Cigarette smoke modifies neutrophil chemotaxis, neutrophil extracellular trap formation and inflammatory response‐related gene expression

Background and Objective Cigarette smoking is a major risk factor for periodontitis, and smoking perturbs neutrophil reactive oxygen species production. This study tested the hypothesis that cigarette smoke extract (CSE) and its components/metabolites nicotine, cotinine and thiocyanate (SCN‐), may i...

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Bibliographic Details
Published in:Journal of periodontal research 2018-08, Vol.53 (4), p.525-535
Main Authors: White, P. C., Hirschfeld, J., Milward, M. R., Cooper, P. R., Wright, H. J., Matthews, J. B., Chapple, I. L.C.
Format: Article
Language:English
Subjects:
Acetic acid
Apoptosis - drug effects
Cell activation
Chemotaxis
Chemotaxis - drug effects
Cigarette smoke
Cigarette smoking
Cotinine
Cotinine - metabolism
Dentistry
Extracellular Traps - drug effects
Flow Cytometry
Gene expression
Gene Expression - drug effects
Gum disease
Humans
Hypochlorous acid
Immune response
Inflammation
Innate immunity
Leukocytes (neutrophilic)
Metabolites
Neutrophils
Neutrophils - drug effects
Nicotine
Nicotine - metabolism
Periodontitis
Polymerase chain reaction
Reactive oxygen species
Reactive Oxygen Species - metabolism
Real-Time Polymerase Chain Reaction
Respiratory burst
Smoke - adverse effects
Smoking - adverse effects
thiocyanate
Thiocyanates - metabolism
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Summary:Background and Objective Cigarette smoking is a major risk factor for periodontitis, and smoking perturbs neutrophil reactive oxygen species production. This study tested the hypothesis that cigarette smoke extract (CSE) and its components/metabolites nicotine, cotinine and thiocyanate (SCN‐), may influence neutrophil functions. Material and Methods Chemotaxis was assessed in neutrophils pre‐treated with CSE using real‐time video microscopy. Neutrophil extracellular trap (NET) release in response to CSE, nicotine, cotinine, SCN‐ as well as to phorbol 12‐myristate‐13‐acetate and hypochlorous acid following pre‐treatment with CSE, nicotine, cotinine or SCN‐ was assessed using fluorescence‐based assays. The impact of CSE and SCN‐ treatment on neutrophil respiratory burst‐ and inflammation‐related gene expression (NFKBIE, DNAJB1, CXCL8, NCF1, NCF2, CYBB) was determined by real‐time polymerase chain reaction. Results Both CSE and SCN‐ pre‐treatment inhibited phorbol 12‐myristate‐13‐acetate‐stimulated NET release. Additionally, SCN‐ inhibited hypochlorous acid‐stimulated NET formation, while SCN‐ alone stimulated NET release. Overall, neutrophils pre‐treated with CSE exhibited reduced speed, velocity and directionality relative to untreated neutrophils. Although CSE and SCN‐ promoted DNAJB1 expression, increased redox‐related gene expression was only detected in response to SCN‐. Conclusion These results suggest that CSE can alter ex vivo neutrophil activation by mechanisms independent of SCN‐ and nicotine, and SCN‐ may contribute to the perturbed innate immune responses observed in smokers.
ISSN:0022-3484
1600-0765
DOI:10.1111/jre.12542