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Concomittant inhalation of cigarette smoke and aerosolized protein activates airway dendritic cells and induces allergic airway inflammation in a TLR-independent way

Lander Robays (UGent) , Ellen Lanckacker (UGent) , Katrien Moerloose (UGent) , Tania Maes (UGent) , Ken Bracke (UGent) , Guy Brusselle (UGent) , Guy Joos (UGent) and Karim Vermaelen (UGent)
(2009) Journal of Immunology. 183(4). p.2758-2766
Author
Organization
Abstract
Abstract: Cigarette smoking is associated with the development of allergic asthma. In mice, exposure to cigarette smoke sensitizes the airways toward coinhaled OVA, leading to OVA-specific allergic inflammation. Pulmonary dendritic cells (DCs) are professional APCs involved in immunosurveillance and implicated in the induction of allergic responses in lung. We investigated the effects of smoking on some of the key features of pulmonary DC biology, including trafficking dynamics and cellular activation status in different lung compartments. We found that cigarette smoke inhalation greatly amplified DC-mediated transport of inhaled Ags to mediastinal lymph nodes, a finding supported by the up-regulation of CCR7 on airway DCs. Pulmonary plasmacytoid DCs, which have been involved in inhalational tolerance, were reduced in number after smoke exposure. In addition, combined exposure to cigarette smoke and OVA aerosol increased surface expression of MHC class II, CD86, and PDL2 on airway DCs, while ICOSL was strongly down-regulated. Although inhaled endotoxins, which are also present in cigarette smoke, have been shown to act as DC activators and Th2-skewing sensitizers, TLR4-deficient and MyD88 knockout mice did not show impaired eosinophilic airway inflammation after concomitant exposure to cigarette smoke and OVA. From these data, we conclude that cigarette smoke activates the pulmonary DC network in a pattern that favors allergic airway sensitization toward coinhaled inert protein. The TLR independency of this phenomenon suggests that alternative immunological adjuvants are present in cigarette smoke. The Journal of Immunology, 2009, 183: 2758-2766.
Keywords
respiratory-tract, linking innate, mouse model, inhaled antigen, adaptive immunity, thoracic lymph-nodes, th2 immune-responses, Induced pulmonary inflammation, environmental tobacco-smoke, in-vitro

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MLA
Robays, Lander et al. “Concomittant Inhalation of Cigarette Smoke and Aerosolized Protein Activates Airway Dendritic Cells and Induces Allergic Airway Inflammation in a TLR-independent Way.” Journal of Immunology 183.4 (2009): 2758–2766. Print.
APA
Robays, L., Lanckacker, E., Moerloose, K., Maes, T., Bracke, K., Brusselle, G., Joos, G., et al. (2009). Concomittant inhalation of cigarette smoke and aerosolized protein activates airway dendritic cells and induces allergic airway inflammation in a TLR-independent way. Journal of Immunology, 183(4), 2758–2766.
Chicago author-date
Robays, Lander, Ellen Lanckacker, Katrien Moerloose, Tania Maes, Ken Bracke, Guy Brusselle, Guy Joos, and Karim Vermaelen. 2009. “Concomittant Inhalation of Cigarette Smoke and Aerosolized Protein Activates Airway Dendritic Cells and Induces Allergic Airway Inflammation in a TLR-independent Way.” Journal of Immunology 183 (4): 2758–2766.
Chicago author-date (all authors)
Robays, Lander, Ellen Lanckacker, Katrien Moerloose, Tania Maes, Ken Bracke, Guy Brusselle, Guy Joos, and Karim Vermaelen. 2009. “Concomittant Inhalation of Cigarette Smoke and Aerosolized Protein Activates Airway Dendritic Cells and Induces Allergic Airway Inflammation in a TLR-independent Way.” Journal of Immunology 183 (4): 2758–2766.
Vancouver
1.
Robays L, Lanckacker E, Moerloose K, Maes T, Bracke K, Brusselle G, et al. Concomittant inhalation of cigarette smoke and aerosolized protein activates airway dendritic cells and induces allergic airway inflammation in a TLR-independent way. Journal of Immunology. Rockville Pike, Bethesda USA: Amer Assoc Immunologists; 2009;183(4):2758–66.
IEEE
[1]
L. Robays et al., “Concomittant inhalation of cigarette smoke and aerosolized protein activates airway dendritic cells and induces allergic airway inflammation in a TLR-independent way,” Journal of Immunology, vol. 183, no. 4, pp. 2758–2766, 2009.
@article{806682,
  abstract     = {Abstract: Cigarette smoking is associated with the development of allergic asthma. In mice, exposure to cigarette smoke sensitizes the airways toward coinhaled OVA, leading to OVA-specific allergic inflammation. Pulmonary dendritic cells (DCs) are professional APCs involved in immunosurveillance and implicated in the induction of allergic responses in lung. We investigated the effects of smoking on some of the key features of pulmonary DC biology, including trafficking dynamics and cellular activation status in different lung compartments. We found that cigarette smoke inhalation greatly amplified DC-mediated transport of inhaled Ags to mediastinal lymph nodes, a finding supported by the up-regulation of CCR7 on airway DCs. Pulmonary plasmacytoid DCs, which have been involved in inhalational tolerance, were reduced in number after smoke exposure. In addition, combined exposure to cigarette smoke and OVA aerosol increased surface expression of MHC class II, CD86, and PDL2 on airway DCs, while ICOSL was strongly down-regulated. Although inhaled endotoxins, which are also present in cigarette smoke, have been shown to act as DC activators and Th2-skewing sensitizers, TLR4-deficient and MyD88 knockout mice did not show impaired eosinophilic airway inflammation after concomitant exposure to cigarette smoke and OVA. From these data, we conclude that cigarette smoke activates the pulmonary DC network in a pattern that favors allergic airway sensitization toward coinhaled inert protein. The TLR independency of this phenomenon suggests that alternative immunological adjuvants are present in cigarette smoke. The Journal of Immunology, 2009, 183: 2758-2766.},
  author       = {Robays, Lander and Lanckacker, Ellen and Moerloose, Katrien and Maes, Tania and Bracke, Ken and Brusselle, Guy and Joos, Guy and Vermaelen, Karim},
  issn         = {0022-1767},
  journal      = {Journal of Immunology},
  keywords     = {respiratory-tract,linking innate,mouse model,inhaled antigen,adaptive immunity,thoracic lymph-nodes,th2 immune-responses,Induced pulmonary inflammation,environmental tobacco-smoke,in-vitro},
  language     = {eng},
  number       = {4},
  pages        = {2758--2766},
  publisher    = {Amer Assoc Immunologists},
  title        = {Concomittant inhalation of cigarette smoke and aerosolized protein activates airway dendritic cells and induces allergic airway inflammation in a TLR-independent way},
  url          = {http://dx.doi.org/10.4049/jimmunol.0802204},
  volume       = {183},
  year         = {2009},
}

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