scholarly journals The expression of RANKL, OPG and TNF-α on cells and/or tissues around alveolar bone during early-stage rat tooth germ development

2011 ◽  
Vol 15 (2) ◽  
pp. 39-43
Author(s):  
Fumiko Fukuhara ◽  
Kenichi Matsuzaka ◽  
Sachie Senzui ◽  
Seikou Shintani ◽  
Takashi Inoue
Keyword(s):  
Alveolar Bone ◽  
Early Stage ◽  
Tooth Germ ◽  
Tnf Α ◽  
Tooth Germ Development

Febuxostat Attenuates the Progression of Periodontitis in Rats

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Naseratun Nessa ◽  
Miyuki Kobara ◽  
Hiroe Toba ◽  
Tetsuya Adachi ◽  
Toshiro Yamamoto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Bone Resorption ◽  
Alveolar Bone ◽  
Alveolar Bone Loss ◽  
Gingival Tissue ◽  
Systemic Effects ◽  
Rt Pcr ◽  
Tnf Α ◽  
And Oxidative Stress

Introduction: Periodontitis is a lifestyle-related disease that is characterized by chronic inflammation in gingival tissue. Febuxostat, a xanthine oxidase inhibitor, exerts anti-inflammatory and antioxidant effects. Objective: The present study investigated the effects of febuxostat on periodontitis in a rat model. Methods: Male Wistar rats were divided into 3 groups: control, periodontitis, and febuxostat-treated periodontitis groups. Periodontitis was induced by placing a ligature wire around the 2nd maxillary molar and the administration of febuxostat (5 mg/kg/day) was then initiated. After 4 weeks, alveolar bone loss was assessed by micro-computed tomography and methylene blue staining. The expression of osteoprotegerin (OPG), a bone resorption inhibitor, was detected by quantitative RT-PCR and immunological staining, and the number of osteoclasts in gingival tissue was assessed by tartrate-resistant acid phosphatase staining. The mRNA and protein expression levels of the proinflammatory cytokines, tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β), in gingival tissue were measured using quantitative RT-PCR and immunological staining. Oxidative stress in gingival tissue was evaluated by the expression of 4-hydroxy-2-nonenal (4-HNE), and 8-hydroxy-2-deoxyguanosine (8-OHdG). To clarify the systemic effects of periodontitis, blood pressure and glucose tolerance were examined. Results: In rats with periodontitis, alveolar bone resorption was associated with reductions in OPG and increases in osteoclast numbers. The gingival expression of TNF-α, IL-1β, 4-HNE, and 8-OHdG was up-regulated in rats with periodontitis. Febuxostat significantly reduced alveolar bone loss, proinflammatory cytokine levels, and oxidative stress. It also attenuated periodontitis-induced glucose intolerance and blood pressure elevations. Conclusion: Febuxostat prevented the progression of periodontitis and associated systemic effects by inhibiting proinflammatory mediators and oxidative stress.

scholarly journals Halofuginone functions as a therapeutic drug for chronic periodontitis in a mouse model

2020 ◽  
Vol 34 ◽  
pp. 205873842097489
Author(s):  
Jiang Wang ◽  
Bo Wang ◽  
Xin Lv ◽  
Yingjie Wang
Keyword(s):  
Alveolar Bone ◽  
Immune Cell ◽  
Critical Role ◽  
Therapeutic Drug ◽  
Mice Model ◽  
T Helper 17 ◽  
Th17 Cell Differentiation ◽  
Tnf Α

Periodontitis is an inflammatory disease caused by host immune response, resulting in a loss of periodontium and alveolar bone. Immune cells, such as T cells and macrophages, play a critical role in the periodontitis onset. Halofuginone, a natural quinazolinone alkaloid, has been shown to possess anti-fibrosis, anti-cancer, and immunomodulatory properties. However, the effect of halofuginone on periodontitis has never been reported. In this study, a ligature-induced mice model of periodontitis was applied to investigate the potential beneficial effect of halofuginone on periodontitis. We demonstrated that the administration of halofuginone significantly reduced the expression levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in vivo, and markedly suppressed immune cell infiltration into the infected sites. Furthermore, we also observed that halofuginone treatment blocked the T-helper 17 (Th17) cell differentiation in vivo and in vitro. We demonstrated for the first time that halofuginone alleviated the onset of periodontitis through reducing immune responses.

Disturbed tooth germ development in the absence of MINT in the cultured mouse mandibular explants

2010 ◽  
Vol 38 (2) ◽  
pp. 777-784 ◽  
Author(s):  
Ming-Hui Zhu ◽  
Wen-Bo Dong ◽  
Guang-Ying Dong ◽  
Ping Zhang ◽  
Yong-Jin Chen ◽  
...  
Keyword(s):  
Tooth Germ ◽  
Tooth Germ Development

scholarly journals Is Inflammation a Friend or Foe for Orthodontic Treatment?: Inflammation in Orthodontically Induced Inflammatory Root Resorption and Accelerating Tooth Movement

2021 ◽  
Vol 22 (5) ◽  
pp. 2388
Author(s):  
Masaru Yamaguchi ◽  
Shinichi Fukasawa
Keyword(s):  
Inflammatory Mediators ◽  
Orthodontic Treatment ◽  
Alveolar Bone ◽  
Tooth Movement ◽  
Root Resorption ◽  
Orthodontic Tooth Movement ◽  
Tnf Α ◽  
Orthodontic Forces ◽  
Necrosis Factor

The aim of this paper is to provide a review on the role of inflammation in orthodontically induced inflammatory root resorption (OIIRR) and accelerating orthodontic tooth movement (AOTM) in orthodontic treatment. Orthodontic tooth movement (OTM) is stimulated by remodeling of the periodontal ligament (PDL) and alveolar bone. These remodeling activities and tooth displacement are involved in the occurrence of an inflammatory process in the periodontium, in response to orthodontic forces. Inflammatory mediators such as prostaglandins (PGs), interleukins (Ils; IL-1, -6, -17), the tumor necrosis factor (TNF)-α superfamily, and receptor activator of nuclear factor (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) are increased in the PDL during OTM. OIIRR is one of the accidental symptoms, and inflammatory mediators have been detected in resorbed roots, PDL, and alveolar bone exposed to heavy orthodontic force. Therefore, these inflammatory mediators are involved with the occurrence of OIIRR during orthodontic tooth movement. On the contrary, regional accelerating phenomenon (RAP) occurs after fractures and surgery such as osteotomies or bone grafting, and bone healing is accelerated by increasing osteoclasts and osteoblasts. Recently, tooth movement after surgical procedures such as corticotomy, corticision, piezocision, and micro-osteoperforation might be accelerated by RAP, which increases the bone metabolism. Therefore, inflammation may be involved in accelerated OTM (AOTM). The knowledge of inflammation during orthodontic treatment could be used in preventing OIIRR and AOTM.

3-methyadenine inhibits lipopolysaccharides-induced pulmonary inflammation at the early stage of silicosis via blocking NF-κB signaling pathway

2021 ◽  
pp. 074823372110394
Author(s):  
Yujing Zhang ◽  
Shuai Huang ◽  
Shiyi Tan ◽  
Mingke Chen ◽  
Shang Yang ◽  
...  
Keyword(s):  
Lung Injury ◽  
Late Stage ◽  
Caspase 3 ◽  
Inflammatory Responses ◽  
Early Stage ◽  
Pulmonary Inflammation ◽  
Mechanism Study ◽  
Silica Dust ◽  
Tnf Α

Occupational exposure to silica dust is related to pulmonary inflammation and silicosis. Lipopolysaccharides (LPSs) could aggravate apoptosis in alveolar macrophages (AMs) of human silicosis through autophagy, yet how the reduction of autophagy attenuated LPS-induced lung injury and the related mechanisms need to be investigated. In the study, we aim to understand the role of 3-methyladenine (3-MA), an inhibitor of autophagy, in LPS-mediated inflammatory responses and fibrosis. We collected AMs from observers/silicosis patients. The results showed that LPS induced NF-κB-related pulmonary inflammation in observers and silicosis patients, as confirmed by an increase in the expression of IL-1β, IL-6, TNF-α, and p65, which could be inhibited by 3-MA treatment. In mice models, at the early stage (7d) of silicosis, but not the late (28d) stage, blocking autophagy reversed the increased levels of IL-1β, IL-6, TNF-α, and p65 caused by LPS. Mechanism study revealed that LPS triggered the expression of LC3 II, p62, and cleaved caspase-3 at the early stage exposed to silica, which could be restored by 3-MA, while there was no difference in the expression of LAMP1 either at the early or late stage of silicosis in different groups. Similarly, 3-MA treatment did not prevent fibrosis characterized by destroyed alveoli, collagen deposition, and increased expression of α-SMA and Col-1 induced by LPS at the late stage of silicosis. The results suggested that 3-MA has a role in the protection of lung injury at the early stage of silicosis and provided an experimental basis for preventive strategies of pulmonary inflammation and silicosis.

Evaluation of urinary TNF-α and KIM-1 biomarkers in T2DM in Upper Egypt

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Magdy EL Sharkawy ◽  
Samir K Abdul-Hamid ◽  
Tarek T Elmelegy ◽  
Mohammed F Adawy
Keyword(s):  
Diabetic Nephropathy ◽  
Early Stage ◽  
Clinical Syndrome ◽  
Diabetic Patients ◽  
University Hospitals ◽  
Type 2 Diabetic Patients ◽  
Cross Sectional ◽  
Tnf Α ◽  
Type 2 Diabetic

Abstract Background Diabetes mellitus (DM) is the most frequent cause of chronic kidney failure in both developed and developing countries. Diabetic nephropathy, is a clinical syndrome characterized by albuminuria (>300 mg/day) with permanent and irreversible decrease in glomerular filtration rate (GFR). Aim of the Work To study the role of urinary TNF-α and urine KIM-1 in type 2 diabetic patients as predictors of DN comparative with albuminuria. Patients and Methods This is a cross-sectional study which include 90 type-2 diabetic patients and 30 controls selected from the outpatient clinic of Assiut University hospitals. All patients gave an informed consent and approval for the study was obtained from the IRB committee of the Assiut Medical Faculty. The recruited patients were divided into three groups: Normo-albuminuria Group (A) (n = 30): UACR less than 30 mg/gm, Microalbuminuria Group (B) (n = 30): UACR between 30-299 mg/gm and Macro-albuminuria Group (C) (n = 30): UACR equal or more than 300 mg/gm. Assess Urinary TNF-α and urine KIM-1 in comparision with albuminuria. Results Urinary KIM-1 and urinary TNF-α are statically significant with albuminuria in patients in the early stage of diabetic nephropathy (eGFR _60 mL/min/1.73 m2).Also there are statically significance between patients with macroalbuminuria than microalbuminuria. Conclusion The results of this study recommend the use of KIM-1 and TNF-α as good predictors of early detection of development of diabetic nephropathy.

In situ cytokine gene expression in early stage of virulent Newcastle disease in chickens

2021 ◽  
pp. 030098582110459
Author(s):  
Corrie Brown ◽  
Jian Zhang ◽  
Mary Pantin-Jackwood ◽  
Kiril Dimitrov ◽  
Helena Lage Ferreira ◽  
...  
Keyword(s):  
B Cells ◽  
Newcastle Disease ◽  
Early Stage ◽  
Severe Disease ◽  
Cytokine Gene Expression ◽  
Lymphoid Tissues ◽  
Tnf Α ◽  
Virulent Newcastle Disease Virus ◽  
Ifn Γ

Selected lymphoid and reproductive tissues were examined from groups of 3-week-old chickens and 62-week-old hens that were inoculated choanally and conjunctivally with 106 EID50 of a virulent Newcastle disease virus (NDV) isolate from the California 2018–2020 outbreak, and euthanized at 1, 2, and 3 days postinfection. In the 3-week-old chickens, immunohistochemistry for NDV and for T and B cell lymphocytes, as well as in situ hybridization for IL-1β, IL-6, IFN-γ, and TNF-α revealed extensive expression of IL-1β and IL-6 in lymphoid tissues, often coinciding with NDV antigen. IFN-γ was only expressed infrequently in the same lymphoid tissues, and TNF-α was rarely expressed. T-cell populations initially expanded but by day 3 their numbers were below control levels. B cells underwent a similar expansion but remained elevated in some tissues, notably spleen, cecal tonsils, and cloacal bursa. Cytokine expression in the 62-week-old hens was overall lower than in the 3-week-old birds, and there was more prolonged infiltration of both T and B cells in the older birds. The strong pro-inflammatory cytokine response in young chickens is proposed as the reason for more severe disease.

scholarly journals Trehalose 6,6′-Dimycolate (Cord Factor) of Mycobacterium tuberculosis Induces Corneal Angiogenesis in Rats

2000 ◽  
Vol 68 (10) ◽  
pp. 5991-5997 ◽  
Author(s):  
Norio Saita ◽  
Nagatoshi Fujiwara ◽  
Ikuya Yano ◽  
Kazuhiko Soejima ◽  
Kazuo Kobayashi
Keyword(s):  
Mycobacterium Tuberculosis ◽  
Neutralizing Antibodies ◽  
Early Stage ◽  
Vascular Endothelial ◽  
Cytokine Network ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Cord Factor ◽  
Factor Alpha ◽  
Endothelial Growth Factor

ABSTRACT Neovascularization or angiogenesis is required for the progression of chronic inflammation. The mechanism of inflammatory neovascularization in tuberculosis remains unknown. Trehalose 6,6′-dimycolate (TDM) purified from Mycobacterium tuberculosis was injected into rat corneas. TDM challenge provoked a local granulomatous response in association with neovascularization. Neovascularization was seen within a few days after the challenge, with the extent of neovascularization being dose dependent, although granulomatous lesions developed 14 days after the challenge. Cytokines, including tumor necrosis factor alpha (TNF-α), interleukin-8 (IL-8), IL-1β, and vascular endothelial growth factor (VEGF), were found in lesions at the early stage (within a few days after the challenge) and were detectable until day 21. Neovascularization was inhibited substantially by neutralizing antibodies to VEGF and IL-8 but not IL-1β. Treatment with anti-TNF-α antibodies resulted in partial inhibition. TDM possesses pleiotropic activities, and the cytokine network plays an important role in the process of neovascularization.

scholarly journals Analysis of factors affected the SARS-CoV-2 viral shedding time of COVID-19 patients in Anhui, China: a retrospective study

2020 ◽  
Author(s):  
You-Hui Tu ◽  
Yuan-Yuan Wei ◽  
Da-Wei Zhang ◽  
Chang-Shan Chen ◽  
Xian-Wei Hu ◽  
...  
Keyword(s):  
T Lymphocytes ◽  
Early Stage ◽  
Serum Glucose ◽  
Viral Shedding ◽  
Cd8 T Lymphocytes ◽  
Cd8 T Lymphocyte ◽  
Tnf Α ◽  
Epidemiological Risk ◽  
Group A ◽  
Group B

Abstract Background The epidemic of Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) has spread worldwide, but the factors that may affect the SARS-CoV-2 viral shedding time in coronavirus disease 2019 (COVID-19) patients were rarely reported. Methods We retrospectively recruited 40 confirmed common COVID-19 patients and classified them into two groups according to the SARS-CoV-2 viral shedding time (group A (less than 10 days) and group B (10 days or more)). The demographic, laboratory parameters and chest computed tomography (CT) features on admission and the 3 rd day after treatment were analyzed respectively. Results Fourteen patients were in group A and 26 patients in group B, the median SARS-CoV-2 viral shedding time of the two groups was 7 and 16 days respectively. Compared to the group A, the comorbidity, epidemiological risk history, serum glucose and CD4/8 on admission were significantly higher in the group B (P<0.05). On the 3 rd day after treatment, the group B got significantly higher IL-6, IL-2R, TNF-α and CD4/8, and lower platelet and CD8 + T lymphocyte counts than group A (P<0.05). Logistic regression analyses revealed that the higher epidemiological risk history, serum glucose and CD4/8 on admission were significantly associated with a longer SARS-CoV-2 viral shedding time (OR=7.5, 11.41, 9.21 respectively, P<0.05), as well as the higher TNF-α and lower CD8 + T lymphocytes on the 3 rd day after treatment (OR=2.36, 0.98 respectively, P<0.05). Conclusions Our study provides the evidence that the prolonged SARS-CoV-2 viral shedding time might be correlated with the patients’ epidemiological risk history, as well as the serum glucose and CD4/8 on admission, TNF-α and CD8 + T lymphocytes on the 3 rd day after treatment. Our result may help clinicians to distinguish the patients with a prolonged viral shedding time at the early stage.

Sign in / Sign up

Export Citation Format

Share Document