Role of Lymphotoxin (alpha) in Cigarette Smoke-Induced Inflammation and Lymphoid Neogenesis
- Author
- Tine Demoor (UGent) , Ken Bracke (UGent) , Tania Maes (UGent) , BERNARD VANDOOREN (UGent) , Dirk Elewaut (UGent) , Charles Pilette, Guy Joos (UGent) and Guy Brusselle (UGent)
- Organization
- Abstract
- In chronic obstructive pulmonary disease (COPD), chronic inflammation is accompanied by peribronchial lymphoid aggregates. Lymphotoxin-alpha (LTalpha), crucial in secondary lymphoid organogenesis, may be involved in lymphoid neogenesis.We examined cigarette smoke (CS)-induced pulmonary lymphoid neogenesis and inflammation in vivo in LTalpha knockout (LTalpha(-/-)) and wild-type (WT) mice and studied expression of lymphoid chemokines by lung fibroblasts in vitro.T-cell numbers (in bronchoalveolar lavage fluid (BALF) and lungs) and lymphoid aggregate numbers were significantly higher in air-exposed LTalpha(-/-) mice than in WT animals, and increased upon chronic CS exposure in both genotypes. In contrast, local IgA responses upon chronic CS exposure were attenuated in LTalpha(-/-) mice. CXCL13 and CCL19 mRNA in total lung and CXCL13 protein level in BALF increased upon CS exposure in WT, but not in LTalpha(-/-) mice. In vitro lymphotoxin-beta receptor (LTbetaR) stimulation induced CXCL13 and CCL19 mRNA in WT lung fibroblasts. Furthermore, in vitro exposure to cigarette smoke extract (CSE) up-regulated CXCL13 mRNA expression in WT, but not in LTbetaR(-/-), lung fibroblasts.In this murine model of COPD, CS induces pulmonary expression of lymphoid chemokines CXCL13 and CCL19 in a LTalphabeta-LTbetaR-dependent fashion. However, LTalpha is not required for CS-induced pulmonary lymphocyte accumulation and neogenesis of lymphoid aggregates.
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-665408
- MLA
- Demoor, Tine, et al. “Role of Lymphotoxin (Alpha) in Cigarette Smoke-Induced Inflammation and Lymphoid Neogenesis.” EUROPEAN RESPIRATORY JOURNAL, vol. 34, no. 2, 2009, pp. 405–16, doi:10.1183/09031936.00101408.
- APA
- Demoor, T., Bracke, K., Maes, T., VANDOOREN, B., Elewaut, D., Pilette, C., … Brusselle, G. (2009). Role of Lymphotoxin (alpha) in Cigarette Smoke-Induced Inflammation and Lymphoid Neogenesis. EUROPEAN RESPIRATORY JOURNAL, 34(2), 405–416. https://doi.org/10.1183/09031936.00101408
- Chicago author-date
- Demoor, Tine, Ken Bracke, Tania Maes, BERNARD VANDOOREN, Dirk Elewaut, Charles Pilette, Guy Joos, and Guy Brusselle. 2009. “Role of Lymphotoxin (Alpha) in Cigarette Smoke-Induced Inflammation and Lymphoid Neogenesis.” EUROPEAN RESPIRATORY JOURNAL 34 (2): 405–16. https://doi.org/10.1183/09031936.00101408.
- Chicago author-date (all authors)
- Demoor, Tine, Ken Bracke, Tania Maes, BERNARD VANDOOREN, Dirk Elewaut, Charles Pilette, Guy Joos, and Guy Brusselle. 2009. “Role of Lymphotoxin (Alpha) in Cigarette Smoke-Induced Inflammation and Lymphoid Neogenesis.” EUROPEAN RESPIRATORY JOURNAL 34 (2): 405–416. doi:10.1183/09031936.00101408.
- Vancouver
- 1.Demoor T, Bracke K, Maes T, VANDOOREN B, Elewaut D, Pilette C, et al. Role of Lymphotoxin (alpha) in Cigarette Smoke-Induced Inflammation and Lymphoid Neogenesis. EUROPEAN RESPIRATORY JOURNAL. 2009;34(2):405–16.
- IEEE
- [1]T. Demoor et al., “Role of Lymphotoxin (alpha) in Cigarette Smoke-Induced Inflammation and Lymphoid Neogenesis,” EUROPEAN RESPIRATORY JOURNAL, vol. 34, no. 2, pp. 405–416, 2009.
@article{665408, abstract = {{In chronic obstructive pulmonary disease (COPD), chronic inflammation is accompanied by peribronchial lymphoid aggregates. Lymphotoxin-alpha (LTalpha), crucial in secondary lymphoid organogenesis, may be involved in lymphoid neogenesis.We examined cigarette smoke (CS)-induced pulmonary lymphoid neogenesis and inflammation in vivo in LTalpha knockout (LTalpha(-/-)) and wild-type (WT) mice and studied expression of lymphoid chemokines by lung fibroblasts in vitro.T-cell numbers (in bronchoalveolar lavage fluid (BALF) and lungs) and lymphoid aggregate numbers were significantly higher in air-exposed LTalpha(-/-) mice than in WT animals, and increased upon chronic CS exposure in both genotypes. In contrast, local IgA responses upon chronic CS exposure were attenuated in LTalpha(-/-) mice. CXCL13 and CCL19 mRNA in total lung and CXCL13 protein level in BALF increased upon CS exposure in WT, but not in LTalpha(-/-) mice. In vitro lymphotoxin-beta receptor (LTbetaR) stimulation induced CXCL13 and CCL19 mRNA in WT lung fibroblasts. Furthermore, in vitro exposure to cigarette smoke extract (CSE) up-regulated CXCL13 mRNA expression in WT, but not in LTbetaR(-/-), lung fibroblasts.In this murine model of COPD, CS induces pulmonary expression of lymphoid chemokines CXCL13 and CCL19 in a LTalphabeta-LTbetaR-dependent fashion. However, LTalpha is not required for CS-induced pulmonary lymphocyte accumulation and neogenesis of lymphoid aggregates.}}, author = {{Demoor, Tine and Bracke, Ken and Maes, Tania and VANDOOREN, BERNARD and Elewaut, Dirk and Pilette, Charles and Joos, Guy and Brusselle, Guy}}, issn = {{0903-1936}}, journal = {{EUROPEAN RESPIRATORY JOURNAL}}, language = {{eng}}, number = {{2}}, pages = {{405--416}}, title = {{Role of Lymphotoxin (alpha) in Cigarette Smoke-Induced Inflammation and Lymphoid Neogenesis}}, url = {{http://doi.org/10.1183/09031936.00101408}}, volume = {{34}}, year = {{2009}}, }
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