Short-term heat pre-treatment modulates the release of HMGB1 and pro-inflammatory cytokines in hPDL cells following mechanical loading and affects monocyte behavior

2015 ◽  
Vol 20 (5) ◽  
pp. 923-931 ◽  
Author(s):  
Michael Wolf ◽  
Stefan Lossdörfer ◽  
Piero Römer ◽  
Christian Kirschneck ◽  
Katharina Küpper ◽  
...  
Keyword(s):  
Mechanical Loading ◽  
Inflammatory Cytokines ◽  
Short Term ◽  
Pre Treatment ◽  
Pro Inflammatory Cytokines

scholarly journals Adenosine A2A receptor agonist polydeoxyribonucleotide ameliorates short-term memory impairment by suppressing cerebral ischemia-induced inflammation via MAPK pathway

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0248689
Author(s):  
Il-Gyu Ko ◽  
Jun-Jang Jin ◽  
Lakkyong Hwang ◽  
Sang-Hoon Kim ◽  
Chang-Ju Kim ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Inflammatory Cytokines ◽  
Memory Impairment ◽  
Carotid Arteries ◽  
Short Term Memory ◽  
Mapk Signaling ◽  
Short Term ◽  
The Common ◽  
Common Carotid Arteries ◽  
Pro Inflammatory Cytokines

Cerebral ischemia causes tissue death owing to occlusion of the cerebral blood vessels, and cerebral ischemia activates mitogen-activated protein kinase (MAPK) and induces secretion of pro-inflammatory cytokines. Adenosine A2A receptor agonist, polydeoxyribonucleotide (PDRN), suppresses the secretion of pro-inflammatory cytokines and exhibits anti-inflammatory effect. In the current study, the therapeutic effect of PDRN on cerebral ischemia was evaluated using gerbils. For the induction of cerebral ischemia, the common carotid arteries were exposed, and then aneurysm clips were used to occlude the common carotid arteries bilaterally for 7 minutes. In the PDRN-treated groups, the gerbils were injected intraperitoneally with 0.3 mL of saline containing 8 mg/kg PDRN, per a day for 7 days following cerebral ischemia induction. In order to confirm the participation of the adenosine A2A receptor in the effects mediated by PDRN, 8 mg/kg 7-dimethyl-1-propargylxanthine (DMPX), adenosine A2A receptor antagonist, was treated with PDRN. In the current study, induction of ischemia enhanced the levels of pro-inflammatory cytokines and increased phosphorylation of MAPK signaling factors in the hippocampus and basolateral amygdala. However, treatment with PDRN ameliorated short-term memory impairment by suppressing the production of pro-inflammatory cytokines and inactivation of MAPK signaling factors in cerebral ischemia. Furthermore, PDRN treatment enhanced the concentration of cyclic adenosine-3,5’-monophosphate (cAMP) as well as phosphorylation of cAMP response element-binding protein (p-CREB). Co-treatment of DMPX and PDRN attenuated the therapeutic effect of PDRN on cerebral ischemia. Based on these findings, PDRN may be developed as the primary treatment in cerebral ischemia.

Short-term effect of multilevel surgery on adipokines and pro-inflammatory cytokines in patients with obstructive sleep apnea

2010 ◽  
Vol 130 (12) ◽  
pp. 1394-1398 ◽  
Author(s):  
Young Gyu Eun ◽  
Myung Gu Kim ◽  
Kee Hwan Kwon ◽  
Seung Youp Shin ◽  
Joong Saeng Cho ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Inflammatory Cytokines ◽  
Term Effect ◽  
Short Term ◽  
Short Term Effect ◽  
Multilevel Surgery ◽  
Obstructive Sleep ◽  
Pro Inflammatory Cytokines

scholarly journals Identification of Atypical Mitogen-Activated Protein Kinase MAPK4 as A Novel Regulator in Acute Lung Injury

2020 ◽  
Author(s):  
Ling Mao ◽  
Ya Zhou ◽  
Longqing Chen ◽  
Lin Hu ◽  
Shiming Liu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Survival Time ◽  
Inflammatory Cytokines ◽  
Mitogen Activated Protein Kinase ◽  
Lps Challenge ◽  
Mitogen Activated Protein ◽  
Pre Treatment ◽  
Pro Inflammatory Cytokines

Abstract Background: Acute lung injury (ALI) is a serious disease with highly morbidity and mortality that causes serious health problems worldwide. Atypical mitogen activated protein kinases (MAPKs) play critical roles in the development of tissues and have been proposed as promising therapeutic targets for various diseases. However, the potential role of atypical MAPKs in ALI remains elusive. In this study, we investigated the role of atypical MAPKs family member MAPK4 in ALI using LPS-induced murine ALI model. Results: We found that MAPK4 deficiency mice exhibited prolonged survival time after LPS challenge, accompanied by alleviated pathology in lung tissues, decreased levels of pro-inflammatory cytokines and altered composition of immune cells in BALF. Furthermore, the transduction of related signaling pathways, including MK5, AKT, JNK, and p38 MAPK pathways, was reduced obviously in LPS-treated MAPK4-/- mice. Notably, the expression of MAPK4 was up-regulated in lung tissues of ALI model, which was not related with MAPK4 promoter methylation, but negatively orchestrated by transcriptional factors NFKB1 and NR3C1. Further studies have shown that the expression of MAPK4 was also increased in LPS-treated macrophages. Meanwhile, MAPK4 deficiency reduced the expression of related pro-inflammatory cytokines in macrophage in response to LPS treatment. Finally, MAPK4 inhibition using shRNA pre-treatment could ameliorate the pathology of lung tissues and prolong the survival time of mice after LPS challenge. Conclusions: Collectively, these findings reveal an important biological function of atypical MAPK in mediating the pathology of ALI, indicating that MAPK4 might be a novel potential therapeutic target for ALI treatment.

scholarly journals Vitamin D3 controls TLR4- and TLR2-mediated inflammatory responses of endometrial cells

2019 ◽  
Author(s):  
Alireza Ghanavatinejad ◽  
Nesa Rashidi ◽  
Mahroo Mirahmadian ◽  
Simin Rezania ◽  
Mahdokht Mosalaei ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Vitamin D3 ◽  
Inflammatory Responses ◽  
Female Reproductive Tract ◽  
Endometrial Stromal Cells ◽  
Endometrial Cells ◽  
Tnf Α ◽  
Pre Treatment ◽  
Tract Infections ◽  
Pro Inflammatory Cytokines

Abstract Background: There is a significant association between intrauterine infection-associated inflammatory responses and such pregnancy complications as abortion and preterm labor. Here, we aimed to investigate anti-inflammatory effects of 1,25 (OH)2 D3 on pro-inflammatory cytokines secretion and expression of TLR2, TLR4 and MyD88 in endometrial stromal cells (ESCs) and whole endometrial cells (WECs). Method: WECs were treated with either lipopolysaccharide (LPS) or lipoteichoic acid (LTA) and ESCs were treated with LPS. IL-6, IL8 and TNF-α were quantified using ELISA technique. TLR2, TLR4 and MyD88 expression were assessed by RT-qPCR. TLR4 expression at the protein level was studied by Western blot technique. Results: 1,25 (OH)2 D3 significantly reduced TNF-α production in LPS-activated ESCs and TNF-α and IL-6 production by LTA-stimulated WECs. In contrast, 1,25 (OH)2 D3 pre-treatment increased production of IL-8 by LPS- and LTA-stimulated endometrial cells. 1,25 (OH)2 D3 pre-treatment markedly reduced LPS-induced TLR-4 protein expression by ESCs. LPS treatment of ESCs significantly induced MyD88 gene expression. This effect was reversed when these cells were pre-treated with 1,25 (OH)2 D3 before stimulation with LPS. Conclusion: 1,25 (OH)2 D3 is an immunomodulatory molecule essential for maintenance of endometrial immune homeostasis through controlling potentially harmful inflammatory responses associated with female reproductive tract infections. Key words: Vitamin D3, Endometrium, Inflammation, Toll like receptors, Pro-inflammatory cytokines

Abstract 246: Global Analysis of Differentially Expressed Genes in the Aortae of Apoe-deficient Mice Infused with Insulin-like Growth Factor I: Novel Mechanisms of the Anti-atherogenic Effect of IGF-1

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Charlotte E Vaughn ◽  
Jane S Titterington ◽  
Sergiy Sukhanov ◽  
Patrick Delafontaine
Keyword(s):  
Gene Expression ◽  
Growth Factor ◽  
Adhesion Molecules ◽  
Inflammatory Cytokines ◽  
Interferon Γ ◽  
Scavenger Receptors ◽  
Saline Control ◽  
Short Term ◽  
Factor I ◽  
Pro Inflammatory Cytokines

We have previously shown that insulin like growth factor-I (IGF-1) suppresses atherosclerosis progression in ApoE-null mice. To determine mechanisms, ApoE-null mice were chronically infused with IGF-1 (1.5 mg/kg/d, 12 weeks) or saline (control) or treated short-term with IGF-1 (0.4 mg/kg/d, i.p., 1 week) or saline (control). Aortic gene expression of 84 atherosclerosis-related genes-of-interest was analyzed with RT-PCR arrays. Chronic IGF-1 infusion decreased expression levels of pro-apoptotic molecules (Bax, 0.62, BID, 0.26), adhesion molecules (integrin β2, 0.32, integrin α2, 0.28, VCAM-1, 0.43), pro-inflammatory cytokines (TNFα, 0.22, interferon γ, 0.30) and lipoprotein lipase (LPL, an enzyme mediating lipid hydrolysis and tissue uptake of oxidized low density lipoprotein (OxLDL), 0.69). These changes in gene expression correlated with a reduction in atherosclerotic plaque burden (Oil Red-positive aortic valve lesion area, ×000 pixels 2 , IGF-1, 228±13, saline, 268±22), suppression of plaque apoptosis (% apoptotic cells per plaque, IGF-1, 3.4±0.7, saline, 5.8±0.5, P<0.05, TUNEL assay), decrease in plaque TNFα levels (58% reduction vs. saline, P<0.05, immunostaining), and inhibition of serum LPL activity (IGF-1, 1.1±0.2, saline, 3.7±0.4, P<0.05, fluorescence assay). Short-term IGF-1 treatment similarly decreased mRNA levels of Bax (0.68), BID (0.61), integrin β2 (0.62), TNFα (0.50), interferon γ (0.37), LPL (0.42) and also downregulated a group of scavenger receptors (CD36, 0.44, MSR-1, 0.48, MSR-2, 0.52). To further characterize the effect of IGF-1 on LPL we exposed THP-1-derived macrophages to OxLDL (80 ug/ml, 16 h) in the presence or absence of IGF-1. OxLDL increased LPL activity in conditioned media (>5 fold, P<0.01), but pre-treatment with IGF-1 (25 ng/ml, 24 h) reversed LPL upregulation by 52% and suppressed lipid internalization by 88% (P<0.05, Oil Red staining). In summary IGF-1 reduces pro-inflammatory cytokines, pro-apoptotic molecules, adhesion molecules, scavenger receptors, and lipoprotein lipase expression in ApoE-null mice and markedly blunts OxLDL-induced upregulation of LPL and lipid uptake in THP-derived macrophages. These data provide major insights into mechanisms whereby IGF-1 is atheroprotective.

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