Volume 12 Supplement 1

11th Annual Conference of the International Society for the Prevention of Tobacco Induced Diseases (ISPTID)

Open Access

Nicotinic augmentation of anti-inflammatory GSK3b signaling

  • David A Scott1Email author,
  • Richard J Lamont1,
  • Akhilesh Kumar1 and
  • Huizhi Wang1
Tobacco Induced Diseases201412(Suppl 1):A15

https://doi.org/10.1186/1617-9625-12-S1-A15

Published: 6 June 2014

Background

Glycogen synthesis kinase 3β (GSK3β) has been shown to be a critical mediator of the intensity and direction of the innate immune system responding to bacterial stimuli. Stimulation of the anti-cholinergic anti-inflammatory system by tobacco alkaloids (nicotine; cotinine) leads to phosphorylation and inactivation of GSK3β and, subsequently, to immune suppression. This presentation will review the tobacco-induced dysregulation of GSK3β signaling and provide insight into the increased susceptibility of smokers to multiple bacterial diseases, including those caused by Mycobacterium tuberculosis, Legionella pneumophila, and Neisseria meningitidis. The extensive ongoing efforts to exploit GSK3β for its therapeutic potential in the control of infectious diseases will also be reviewed.

Authors’ Affiliations

(1)
School of Dentistry, University of Louisville

Copyright

© Scott 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/4.0), 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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