scholarly journals Basic research on the potential therapeutic effect of endogenous anti-inflammatory molecule DEL-1 on periodontal disease

Author(s):  
Tomoki Maekawa
2014 ◽  
Vol 4 (1_suppl) ◽  
pp. s-0034-1376756-s-0034-1376756
Author(s):  
Makarand V. Risbud

2021 ◽  
Vol 22 (7) ◽  
pp. 3728
Author(s):  
Masahiro Hatasa ◽  
Sumiko Yoshida ◽  
Hirokazu Takahashi ◽  
Kenichi Tanaka ◽  
Yoshihito Kubotsu ◽  
...  

Periodontal disease is an inflammatory disease caused by pathogenic oral microorganisms that leads to the destruction of alveolar bone and connective tissues around the teeth. Although many studies have shown that periodontal disease is a risk factor for systemic diseases, such as type 2 diabetes and cardiovascular diseases, the relationship between nonalcoholic fatty liver disease (NAFLD) and periodontal disease has not yet been clarified. Thus, the purpose of this review was to reveal the relationship between NAFLD and periodontal disease based on epidemiological studies, basic research, and immunology. Many cross-sectional and prospective epidemiological studies have indicated that periodontal disease is a risk factor for NAFLD. An in vivo animal model revealed that infection with periodontopathic bacteria accelerates the progression of NAFLD accompanied by enhanced steatosis. Moreover, the detection of periodontopathic bacteria in the liver may demonstrate that the bacteria have a direct impact on NAFLD. Furthermore, Porphyromonas gingivalis lipopolysaccharide induces inflammation and accumulation of intracellular lipids in hepatocytes. Th17 may be a key molecule for explaining the relationship between periodontal disease and NAFLD. In this review, we attempted to establish that oral health is essential for systemic health, especially in patients with NAFLD.


2011 ◽  
Vol 46 (2) ◽  
pp. 269-279 ◽  
Author(s):  
M. R. Guimarães ◽  
L. S. Coimbra ◽  
S. G. de Aquino ◽  
L. C. Spolidorio ◽  
K. L. Kirkwood ◽  
...  

Author(s):  
Hiroshi TAWARA ◽  
Miyoko MATSUE ◽  
Eisuke MIYAKAWA ◽  
Shinya YAMAGUCHI ◽  
Johng-ha LEE ◽  
...  

2018 ◽  
Vol 27 (9) ◽  
pp. 1352-1367 ◽  
Author(s):  
Fu Yuan Yang ◽  
Rui Chen ◽  
Xiaohu Zhang ◽  
Biao Huang ◽  
Lai Ling Tsang ◽  
...  

Mesenchymal stem cell (MSC)-based cell therapy has been demonstrated as a promising strategy in the treatment of inflammatory bowel disease (IBD), which is considered an immune disease. While the exact mechanisms underlying the therapeutic effect of MSCs are still unclear, MSCs display anti-inflammatory and immunomodulatory effects by interacting with various immunoregulatory cells. Our previous studies have shown that MSCs can be preconditioned and deconditioned with enhanced cell survival, differentiation and migration. In this study, we evaluated the effect of preconditioning on the immunoregulatory function of human umbilical cord-derived MSCs (hUCMSCs) and their therapeutic effect on treating IBD. Our results show that intraperitoneal administration of deconditioned hUCMSCs (De-hUCMSCs) reduces the disease activity index (DAI), histological colitis score and destruction of the epithelial barrier, and increases the body weight recovery more intensively than that of un-manipulated hUCMSCs. In addition, De-hUCMSCs but not hUCMSCs elicit anti-apoptotic effects via induction of the ERK pathway during the early stage of IBD development. In vitro co-culture studies indicate that De-hUCMSCs suppress T-cell proliferation and activation more markedly than hUCMSCs. Moreover, De-hUCMSCs block the induction of inflammatory cytokines such as tumor necrosis factor (TNF)α and interleukin (IL)-2, while promoting the secretion of the anti-inflammatory cytokine IL-10 in T-cells. Mechanically, we find that prostaglandin E2 (PGE2) secretion is significantly increased in De-hUCMSCs, the suppression of which dramatically abrogates the inhibitory effect of De-hUCMSCs on T-cell activation, implying that the crosstalk between De-hUCMSCs and T-cells is mediated by PGE2. Together, we have demonstrated that preconditioning enhances the immunosuppressive and therapeutic effects of hUCMSCs on treating IBD via increased secretion of PGE2.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Adeyinka C Adejumo ◽  
Samson Alliu ◽  
Oluwole M Adegbala ◽  
Nnaemeka E Onyeakusi ◽  
Tokunbo O Ajayi ◽  
...  

Introduction: Cannabis is a commonly utilized recreational substance which contains numerous bioactive agents. As more states legalize the use of marijuana, it’s effect on various disease conditions is expected to become more pronounced. Cannabis’ anti-inflammatory effects could suppress pro-inflammatory conditions. For example, chronic inflammation with extracellular matrix degradation resulting in weakness and abnormal dilatation of the aortic wall is a hallmark of Aortic Aneurysm. We, therefore, hypothesized that cannabis users would have less prevalence of aortic aneurysms. Objective: To identify the relationship between chronic cannabis use (CU) and diagnosis of aortic aneurysms (AA) among hospitalized patients. Methods: After selecting patients who were 55 years and above from 2012 to 2014 National Inpatient Sample database, we identified those who had a diagnosis of Aortic Aneurysm and those who utilize Cannabis. We then stratified the CU into two groups: nondependent (NDU) and dependent users (DU). Using logistic regression, we estimated the Odds Ratio (AOR) after controlling for numerous factors. Results: In our total 10,461,694 sample, 99.6% (10,419,972) are non-users, 0.37% (38,514) are nondependent users and 0.03% (3,208) are dependent users. About 3.21% (336,202) of the patients had a diagnosis of AA versus 96.79% (10,125,492) without a diagnosis of AA. Compared to non-users of cannabis, the odds of AA is about 35% less among CU (AOR 0.66[0.62-0.71]), 40% less among DU (aOR 0.58[0.44-0.76]), and 33% less among NDU (AOR 0.67[0.62-0.72]). The odds of AA was lower in females (AOR 0.61[0.60-0.610]), but higher in many conditions such as: among >=65 years (AOR 1.16[1.15-1.17]), tobacco users (AOR 1.18[1.17-1.19]), predisposing hereditary conditions (AOR 5.31[4.60-6.13]), and atherosclerosis (AOR 3.04[3.00-3.08]). Conclusions: Our result shows that Cannabis use is associated with less occurrence of AA. Cannabidiol, an anti-inflammatory alkaloid in Cannabis could potentially suppress the release of proteolytic inflammatory mediators which might be responsible for the gradual weakening of the vascular walls. We recommend more basic research to evaluate this effect of Cannabidiol.


2020 ◽  
Vol 21 (22) ◽  
pp. 8870 ◽  
Author(s):  
Jakub Mlost ◽  
Marta Bryk ◽  
Katarzyna Starowicz

Cannabis has a long history of medical use. Although there are many cannabinoids present in cannabis, Δ9tetrahydrocannabinol (Δ9-THC) and cannabidiol (CBD) are the two components found in the highest concentrations. CBD itself does not produce typical behavioral cannabimimetic effects and was thought not to be responsible for psychotropic effects of cannabis. Numerous anecdotal findings testify to the therapeutic effects of CBD, which in some cases were further supported by research findings. However, data regarding CBD’s mechanism of action and therapeutic potential are abundant and omnifarious. Therefore, we review the basic research regarding molecular mechanism of CBD’s action with particular focus on its analgesic potential. Moreover, this article describes the detailed analgesic and anti-inflammatory effects of CBD in various models, including neuropathic pain, inflammatory pain, osteoarthritis and others. The dose and route of the administration-dependent effect of CBD, on the reduction in pain, hyperalgesia or allodynia, as well as the production of pro and anti-inflammatory cytokines, were described depending on the disease model. The clinical applications of CBD-containing drugs are also mentioned. The data presented herein unravel what is known about CBD’s pharmacodynamics and analgesic effects to provide the reader with current state-of-art knowledge regarding CBD’s action and future perspectives for research.


Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1153 ◽  
Author(s):  
Takuji Hayashi ◽  
Kazutoshi Fujita ◽  
Makoto Matsushita ◽  
Norio Nonomura

Prostate cancer is the most common type of cancer and the leading cause of cancer deaths among men in many countries. Preventing progression is a major concern for prostate cancer patients on active surveillance, patients with recurrence after radical therapies, and patients who acquired resistance to systemic therapies. Inflammation, which is induced by various factors such as infection, microbiome, obesity, and a high-fat diet, is the major etiology in the development of prostate cancer. Inflammatory cells play important roles in tumor progression. Various immune cells including tumor-associated neutrophils, tumor-infiltrating macrophages, myeloid-derived suppressor cells, and mast cells promote prostate cancer via various intercellular signaling. Further basic studies examining the relationship between the inflammatory process and prostate cancer progression are warranted. Interventions by medications and diets to control systemic and/or local inflammation might be effective therapies for prostate cancer progression. Epidemiological investigations and basic research using human immune cells or mouse models have revealed that non-steroidal anti-inflammatory drugs, metformin, statins, soy isoflavones, and other diets are potential interventions for preventing progression of prostate cancer by suppressing inflammation. It is essential to evaluate appropriate indications and doses of each drug and diet.


2005 ◽  
Vol 276 (1-2) ◽  
pp. 219-225 ◽  
Author(s):  
Noor Mohamed Jameel ◽  
Brigitte M. Frey ◽  
Felix J. Frey ◽  
T. Veerabasappa Gowda ◽  
Bannikuppe S. Vishwanath

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