Variety Of Inflammatory Factors Research Articles

Changes in the Expression and Functional Activities of C-X-C Motif Chemokine Ligand 13 (CXCL13) in Hyperplastic Prostate

C-X-C motif chemokine ligand 13 (CXCL13), a member of the CXC subtype in chemokine superfamily, affects numerous biological processes of various types of cells and the progress of a great number of clinical diseases. The purpose of the current study was to reveal the internal mechanism between CXCL13 and benign prostatic hyperplasia (BPH). Human serum, prostate tissues and human prostate cell lines (BPH-1, WPMY-1) were utilized. The effect of recombinant human CXCL13 (rHuCXCL13) protein and the influences of the knockdown/overexpression of CXCL13 on two cell lines were studied. Rescue experiments by anti-CXCR5 were also conducted. In vivo, rHuCXCL13 was injected into the ventral prostate of rats. Additionally, a tissue microarray of hyperplastic prostate tissues was constructed to analyze the correlations between CXCL13 and clinical parameters. CXCL13 was highly expressed in the prostate tissues and upregulated in the BPH group. It was observed that CXCL13 modulated cell proliferation, apoptosis, and the epithelial-mesenchymal transition (EMT) through CXCR5 via AKT and the ERK1/2 pathway in BPH-1, while it contributed to inflammation and fibrosis through CXCR5 via the STAT3 pathway in WPMY-1. In vivo, rHuCXCL13 induced the development of rat BPH. Additionally, CXCL13 was positively correlated with the prostate volume and total prostate specific antigen. Our novel data demonstrated that CXCL13 modulated cell proliferation, cell cycle, the EMT of epithelial cells, and induced the fibrosis of prostatic stromal cells via a variety of inflammatory factors, suggesting that CXCL13 might be rediscovered as a potential therapeutic target for the treatment of BPH.

Paeoniflorin Alleviates Skeletal Muscle Atrophy in Ovariectomized Mice through the ERα/NRF1 Mitochondrial Biogenesis Pathway

Muscle atrophy in postmenopausal women is caused by estrogen deficiency and a variety of inflammatory factors, including tumor necrosis factor alpha (TNFα). Paeoniflorin (PNF), a natural compound with anti-inflammatory properties, improves estradiol synthesis. Here, we demonstrate that PNF inhibits the progression of TNFα-induced skeletal muscle atrophy after menopause by restoring mitochondrial biosynthesis. Differentiated myoblasts damaged by TNFα were restored by PNF, as evident by the increase in the expression of myogenin (MyoG) and myosin heavy chain 3 (Myh3)—the markers of muscle differentiation. Moreover, diameter of atrophied myotubes was restored by PNF treatment. TNFα-repressed nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM) (a major regulator of mitochondrial biosynthesis) were restored by PNF, via regulation by estrogen receptor alpha (ERα), an upregulator of NRF1. This mechanism was confirmed in ovariectomized (OVX) mice with a ~40% reduction in the cross-sectional area of the anterior tibialis muscle. OVX mice administered PNF (100, 300 mg/kg/day) for 12 weeks recovered more than ~20%. Behavioral, rotarod, and inverted screen tests showed that PNF enhances reduced muscle function in OVX mice. ERα restored expression of mitofusin 1 (MFN1) and mitofusin 2 (MFN2) (mitochondrial fusion markers) and dynamin-related protein (DRP1) and fission 1 (FIS1) (mitochondrial fission markers). Therefore, PNF can prevent muscle atrophy in postmenopausal women by inhibiting dysfunctional mitochondrial biogenesis.

IL-17-induced inflammation modulates the mPGES-1/PPAR-γ pathway in monocytes/macrophages.

Recent biochemical and pharmacological studies have reported that in several tissues and cell types, microsomal PGE2 synthase (mPGES) and PPAR-γ expression are modulated by a variety of inflammatory factors and stimuli. Considering that very little is known about the biological effects promoted by IL-17 in the context of mPGES-1/PPAR-γ modulation, we sought to investigate the contribution of this unique cytokine on this integrated pathway during the onset of inflammation. We evaluated effects of PF 9184 (mPGES-1 inhibitor) and troglitazone (PPAR-γ agonist) in vitro, using the mouse macrophage cell line J774A.1. In vivo, the dorsal air pouch model in CD1 mice was used, and inflammatory infiltrates were analysed by flow cytometry. Locally produced cyto-chemokines and PGs were assessed using elisa assays. Western blots were also employed to determine the activity of various enzymes involved in downstream signalling pathways. PF 9184 and troglitazone, in a time- and dose-dependent manner, modulated leukocyte infiltration, myeloperoxidase activity, and the expression of COX-2/mPGES-1, NF-кB/IкB-α, and mPTGDS-1/PPAR-γ, induced by IL-17. Moreover, both PF 9184 and troglitazone modulated PG (PGE2 , PGD2 , and PGJ2 ) production, the expression of different pro-inflammatory cyto-chemokines, and the recruitment of inflammatory monocytes, in response to IL-17. Our data suggest that IL-17 may constitute a specific modulator of inflammatory monocytes during later phases of the inflammatory response. The results of this study show, for the first time, that the IL-17/mPGES-1/PPAR-γ pathway could represent a potential therapeutic target for inflammatory-based and immune-mediated diseases. This article is part of a themed issue on Inflammation, Repair and Ageing. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.9/issuetoc.

The mechanism of hyperbaric oxygen regulating HMGB1 in the prevention and treatment of encephalopathy after acute CO poisoning

Objective: To study the expression of high mobility group protein 1 (HMGB1) in the brain of rats after hyperbaric oxygen (HBO) treatment of acute carbon monoxide poisoning (DEACMP) , and to explore the mechanism of HBO in the prevention and treatment of DEACMP pathological process by regulating HMGB1. Methods: 108 SD rats were randomly divided into control group (NC group) and co group (CO group) . HBO treatment group (HBO group) , 48 rats in each group. Co group and HBO group were used to establish CO poisoning model, HBO group were treated with hyperbaric oxygen once a day. Water maze test was used to detect and analyze the memory retention ability of three groups of rats in 3 d, 7 d, 14 d. ELISA was used to detect the plasma concentration of HMGB1、IL-6、TNF-α in three groups of rats on the 1 d, 3 d, 7 d, 14 d, 21 d Concentration. Western blotting was used to detect the expression of HMGB1 and Caspase-3 in the brain of the three groups on the 1 d, 3 d, 7 d, 14 d, 21 d. TUNEL staining was used to detect the apoptosis of hippocampal neurons in the three groups. Results: Compared with NC group, the average escape latency of rats in CO group and HBO group was significantly prolonged, and the activity time of platform quadrant in CO group was significantly shortened on 14 d and 21 d (P<0.05) ; compared with CO group, the average escape latency of HBO group on 7 d, 14 d and 21 d was significantly shortened (P<0.05) . Compared with NC group, plasma HMGB1 in CO group and HBO group were significantly increased (P<0.05) ; after 3 days, HBO group was significantly lower than co group, the difference was statistically significant (P<0.05) . The levels of IL-6 and TNF-α in HBO group and co group increased rapidly and then decreased gradually. The increased levels of IL-6 and TNF-α in HBO group were significantly lower than those in CO group (P<0.05) . Compared with NC group, the expression of HMGB1 and Caspase-3 in CO group was significantly increased on 3 d, 7 d and 14 d (P<0.05) ; the expression of HMGB1 and Caspase-3 in HBO group was significantly increased on 3 d, 7 d, 14 d and 21 d (P<0.05) ; compared with CO group, the expression of HMGB1 and Caspase-3 in HBO group decreased significantly on 3 d, 7 d, 14 d and 21 d (P<0.05) . The apoptotic index of nerve cells in CO group began to increase at 3 days, which was significantly different from that of NC group (P<0.05) , and the difference was still statistically significant on 21 d (P<0.05) ; the apoptotic index of nerve cells in HBO group was slightly increased, but there was no significant difference compared with NC group (P>0.05) , and the apoptotic index of 3 d, 7 d, 14 d and 21 d in HBO group was significantly lower than that in CO group (P<0.05) . Conclusion: acute CO poisoning can induce the release of HMGB1 and a variety of inflammatory factors. HMGB1 can promote the apoptosis of nerve cells after acute CO poisoning by up regulating the expression of caspase-3 protein, and participate in the pathological process of DEACMP. HBO can down regulate the expression of HMGB1, IL-6, TNF-α and caspase-3 protein, inhibit the apoptosis of nerve cells, and play a protective role on nerve cells.

Serum and Plasma Tumor Necrosis Factor Alpha Levels in Individuals with Obstructive Sleep Apnea Syndrome: A Meta-Analysis and Meta-Regression.

Background: Obstructive sleep apnea syndrome (OSAS) is associated with a variety of inflammatory factors. Specifically, proinflammatory cytokines appear to be associated with the pathogenesis of OSAS. Methods: For the present meta-analysis and meta-regression on serum and plasma tumor necrosis factor alpha (TNF-α) levels in individuals with and without OSAS, we performed a systematic search without any restrictions of the PubMed/Medline, Scopus, Cochrane Library, and Web of Science databases to find relevant articles published up to 1 February 2020. Results: Fifty-five (adults: 29 studies on serum and 17 studies on plasma; children: 4 studies on serum and 5 studies on plasma) were included and analyzed. Always compared to age-matched healthy controls, the pooled MDs were as follows: adults, serum: 10.22 pg/mL (95% CI = 8.86, 11.58; p < 0.00001); adults, plasma: 5.90 pg/mL (95% CI = 4.00, 7.80; p < 0.00001); children, serum: 0.21 pg/mL (95% CI = 0.05, 0.37; p = 0.01); children, plasma: 5.90 pg/mL (95% CI = 4.00, 7.80; p < 0.00001). Conclusions: Compared to healthy and age-matched controls, adult individuals with OSAS had significantly higher serum/plasma TNF-α levels. For children with OSAS, significantly higher levels were observed for TNF-α in serum but not in plasma.

Research progress in the role of nuclear factor-kappa B in neuropathic pain

Chronic pain is a worldwide public health problem in which neuropathic pain (NP) caused by nerve damage is the most common chronic pain. At present, NP lacks effective treatment for any reason. In recent years, increasing studies have shown that neuroimmunity and neuroinflammation play a key role in mediating NP, and nuclear factor-kappa B (NF-κB) plays the most important role in the expression of pain inducers and effectors in the immune and inflammatory systems. NF-κB promotes transcriptional up-regulation by a promoter that links to a variety of inflammatory factors. Therefore, this paper reviews the research status of the role of NF-κB in NP. Key words: NF-κappa B; Neuralgia; Neuroimmunomodulation; Review

Study progress of chorioamnionitis and lung disease in preterm infants

Preterm birth is a major cause of perinatal mortality and long-term morbidity, chorioamnionitis (CAM) is a common cause of preterm birth and characterized by inflammation.CAM produces variety of inflammatory factors in fetal, results in structural and functional impairment, and affects the contractile function of pulmonary blood vessels, so, CAM can have impact on the morbidity of lung disease in premature, and it may even affect the long-term pulmonary function. Key words: Chorioamnionitis; Infant, preterm; Respiratory distress syndrome; Bronchopulmonary dysplasia; Persistent pulmonary hypertension; Pneumonia

Sufentanil Preconditioning Protects Against Hepatic Ischemia-Reperfusion Injury by Suppressing Inflammation.

BackgroundInflammation is one of the most significant mechanisms of hepatic ischemia-reperfusion injury (IRI). Sufentanil has a protective effect against liver injury by reducing inflammatory response. In this study, we used a cellular hepatic ischemic/reoxygenated (IR) model to determine whether sufentanil preconditioning protects against hepatic IRI.Material/MethodsThe human normal liver cells line L-O2 was studied. The levels of glutamic oxaloacetic transaminase (AST), lactate dehydrogenase (LDH), malonaldehyde (MDA), and superoxide dismutase (SOD) were measured using corresponding assay kits. The protein levels of total and phosphorylated ERK1/2, JNK, and p38, and the expression of p65 and COX2 genes, were measured by Western blotting. The levels of inflammatory factors were examined by ELISA. The Cell Counting Kit-8 (CCK-8) was used to determine if the viability of L-O2 cells was affected by sufentanil. The effects of sufentanil on IR-induced cell apoptosis were examined by flow cytometry.ResultsIR-induced caused L-O2 cells to become rounded and to have a lower adhesive rate than normal cells. The levels of AST, LDH, and MDA were higher but the level of SOD was lower in the IR group than in the control group. The phosphorylated protein levels of ERK1/2, JNK, and p38, along with the expression of p65 and COX2, were upregulated in the IR group compared to the normal group. In addition, a variety of inflammatory factors were secreted in L-O2 cells after IR. The viability of L-O2 cells decreased and cell apoptosis increased significantly after IR treatment. All indexes of cell injury were reversed by sufentanil in a concentration-dependent manner.ConclusionsSufentanil stimulation triggers downregulation of inflammatory factors such as HIF-1α, TNF-α, IL-1β, and IL-6, possibly through suppressing the p38/ERK/JNK/NF-κB-p65/COX2 pathways, and thereby reduces the damage to IR hepatic cells.

PO-052 Study on the Expression of Inflammatory Factor, chemotactic factor in the Repair of Skeletal Muscle Contusion in Mic

Objective To investigate the regulation of muscle inflammatory factors and chemotactic factors during the repair of skeletal muscle contusion in mice.&#x0D; Methods Forty C57 male mice were needed. Eight for control group (C, n=8) and thirty-tow for muscle contusion group (S, n=32). Subsequently, their gastrocnemius muscles were harvested at 0d, 1d, 3d, 7d, 14d after injury. Hematoxylinand eosin (HE) stain were used to assess the changes of muscle morphology. In addition, the gene expression of inflammatory factors and chemotactic factors was analyzed by real-time polymerase chain reaction.&#x0D; Results 1、Morphology of skeletal muscles showed signs of regeneration at 3d post injury. The maximumamount of regeneration muscle fibers appeared during one week post contusion. Two weeks post-injury morphology of myofibers nearly recovered to normal. 2、After skeletal muscle injury, macrophage markers (CD68, CD163, CD206), a variety of inflammatory factors (IL-1, IL-6, IL-10) were up-regulated. 3、chemotactic factors (CCL2, CCL3, CCL5, CCL8, CXCL9, CXCL10, CXCL12, mRNA) were up-regulated。&#x0D; Conclusions After skeletal muscle contusion, the expression of a variety of chemotactic factors is up-regulated, which promotes macrophage infiltration and produces a variety of inflammatory factors. They may be involved in the inflammatory response and regeneration process after skeletal muscle contusion.

Reduced inflammatory factor expression facilitates recovery after sciatic nerve injury in TLR4 mutant mice

Toll-like receptors (TLRs) are extremely significant pattern recognition receptors. When nerve injury occurs, a variety of inflammatory factors are generated, leading to an exceedingly complex micro-environment. TLRs recognize damage-associated molecular patterns. To investigate the correlation between TLR4 and recovery after sciatic nerve injury, the model of sciatic nerve injury was conducted using TLR4-mutated mice (C3H/HeJ) and wild mice (C3H/HeN). Our goal was to identify short-stage and long-stage changes after sciatic nerve injury, mainly by checking the expression changes of inflammation factors in the short-stage and the differences in the recovery of the injured sciatic nerve in the long-stage. The results show that the increase of changes in the HeN group of IL-1β, IL-6, TNF-α and MCP-1 are more obvious than in the HeJ group, with caspase1 expression higher and Nlrp3 expression lower in the former group. Further results reveal intense inflammation occurred in the HeN group showing more neutrophils and macrophages. Nlrp3 and caspase1 showed little difference by Immunohistochemistry, with Nlrp6 expression differing between the HeJ group and the HeN group. The results led us to conclude that better recovery of the injured sciatic nerve occurred in the HeJ group because the expression of GAP-43 and p75NTR was higher and had a better SFI figure. TLR4 mutation can decrease the expression of inflammatory factors and enhance the speed of recovery after sciatic nerve injury. The changes in the expression of Nlrp6, which are related to the TLR4 mutation, may influence recovery of the injured sciatic nerve. Further studies will be conducted to confirm these results.

Study on the Dynamic Changes in Synaptic Vesicle-Associated Protein and Axonal Transport Protein Combined with LPS Neuroinflammation Model

Microglia activation is the major component of inflammation that constitutes the characteristic of neurodegenerative disease. A large amount of researches have demonstrated that inflammation involved in the pathogenesis of PD process activated microglia acting on the neurons through the release of a variety of inflammatory factors. However, the molecular mechanism underlying how it does work on neurons is still unclear. Here, we show that intracerebral injections of LPS induced Parkinson's disease pathology in C57BL/6J mice. Furthermore, study on the dynamic changes in Synaptic vesicle-associated protein and axonal transport Protein in this process. The results indicated that after administration of LPS in the brain, the inflammatory levels of TNF-α and IL-1β both are elevated, and have a time-dependent.

E0464 Clinical significance of the changes of serum TNF-α, IFN-γ, MMP-9

A variety of inflammatory factors in atherosclerosis (AS) plays a complex role, the combination of two or more of the inflammatory mediators can increase inflammatory mediators in coronary heart disease...