Synergy of TLR2 and H1R on Cox-2 Activation in Pulpal Cells

2009 ◽  
Vol 89 (2) ◽  
pp. 180-185 ◽  
Author(s):  
C. Park ◽  
S.Y. Lee ◽  
H.J. Kim ◽  
K. Park ◽  
J.S. Kim ◽  
...  
Keyword(s):  
Dental Pulp ◽  
Histamine Receptor ◽  
Cell Type ◽  
Microbial Infection ◽  
Synergistic Activation ◽  
Major Cell Type ◽  
Cox 2 ◽  
Micro Organisms ◽  
Stimulation Of

Although pulp fibroblasts are a major cell type in dental pulp, their roles in microbial recognition and pulpal inflammation are not well-understood. Considering the pivotal role of Toll-like receptors (TLRs) in the recognition of micro-organisms, we hypothesized that TLRs on pulp fibroblasts may induce inflammatory signals in dental pulp. In human pulp fibroblasts, TLR2, 3, 4, and 5 were constitutively expressed. Stimulation of TLR2 and 3 induced the expression of pro-inflammatory genes such as CXCL10, CCL5, and/or Cox-2 in pulp fibroblasts. Interestingly, histamine synergistically activated TLR2-mediated Cox-2 expression and PGE2 production. The synergistic effect of histamine is mediated by histamine receptor-1 (H1R). Studies on the intra-cellular signaling pathways revealed that p38 activation is required for the synergistic activation of Cox-2 by TLR2 and histamine. Analysis of these data suggests that TLR2 on pulp fibroblasts, in concert with H1R, can induce an inflammatory response during microbial infection in dental pulp.

Histamine H2 receptor mediates keratan sulfate secretion in rabbit chondrocytes: role of cAMP

1993 ◽  
Vol 265 (6) ◽  
pp. C1653-C1657 ◽  
Author(s):  
K. Fukuda ◽  
F. Matsumura ◽  
S. Tanaka
Keyword(s):  
Keratan Sulfate ◽  
Histamine Receptor ◽  
Intracellular Camp ◽  
Continuous Exposure ◽  
Short Term ◽  
Single Class ◽  
Histamine H2 Receptor ◽  
H2 Receptor ◽  
Stimulation Of

We obtained evidence for the presence of a single class of histamine H2 receptor on rabbit chondrocytes. Stimulation of these receptors with specific H2 agonists led to an inhibition of keratan sulfate secretion and rapid (15 min) accumulation of intracellular adenosine 3',5'-cyclic monophosphate (cAMP). Factors such as prostaglandin E2 and parathyroid hormone, which stimulate short-term increases in cAMP, also caused a reduction in keratan sulfate secretion. Conversely, cholera toxin and forskolin, which enhance cAMP accumulation over 48 and 4 h, respectively, as well as a continuous exposure to dibutyryl cAMP, stimulated keratan sulfate secretion. These data suggest that intracellular cAMP must be kept above a certain level for a prolonged period to stimulate keratan sulfate secretion. We conclude that inhibition of keratan sulfate secretion is coupled with activation of the H2 histamine receptor.

The role of intracanal medicaments in inhibition of bacteria isolated from root canals of infected primary molars

2019 ◽  
Vol 14 (1) ◽  
pp. 92
Author(s):  
Dr. Maha Abdul- Kareem Mahmood ◽  
Dr. Huda Elias Ali ◽  
Dr. Haraa Khairi Abdul-Kadher
Keyword(s):  
Antimicrobial Activity ◽  
Streptococcus Mutans ◽  
Normal Saline ◽  
Root Canal ◽  
Primary Teeth ◽  
Primary Molars ◽  
Root Canals ◽  
Etiologic Agents ◽  
Micro Organisms

Microbes are considered as the primary etiologic agents in endodontic diseases.Disinfection of the root canal is obtained by the combined effect of biomechanicalpreparation, irrigation and intra canal medicament. The aim of the present study wasto assess the antimicrobial activity of intracanal medicaments (formocresol andEndosepton) against two micro organisms (Streptococcus mutans and staphylococcusaureus) isolated from 15 necrotic pulps of primary molars indicated for pulpectomyprocedure. The samples were cultured, and purified using microbiological evaluation.Broth dilution test was performed in our study by preparing test tubes containing10 ml of BHI broth (pH. 7) which then inoculated with strains of the tested bacteriaand incubated at 37 C° for 24 h. After over night incubaction, ten fold dilution weremade in test tubes containing 9 ml of normal saline by adding 1 ml of the inoculum tothe first tube . Then from dilution 10-1 , 0.1 ml of cell suspension was added to 9.9 mlof formocresol and endosepton, then 0.1 ml was taken and spread on duplicates ofBHI agar plates at different intervals and incubated aerobically for 24 h. at 37 C°.Colonies on the plates were counted after incubation and CFU/mL (colony formingunit) was calculated. Our results indicating that there were no significant differencesbetween the intracanal medicaments, but there were high significant differencesbetween the intervals time of the study. We concluded that both materials had greatantibacterial effect against the pathogens commonly isolated from necrotic pulpaltissue of primary teeth.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

In Vitro Evidence of the Role of COX-2 in Attenuating Gastric Inflammation and Promoting Gastric Carcinogenesis

2002 ◽  
Vol 21 (2) ◽  
pp. 12 ◽  
Author(s):  
Ki-Baik Hahm ◽  
Ho-Yeong Lim ◽  
Seonghyang Sohn ◽  
Hyuk-Jae Kwon ◽  
Ki-Myung Lee ◽  
...  
Keyword(s):  
Gastric Carcinogenesis ◽  
Cox 2

The emerging role of COX-2, 15-LOX, and PPARγ in metabolic diseases and cancer: An introduction to novel multi-target directed ligands (MTDLs)

2020 ◽  
Vol 27 ◽  
Author(s):  
Rana A. Alaaeddine ◽  
Perihan A. Elzahhar ◽  
Ibrahim AlZaim ◽  
Wassim Abou-Kheir ◽  
Ahmed S.F. Belal ◽  
...  
Keyword(s):  
Metabolic Diseases ◽  
Biological Effects ◽  
Arachidonic Acid Metabolism ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cellular Targets ◽  
Design And Synthesis ◽  
Early Results ◽  
Cox 2

: Emerging evidence supports an intertwining framework for the involvement of different inflammatory pathways in a common pathological background for a number of disorders. Of importance are pathways involving arachidonic acid metabolism by cyclooxygenase-2 (COX-2) and 15-lipoxygenase (15-LOX). Both enzyme activities and their products are implicated in a range of pathophysiological processes encompassing metabolic impairment leading to adipose inflammation and the subsequent vascular and neurological disorders, in addition to various pro-and anti-tumorigenic effects. A further layer of complexity is encountered by the disparate, and often reciprocal, modulatory effect COX-2 and 15-LOX activities and metabolites exert on each other or on other cellular targets, the most prominent of which is peroxisome proliferator-activated receptor gamma (PPARγ). Thus, effective therapeutic intervention with such multifaceted disorders requires the simultaneous modulation of more than one target. Here, we describe the role of COX-2, 15-LOX, and PPARγ in cancer and complications of metabolic disorders, highlight the value of designing multi-target directed ligands (MTDLs) modifying their activity, and summarize the available literature regarding the rationale and feasibility of design and synthesis of these ligands together with their known biological effects. We speculate on the potential impact of MTDLs in these disorders as well as emphasize the need for structured future effort to translate these early results facilitating the adoption of these, and similar, molecules in clinical research.

The Role of Formyl Peptide Receptors in Microbial Infection and Inflammation

2003 ◽  
Vol 2 (1) ◽  
pp. 83-93 ◽  
Author(s):  
Yingying Le ◽  
Ronghua Sun ◽  
Guoguang Ying ◽  
Pablo Iribarren ◽  
Ji Wang
Keyword(s):  
Microbial Infection ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
Infection And Inflammation

scholarly journals Pre-motor versus motor cerebral cortex neuromodulation for chronic neuropathic pain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Cerebral Cortex ◽  
Motor Cortex ◽  
Initial Assessment ◽  
Motor Cortex Stimulation ◽  
Chronic Neuropathic Pain ◽  
Long Term Effect ◽  
Stimulation Of

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.

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