Smoking reduces cathelicidin LL‐37 and human neutrophil peptide 1–3 levels in the gingival crevicular fluid of patients with periodontitis

Soldati, Kahena Rodrigues; Toledo, Felipe A.; Aquino, Sabrina García de; Rossa, Carlos; Deng, Dongmei; Zandim-Barcelos, Daniela Leal

doi:10.1002/jper.20-0098

Cited by 8 publications

(7 citation statements)

References 49 publications

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“…And NP-1 has been shown to promote immune sterilization in vivo by increasing the ability of macrophages [ 31 ] . The results published by Rivas-Santiago and Soldati, et al, who demonstrated that NP-1 was lowered in elderly people [32] and smokers [33] , are consistent with our observation that NP-1 was decreased in cardiac remodeling and hypertrophic cardiomyocytes. While Kou et al found that there was no discernible difference in protein expression between Schwann cells treated with NP-1 and those in the control group [ 25 ] , there are variances between our work and theirs.…”

Section: Discussionsupporting

confidence: 94%

NP-1 Reverses Left Ventricular Remodeling in Hypertension through Inhibiting NF-KB Signaling Pathway

duan

Zhou

Si³

et al. 2022

Preprint

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BACKGROUND Reversing hypertensive ventricular remodeling could reduce cardiovascular disease, but it’s reversal rate is low. Neutrophil Peptide 1 ( NP-1 ) is under intensive investigation as a potential therapeutic agent. But it’s role in hypertensive ventricular remodeling remains unclear. METHODS We collected data from hypertensive patients and measured NP-1 levels using an ELISA. We established hypertensive ventricular remodeling models and then treated with NP-1 or BAY 11-7082, an inhibitor of NF-кB. The cardiac hypertrophy markers and NF-кB factors were detected through HE, Masson, IHC, qPCR, and WB. We also established hypertrophic cardiomyocyte models and then dealt with NP-1 or BAY 11-7082. The myocardial hypertrophy indicators and NF-кB factors were measured by IF, qPCR, and WB. RESULTS We found the NP-1 level was decreased in patients with hypertensive ventricular remodeling. It’s demonstrated that NP-1 expression was decreased in hypertensive ventricular remodeling models. While NP-1 treatment has the potential to raise NP-1 levels and reverse ventricular remodeling. It’s also noticed a decrease with NP-1 in hypertrophic cardiomyocyte models. NP-1 disposal could improve NP-1 expression and reverse cardiomyocyte hypertrophy. Besides, our study found the activation of NF-кB in animal and cell models. And it could be inhibited by dealing with NP-1, which was similar to an inhibitor of NF-кB. CONCLUSIONS NP-1 could reverse ventricular remodeling and cardiomyocyte hypertrophy through inhibiting the activation of NF-кB. This may serve as a potential therapeutic target for cardiovascular disease.

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Section: Discussionsupporting

confidence: 94%

NP-1 Reverses Left Ventricular Remodeling in Hypertension through Inhibiting NF-KB Signaling Pathway

duan

Zhou

Si³

et al. 2022

Preprint

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“…There are few data in the literature concerning factors that could independently impact AMPs levels in biological fluids. No correlation was found between serum cathelicidin levels and race/ethnicity, BMI and body fat percentage in healthy children, but data concerning age, gender or smoke exposure are conflicting [19][20][21][22][23] . Finally, in a study of 115 infants, cord plasma LL-37 levels were three-times higher after normal vaginal delivery compared with Caesarean section 24 .…”

Section: Discussionmentioning

confidence: 96%

LL-37 levels in nasal secretions are associated with the severity of acute bronchiolitis

Papadaki¹,

Marmarinos²,

Τσολιά³

et al. 2020

Preprint

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Objective: Τo investigate the association of serum vitamin D and nasal secretion antimicrobial peptides (AMPs) levels with the severity of acute bronchiolitis. Study design: We conducted a prospective single pediatric tertiary care center cohort study of inpatients aged 0-18 months with a first episode of acute bronchiolitis from November 1st 2014 to April 30th 2017. Disease severity was determined by the length of hospitalization and supplemental hospital data. Qualitative measurements included serum 25(OH)D and nasal secretion LL-37 and β-defensin-2 levels. Correlations were examined with the Mann-Whitney and Kruskal-Wallis criteria for qualitative and the correlation coefficient Spearman’s rho for quantitative factors. Multiple linear and logarithmic regression were performed in order to adjust for confounding factors. Results: The study population consisted of 153 infants and toddlers with mean age 3.6 months (SD: +2.8). The median level of serum 25(OH)D was 51.4 nmol/L (IQR: 29.7-72.2). No association was found between serum 25(OH)D and AMPs nasal secretions levels. Serum 25(OH)D and nasal secretion β-defensin-2 levels were not associated with the severity of bronchiolitis. In contrast, LL-37 levels were inversely associated with the length of hospitalization (rho = -0.340, p = 0.001) and the need for medication use (p = 0.001) and this association remained significant after adjustment for potential confounders. Conclusion: A significant association between LL-37 nasal secretions levels with the severity of acute bronchiolitis was found in hospitalized infants and toddlers. The role of LL-37 in the pathogenesis of bronchiolitis merits further investigation.

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“…Previous studies have reported diminished HNP-1 levels in older people, smokers, people who are toothless or have tooth decay, and people with lipid metabolism disorders or vasodilation responses [60][61][62]. Decreased HNP-1 is associated with aging, decreased immune resistance, lipid metabolism disorders, and a diminished vasodilation response [63,64].…”

Section: Discussionmentioning

confidence: 98%

HNP-1 Reverses Hypertensive Left Ventricular Hypertrophy by Inhibiting the NF-кB Signaling Pathway

Duan,

2023

CVIA

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Background: Human neutrophil peptide-1 (HNP-1) is a commonly investigated therapeutic agent. However, its role in hypertensive left ventricular hypertrophy (HLVH) remains unclear. Methods: We measured HNP-1 levels in patients with hypertension and treated HLVH rat and H9c2 cell hypertrophy models with HNP-1. Cardiomyocyte hypertrophy indexes (i.e., single-cell surface area, left ventricular fibrosis area, BNP levels, and β-MHC levels) were measured with hematoxylin-eosin and Masson’s trichrome staining and WB. NF-кB signaling factors (i.e., IKKβ, p-IKKβ, IкBα, p-IкBα, p65, and p-p65) were measured with WB and qPCR. Finally, inflammatory factors (i.e., IL-6, IL-1α, and TNF-α) were measured with ELISA. Results: HNP-1 levels were lower in the exposure than the control groups (M (95% CI), 48.83 (45.64–52.26) vs. 59.03 (55.62–62.54), P = 0.000). Diminished HNP-1 was associated with HLVH occurrence in patients. HLVH rat and H9c2 cell hypertrophy models revealed elevated cardiomyocyte hypertrophy indexes and NF-кB signaling and inflammatory factors. However, each HNP-1 treatment group showed lower levels of the aforementioned indices than were observed in the model groups. Conclusion: Diminished HNP-1 is a risk factor for HLVH. HNP-1 treatment may reverse HLVH by inhibiting NF-кB signaling pathways.

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Smoking reduces cathelicidin LL‐37 and human neutrophil peptide 1–3 levels in the gingival crevicular fluid of patients with periodontitis

Cited by 8 publications

References 49 publications

NP-1 Reverses Left Ventricular Remodeling in Hypertension through Inhibiting NF-KB Signaling Pathway

NP-1 Reverses Left Ventricular Remodeling in Hypertension through Inhibiting NF-KB Signaling Pathway

LL-37 levels in nasal secretions are associated with the severity of acute bronchiolitis

HNP-1 Reverses Hypertensive Left Ventricular Hypertrophy by Inhibiting the NF-кB Signaling Pathway

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