Cigarette smoke extract modulates human β‐defensin‐2 and interleukin‐8 expression in human gingival epithelial cells

Abstract

Human gingival epithelial cells play a critical role in orchestrating the innate immune responses of periodontal tissue via TLR signalling. Our results represent the first demonstration that CSE can modulate HGEC function by suppressing hBD-2 and enhancing IL-8 production, and this may be, in part, a possible mechanism which promotes periodontal disease.

Effect of Smoking on the Expression of Human Beta-Defensin-2 in Gingival Crevicular Fluid after Non Surgical Periodontal Therapy

“…Correspondingly, the activated immune response limits innate response and, hence, secretion of β-defensins (42) . Our findings were in agreement with previous studies shown that smoking downregulates hβD-2 expression (37,39,43) .…”

“…At three months greater mean hβD-2 level was recorded in non-smokers group, with no statistically significant difference. At baseline, the low level of hβD-2 in smoker's group could be explained by the fact that periodontopathogenic microorganisms mainly P.gingivalis, which had a specific role in β-defensins degradation was found in smokers more than in non-smokers (39,40) . Moreover, bacteria with resistance to β-defensins, such as T. denticola and P.gingivalis, survive and colonize on epithelial surfaces, and eventually, invade gingival tissues (41) .…”

Air Pollution Particulate Matter Alters Antimycobacterial Respiratory Epithelium Innate Immunity

“…It is therefore possible that vanadium contributed to the inhibition of HBD-2 production in response to M. tuberculosis. Interestingly, exposure of gingival epithelial and normal human bronchial epithelial cells to cigarette smoke, which also contains vanadium, similarly reduces HBD-2 mRNA expression and peptide production in vitro in response to LPS from Pseudomonas aeruginosa (51). It has been proposed that the downregulation of HBD-2 in P. aeruginosainfected cells by cigarette smoke may be due to the downregulation of fatty acid-binding protein 5 (FABP5).…”

Cigarette smoke enhances -defensin 2 expression in rat airways via nuclear factor- B activation

“…Antimicrobial peptides are important effector molecules of the lung innate immune system, and BDs, especially BD-2, are the principal family of antimicrobial peptides in respiratory tract, which are mainly produced by airway epithelial cells [1]. Several studies have recently demonstrated a suppressive effect of CS on hBD-2 expression by cultured human sinonasal, gingival and airway epithelial cells in vitro and decreased hBD-2 levels in pharyngeal washing fluid and sputum from smokers with acute pneumonia in vivo [9][10][11], indicating that CS exposure possibly inhibits airway epithelial hBD-2 production, which links cigarette smoking with increased susceptibility of respiratory tract to microbial infections. However, SHIBATA et al [12] reported upregulated mBD-2 mRNA expression in lung tissues after 6-month CS exposure, and we have further demonstrated, in the present study, that 4-week repeated CS exposure stimulated rBD-2 mRNA and protein expression in rat airways.…”

“…However, little is known about the effect of CS on BD-2 expression. Very recently, LEE et al [9] and MAHANONDA et al [10] reported that acrolein (a major component of cigarette smoke) and cigarette smoke extract, suppressed hBD-2 expression by sinonasal epithelial cells and gingival epithelial cells. Results from a study by HERR et al [11] showed decreased levels of hBD-2 in pharyngeal washing fluid and sputum from current and former smokers with acute pneumonia compared with that from never smokers, and demonstrated that smoke exposure reduced in vitro hBD-2 expression in airway epithelium in response to bacterial stimulation.…”