Cigarette smoking and inflammation: Cellular and molecular mechanisms

Research output: Contribution to journalArticle

224 Citations (Scopus)

Abstract

Cigarette smoke (CS) causes considerable morbidity and mortality by inducing cancer, chronic lung and vascular diseases, and oral disease. Despite the well-recognized risks associated with smoking, the habit remains unacceptably prevalent. Several toxins present in CS have immunomodulatory effects. CS also contains trace amounts of microbial cell components, including bacterial lipopolysaccharide. These and other CS constituents induce chronic inflammation at mucosal surfaces and modify host responses to exogenous antigens. The effects of CS on immunity are far-reaching and complex; both pro-inflammatory and suppressive effects may be induced. The net effect of CS on immunity depends on many variables, including the dose and type of tobacco, the route and chronicity of exposure, and the presence of other factors at the time of immune cell stimulation, such as Toll receptor ligands or other inflammatory mediators. CS impairs innate defenses against pathogens, modulates antigen presentation, and promotes autoimmunity. CS also impairs immunity in the oral cavity and promotes gingival and periodontal disease and oral cancer. The recognition of specific mechanisms by which CS affects host immunity is an important step toward elucidating mechanisms of tobacco-induced disease and may identify novel therapeutic approaches for the management of diseases that afflict smokers.Abbreviations: AP-1, activator protein-1; CD, cluster of differentiation; COPD, chronic obstructive pulmonary disease; HLA, human leukocyte antigen; IFNγ, interferon gamma; IL, interleukin; LPS, lipopolysaccharide; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor kappa-B; RAGE, receptors for advanced glycation end-products; ROS, reactive oxidative species; RORγτ, retinoic acid receptor-related orphan receptor transcription factor; STAT, signal transducer and activator of transcription; T-bet, T-box transcription factor; Th, T-helper; TLR, Toll-like receptors; TNFα, Tumor necrosis factor alpha; and TSLP, thymic stromal lymphopoeitin.

Original languageEnglish (US)
Pages (from-to)142-149
Number of pages8
JournalJournal of Dental Research
Volume91
Issue number2
DOIs
StatePublished - Feb 2012

Fingerprint

Smoke
Tobacco Products
Smoking
Inflammation
Immunity
Transcription Factor AP-1
Chronic Obstructive Pulmonary Disease
Tobacco
Lipopolysaccharides
Mouth Diseases
Gingival Diseases
Retinoic Acid Receptors
NF-kappa B
Toll-Like Receptors
Interleukins
Mouth Neoplasms
Antigen Presentation
Periodontal Diseases
Cellular Structures
Disease Management

Keywords

  • autoimmunity
  • cigarette smoke
  • immunity
  • inflammation
  • nicotine
  • tobacco

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Cigarette smoking and inflammation : Cellular and molecular mechanisms. / Lee, J.; Taneja, Veena D; Vassallo, Robert.

In: Journal of Dental Research, Vol. 91, No. 2, 02.2012, p. 142-149.

Research output: Contribution to journalArticle

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