Gingival crevicular fluid levels of human beta‐defensin‐2 and cathelicidin in smoker and non‐smoker patients: a cross‐sectional study

Ertuğrul, Abdullah Seçkin; Sahin, Hacer; Dikilitaş, Ahu; Alpaslan, Nuh; Bozoğlan, Alihan; Tekin, Yasin

doi:10.1111/jre.12105

Cited by 23 publications

(27 citation statements)

References 55 publications

(66 reference statements)

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“…Several in vitro studies have determined that smoking can affect the expression of AMPs in gingival epithelial cells or skin keratinocytes (Table ). Besides, some cross‐sectional, in vivo studies have sought to identify the effect of smoking or nicotine use on AMP expression in saliva or gingival crevicular fluid of periodontitis patients (Table ). The net effect of smoking on AMP expression in the gingival or salivary niches in periodontitis subjects seems to be complicated and remains unclear, chiefly, as the literature in this regard has addressed different natures of target AMPs (human neutrophil peptides [HNP, alpha‐defensins], human beta defensins [HBD] or LL‐37) and oral sample types (gingival crevicular fluid, saliva or tissue).…”

Section: Resultsmentioning

confidence: 99%

“…HBD‐2 expression has been associated with proinflammatory stimulation such as that from bacterial lipopolysaccharides (LPS) . HBD‐2 levels are shown as significantly higher in smokers with generalized aggressive periodontitis as compared with non‐smokers and similarly higher in smokers with gingivitis when compared to non‐smokers with gingivitis . In addition, HBD‐2 levels in non‐inflamed gingival tissues were shown to be significantly reduced in smokers compared with non‐smokers .…”

Section: Resultsmentioning

confidence: 99%

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Antimicrobial peptides as a possible interlink between periodontal diseases and its risk factors: A systematic review

Schmalz

Schmidt

et al. 2017

J of Periodontal Research

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Antimicrobial peptides (AMPs) play a critical role in controlling innate and acquired immune responses. Local dysregulation of AMP is implicated in the pathogenesis of periodontal diseases as a response to periodontal pathogen challenge. Changes in AMP expression also characterize tobacco smoking, diabetes mellitus, obesity and rheumatoid arthritis, which are established risk factors of periodontal diseases, suggesting AMP may act as putative mechanistic links between these. The aim was to evaluate and summarize critically the current evidence pertaining to interrelationships between AMPs, periodontal diseases and selected periodontal disease risk factors. General and theme specific keywords were used to search the PUBMED database for studies relevant to AMP, periodontal diseases, smoking, diabetes mellitus, obesity and rheumatoid arthritis and critically reviewed. A total of 131 abstracts and 119 full text articles were screened for relevance; 13 studies were selected for inclusion after critical review. Local AMP dysregulation characteristic to periodontal diseases appears to occur within a broader landscape of complex systemic immune perturbations independently induced by smoking, metabolic and rheumatoid disease. The nature of these interactions and mechanistic pathways involved are inadequately understood. AMPs could be possible mechanistic interlinks between periodontal diseases and its risk factors. However, such evidence is very limited and more in vivo and in vitro studies are necessary to clarify the nature of such relationships. A greater understanding of AMPs as shared mediators is essential for unraveling their value as therapeutic or biomarker candidates.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Antimicrobial peptides as a possible interlink between periodontal diseases and its risk factors: A systematic review

Schmalz

Schmidt

et al. 2017

J of Periodontal Research

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“…Another study suggested that the pre-treatment with nicotine reduced a stimulating effect of TNF-α on the gene expression of hBD-2 in HaCaT keratinocytes [47]. It was found that hBD-2 protein level in gingival crevicular fluid was significantly higher in smoker patients with gingivitis than that of non-smoker patients with gingivitis, while hBD-2 level in the gingival crevicular fluid was significantly higher in smoker patients with generalized aggressive periodontitis than that of non-smoker patients with generalized aggressive periodontitis [48]. It was reported that whole cigarette smoke exposure up-regulated hBD-2 and hBD-3 [10].…”

Section: Discussionmentioning

confidence: 81%

Cigarette Smoke Modulates NOD1 Signal Pathway and Human ß Defensins Expression in Human Oral Mucosa

Qian¹,

Wang²,

Gao³

et al. 2015

Cell Physiol Biochem

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Background/Aims: Nucleotide binding oligomerization domain 1 (NOD1) signal pathway and human ß defensins (hBDs) play crucial roles in innate immune. Cigarette smoke has been confirmed to dampen innate immune in some human tissues, such as oral mucosa. The aim of this study was to evaluate potential effects of smoking on NOD1 signaling and hBDs expression in oral mucosa. Methods: Tissue specimens of normal oral mucosa were collected from donors undergoing routine surgical treatment. All 20 participants were classified equally as two groups: non-smokers and smokers. By using Western blotting and immunohistochemistry, we investigated differential expression of crucial molecules in NOD1 signal pathway, hBD-1, -2, and -3 in oral mucosa tissues between non-smokers and smokers. Immortalized human oral mucosal epithelial (Leuk-1) cells were treated with various concentrations of cigarette smoke extract (CSE) for 24h. Western blotting and immunofluorescence assays were performed to study CSE-induced alteration of protein expression. Leuk-1 cells were treated with 4% CSE, iE-DAP (NOD1 agonist), CSE + iE-DAP, BAY 11-7082 (NF-κB inhibitor), 4% CSE + BAY 11-7082, respectively. Real-time PCR and ELISA were performed to detect the mRNA levels and secretion of hBD-1, -2, and -3, respectively. Results: The levels of NOD1, NF-κB, hBD-1 and hBD-3 significantly reduced in oral mucosa tissues of smokers compared with non-smokers. The levels of RIP2 (receptor-interacting protein 2), phospho-NF-κB (P-NF-κB) and hBD-2 remarkably enhanced in oral mucosal tissues of smokers. CSE treatment suppressed NOD1 and NF-κB expression and activated RIP2 and P-NF-κB expression in Leuk-1 cells. The mRNA and secretory levels of hBD-1 and -3 were down-regulated by CSE, while the mRNA and secretory level of hBD-2 were up-regulated by CSE. The iE-DAP or BAY 11-7082 treatment reversed the regulatory effects of CSE on levels of hBDs. Conclusion: The present study indicated that cigarette smoke could potentially modulate the expression of crucial molecules of NOD1 signal pathway and hBDs in human oral mucosal epithelium. NOD1 signal pathway could play an important role in the regulatory effects of CSE on hBDs levels in oral mucosal epithelial cells.

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“…The diagnosis of AR was made according to the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines (10). Patients who had chronic disease including doctor-diagnosed asthma, whose family members were smokers, and who were using medication including vitamins were not included in the study, because some publications reported that use of vitamins and exposure to smoking affected BD-2 levels (11,12). Twenty-four healthy children who were being followed up in the Outpatient Clinic of Healthy Children and had no known problems, whose parents did not smoke, and who were not using medication were included as the control group.…”

Section: Methodsmentioning

confidence: 99%

Evaluation of nasal fluid β-defensin 2 levels in children with allergic rhinitis

et al. 2017

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Aim: Knowledge about the role of the innate immune system in the pathogenesis of allergic diseases has been expanding in recent years. Defensins are antimicrobial peptides that are components of the innate immune system. Defensins have strong efficacy against bacterial, viral, and fungal infections. Moreover, they have regulatory functions in many physiologic processes such as antitumoral immunity, chemotaxis, inflammation, and wound healing. In this study, we aimed to investigate β-defensin 2 levels in the nasal fluids of children with allergic rhinitis. Material and Methods:Study and control groups consisted of 28 patients with newly diagnosed allergic rhinitis who were not taking any medication, and 23 healthy children. Skin prick tests were performed on patients with allergic rhinitis and disease severity was assessed using the total symptom score. Nasal fluid samples were obtained using a modified polyurethane sponge absorption method from patients and control subjects. Nasal fluid β-defensin 2 levels were determined using an enzyme-linked immunosorbent assay (ELISA). Results:The median value of nasal fluid β-defensin 2 levels were 173.8 pg/mL (interquartile range; 54.8-205.9 pg/mL) in allergic rhinitis group and 241.6 pg/mL (163.5-315.2 pg/mL) in the control group. There was a statistically significant difference between the two groups (p=0.01). Moreover, nasal fluid β-defensin 2 levels showed a significant negative correlation with total symptom scores (rho= -0.78, p<0.001). Conclusions:Children with allergic rhinitis have reduced nasal fluid β-defensin 2 levels compared with controls, and β-defensin 2 levels were negatively correlated with disease severity. A more definite understanding of the roles of defensins and other antimicrobial peptides in allergic inflammation can open up new horizons in the management and treatment of these common diseases. (Turk Pediatri Ars 2017; 52: 79-84)

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Gingival crevicular fluid levels of human beta‐defensin‐2 and cathelicidin in smoker and non‐smoker patients: a cross‐sectional study

Cited by 23 publications

References 55 publications

Antimicrobial peptides as a possible interlink between periodontal diseases and its risk factors: A systematic review

Antimicrobial peptides as a possible interlink between periodontal diseases and its risk factors: A systematic review

Cigarette Smoke Modulates NOD1 Signal Pathway and Human ß Defensins Expression in Human Oral Mucosa

Evaluation of nasal fluid β-defensin 2 levels in children with allergic rhinitis

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