enterotoxin B in mice,” RESPIRATORY RESEARCH, vol. 12, 2011.
@article{2026522,
  abstract     = {Background: Cigarette smoke (CS) is a major risk factor for the development of COPD. CS exposure is associated with an increased risk of bacterial colonization and respiratory tract infection, because of suppressed antibacterial activities of the immune system and delayed clearance of microbial agents from the lungs. Colonization with Staphylococcus aureus results in release of virulent enterotoxins, with superantigen activity which causes T cell activation. 
Objective: To study the effect of Staphylococcus aureus enterotoxin B (SEB) on CS-induced inflammation, in a mouse model of COPD. 
Methods: C57/Bl6 mice were exposed to CS or air for 4 weeks (5 cigarettes/exposure, 4x/day, 5 days/week). Endonasal SEB (10 mu g/ml) or saline was concomitantly applied starting from week 3, on alternate days. 24 h after the last CS and SEB exposure, mice were sacrificed and bronchoalveolar lavage (BAL) fluid and lung tissue were collected. 
Results: Combined exposure to CS and SEB resulted in a raised number of lymphocytes and neutrophils in BAL, as well as increased numbers of CD8(+) T lymphocytes and granulocytes in lung tissue, compared to sole CS or SEB exposure. Moreover, concomitant CS/SEB exposure induced both IL-13 mRNA expression in lungs and goblet cell hyperplasia in the airway wall. In addition, combined CS/SEB exposure stimulated the formation of dense, organized aggregates of B-and T-lymphocytes in lungs, as well as significant higher CXCL-13 (protein, mRNA) and CCL19 (mRNA) levels in lungs. 
Conclusions: Combined CS and SEB exposure aggravates CS-induced inflammation in mice, suggesting that Staphylococcus aureus could influence the pathogenesis of COPD.},
  articleno    = {69},
  author       = {Huvenne, Wouter and Lanckacker, Ellen and Krysko, Olga and Bracke, Ken and Demoor, Tine and Hellings, Peter W and Brusselle, Guy and Joos, Guy and Bachert, Claus and Maes, Tania},
  issn         = {1465-993X},
  journal      = {RESPIRATORY RESEARCH},
  keywords     = {AIRWAY INFLAMMATION,BACTERIAL SUPERANTIGEN,DEPENDENT AIRWAY,CELL-ACTIVATION,IGE-ANTIBODIES,TH17 CELLS,DISEASE,NASAL,SENSITIZATION,PATHOGENESIS},
  language     = {eng},
  pages        = {11},
  title        = {Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus enterotoxin B in mice},
  url          = {http://dx.doi.org/10.1186/1465-9921-12-69},
  volume       = {12},
  year         = {2011},
}

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