Comparison of circulating tumour necrosis factor superfamily cytokines in periodontitis patients undergoing supportive therapy: a case-controlled cross-sectional study comparing smokers and non-smokers in health and disease

Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) reportedly promotes, or conversely, resolves inflammation in asthma. In this study of TRAIL and cell receptors in sputum, bronchoalveolar lavage and biopsy from subjects in the Severe Asthma Research Program at Wake Forest, the high TRAIL group had significant increases in all leucocytes, and was associated with increased type 1, type 2 and type 17 cytokines, but not type 9 interleukin 9. Two variants at loci in the TRAIL gene were associated with higher sputum levels of TRAIL. Increased TRAIL decoy receptor R3/DcR1 was observed on sputum leucocytes compared with death receptor R1/DR4, suggesting reduced apoptosis and prolonged cellular inflammation.

Download Full-text

P3509Leukocyte derived tumour necrosis factor modulates cardiac function in health and disease

European Heart Journal ◽

10.1093/eurheartj/ehz745.0373 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

S Walker ◽

A Gutierrez Del Arroyo ◽

J Sanchez ◽

G L Ackland

Keyword(s):

Ejection Fraction ◽

Cardiac Function ◽

Tumour Necrosis Factor ◽

Tumour Necrosis ◽

Cardiac Injury ◽

Cardiac Cells ◽

Health And Disease ◽

Deficient Mice ◽

Necrosis Factor

Abstract Purpose Tumour necrosis factor alpha (TNFα) regulates both normal and pathophysiological cardiac function. The regulatory role of TNFα derived from different sources (leukocyte versus cardiac cells) in cardiac physiology is unclear. Deficiency of iRhom2 protein prevents circulating immune cells from shedding TNFα (and CD62L, an adhesion molecule essential for effective immune function). Here we investigated the role of leukocyte derived TNFα in constitutive cardiac function and after cardiac injury. Methods Adult iRhom2-deficient mice (KO) and wildtype (Wt) littermates, of both genders, underwent echocardiography to assess cardiac physiologic function at least 1 week before receiving a single dose of isoproterenol (300mg/kg IP) to induce cellular death in 10% of the cardiomyoctes [1]. Cardiac echocardiography was repeated 36 hours after isoproterenol. Peripheral and cardiac-resident leukocytes were phenotyped by flow cytometry and molecular markers of cardiac stress (atrial and brain natriuretic protein, ANP, BNP) and inflammation (NFkB) were quantified using RT-PCR. Results Peripheral leukocytes from iRhom2 KO mice failed to shed CD62L in response to isoproterenol induced cardiac injury (e.g. neutrophils CD62L Mean Fluorescence Intensity KO: 9149±4616, Wt: 972±558, p<0.0001, n=9). iRhom2-deficient mice had higher cardiac output at baseline (KO 23±2 mL/min, n=11) compared to their wildtype littermates (Wt 18±3 mL/min, n=9). Wild type mice increased contractility after isoproterenol (Wt ejection fraction: baseline 60±6%, isoproterenol 68±6%, n=8) whilst iRhom2-deficient mice were unable to (KO ejection fraction: baseline 66±9%, isoproterenol 61±5%, n=8). ANP and BNP mRNA were elevated in ventricular tissue of iRhom2-knockout mice after isoproterenol, when compared to naïve tissue (ANP 2ΔCT: 3x increase, BNP 2ΔCT: 1.6x increase) whereas only ANP was elevated in wildtypes (ANP 2ΔCT: 2.7x increase, BNP 2ΔCT: 0.9x increase). No difference in immune cell infiltration of ventricular cardiac tissue was observed (number of CD45+ cells KO: 3014±3482, Wt: 2555±1411, p=0.7, n=9) NFkB mRNA was upregulated at baseline (2ΔCT KO: 0.2±0.08, Wt: 0.1±0.09) suggesting constitutive cardiac inflammation in iRhom2-deficient mice. Conclusions Inability to shed CD62L and TNFα is associated with constitutive and acquired cardiac dysfunction in iRhom2-deficient mice. These data support the hypothesis that leukocyte-derived TNFα is required for maintaining cardiac function in health and disease. Acknowledgement/Funding National Institute of Academic Anaesthesia/Royal College of Anaesthetists/British Journal of Anaesthesia; National Institute for Health Research

Download Full-text

Potential Protective Effect of Dietary Intake of Non-α-Tocopherols on Cellular Aging Markers Mediated by Tumor Necrosis Factor-α in Prediabetes: A Cross-Sectional Study of Chinese Adults

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/7396801 ◽

2020 ◽

Vol 2020 ◽

pp. 1-9

Author(s):

Yiwen Liu ◽

Chifa Ma ◽

Pingping Li ◽

Chunxiao Ma ◽

Shuli He ◽

...

Keyword(s):

Glucose Tolerance ◽

Dietary Intake ◽

Tumor Necrosis ◽

Cross Sectional Study ◽

Cellular Aging ◽

Sectional Study ◽

Chinese Adults ◽

Cross Sectional ◽

Glucose Tolerance Status ◽

Necrosis Factor

It remains unknown how different glucose tolerance status affects the relationships between dietary intake of different tocopherol isoforms (α-, β-, γ-, and δ-tocopherol) and cellular aging, oxidative stress, and inflammatory markers. The authors conducted a cross-sectional study among 582 Chinese adults with different glucose tolerance status to explore the association between dietary intake of different tocopherol isoforms and cellular aging, oxidative stress, and inflammatory markers. The inverse correlations between non-α-tocopherols and tumor necrosis factor-alpha (TNF-α) varied substantially across different glucose tolerance status, with the strongest observed in prediabetes (r=−0.33 for β-/γ-tocopherol, r=−0.37 for δ-tocopherol, p<0.01), followed by normal glucose tolerance (NGT). While such correlations were abolished in established diabetes. Furthermore, within prediabetes, the strongest inverse correlations between non-α-tocopherols and TNF-α were observed in impaired fasting glucose (IFG) (r=−0.42 for β-/γ-tocopherol, r=−0.55 for δ-tocopherol, p<0.01), while such correlations were significantly attenuated in individuals with impaired glucose tolerance (IGT) and IFG+IGT. And mediation model analysis displayed that TNF-α mediated the protective effect of non-α-tocopherols on leukocyte telomere length and mitochondrial DNA copy number, which was uniquely observed in prediabetes, while such mediation effect was statistically nonsignificant in NGT and established diabetes. In conclusion, our findings indicate that dietary intake of non-α-tocopherols might protect against cellular aging markers mediated by TNF-α in prediabetes. Individuals with prediabetes, especially for IFG, might benefit from increasing dietary intake of non-α-tocopherol in alleviating inflammation and cellular aging, which might provide a new dietary avenue for delaying diabetes onset.

Download Full-text

Prevalence of Peri-Implantitis: A Multi-Centered Cross-Sectional Study on 248 Patients

Dentistry Journal ◽

10.3390/dj8030080 ◽

2020 ◽

Vol 8 (3) ◽

pp. 80

Author(s):

Tommaso Weinstein ◽

Tommaso Clauser ◽

Massimo Del Fabbro ◽

Matteo Deflorian ◽

Andrea Parenti ◽

...

Keyword(s):

Bone Loss ◽

Supportive Therapy ◽

Cross Sectional Study ◽

Smoking Habits ◽

Sectional Study ◽

Related Factors ◽

Pocket Depth ◽

Cross Sectional ◽

History Of ◽

Implant Therapy

The aim of this multicenter cross-sectional study was to determine the prevalence of peri-implantitis and to assess its association with several patient- and implant-related factors. Patients with at least one implant, who came for a recall visit to one of the four centers over a period of five months, were enrolled. Presence of peri-implantitis (defined as bleeding on probing, exudate/suppuration, bone loss > 0.2 mm/year and increased pocket depth) and several other variables (e.g., smoking habits, history of periodontitis, diabetes) were recorded. Out of 248 enrolled patients (1162 implants), 10 patients had at least one implant with peri-implantitis (4.03%); a total of 14 implants were affected (1.20%). A statistically significant association between peri-implantitis and diabetes was found (OR 8.65; CI: 1.94–38.57). Smoking more than 10 cigarettes per day (OR: 0.53; CI 0.03–9.45) and history of periodontitis (OR: 2.42; CI: 0.49–11.89) were not found to be statistically associated with peri-implantitis. Even if implant therapy is a consolidated treatment, biological complications do happen. Strict supportive therapy recalls could lead to lower rates of peri-implantitis and earlier diagnosis.

Download Full-text