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  • Open Access

Acrolein: blocking antibody formation: pro tumor, anti-allergy

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Clinical and Translational Allergy20144 (Suppl 2) :P31

https://doi.org/10.1186/2045-7022-4-S2-P31

  • Published:

Keywords

  • Tumor Growth
  • Acrolein
  • Cytokine Profile
  • Anaphylactic Reaction
  • Passive Smoking

Background

Allergic sensitization has been linked to active and passive smoking in exposed individuals and even their pets. We here investigated the contribution of acrolein, a compound generated in large amounts during smoking, during nasal sensitization and -- based on the surprising preliminary results -- on tumor growth. As a model antigen we used KLH with or without acrolein.

Methods

BALB/c mice were nasally sensitized 5 times in biweekly intervals with KLH alone or with KLH in conjunction with acrolein. Airway hyperreactivity was was measured according to change of enhanced pause and KLH-specific anaphylactic reaction was monitored in vivo Levels of specific antibodies as well as cytokine profile of KLH-stimulated splenocytes were analyzed by ELISA. Further, mouse D2F2-tumor cells were grafted to the flanks and tumor growth monitored in mice previously exposed to acrolein or buffer.

Results

Nasal application of KLH as model antigen induced specific IgG1-, IgG2a-, IgA- and IgE-levels. The same mice secreted elevated levels of IL5, IL13, IL10 and IFN-γ. They showed increased airway-hyperreactivity and had a significant drop in body temperature upon allergen challenge. Pointing towards tolerance, and against our expectations, presence of acrolein in the KLH-antigen significantly reduced specific antibody-titers, resulted in lower splenocyte cytokine production and prevented anaphylaxis. However, the impaired immune response simultaneously led to a significantly higher tumor growth in mice exposed to acrolein than in the control group.

Conclusion

Acrolein in smoke -- best known for its carcinogenic effect - decreases the risk of sensitization towards a specific antigen by inhibiting immune activation. Our data further suggest that Acrolein via the same mechanism acts tumor promoting in smokers.

Authors’ Affiliations

(1)
University of Veterinary Medicine, Messerli Research Institute, Comparative Medicine, Vienna, Austria
(2)
Department of Pathophysiology and Allergy Research, Medical University of Vienna, Vienna, Austria
(3)
Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria
(4)
Medical University of Vienna, Institute of Immunology, Vienna, Austria

Copyright

© Roth-Walter et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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