SEARCH · Search PubMed

Results for “INFLAMMATION”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources

PubMedDate not supplied

Inflammation in patients on peritoneal dialysis is associated with increased extracellular fluid volume.

BACKGROUND: Cardiovascular disorders (CD) are the most frequent cause of death in patients on dialysis. CD have been related to increased extracellular fluid volume, peritoneal transport type (PTT), hypertension, and inflammation. Inflammation is in itself a risk factor for mortality. The aim of this study was to assess the relationship of increased extracellular fluid volume, inflammation, and PTT in patients on continuous ambulatory peritoneal dialysis (CAPD) and automated peritoneal dialysis (APD). METHODS: A cross-sectional study was carried out with 20 healthy controls (C), 21 patients on CAPD, and nine patients on APD. Clinical and demographic variables were measured and registered. Peritoneal equilibrium test (PET) was done. Blood volume (BV), total body water (TBW), inferior vena cava diameter during inspiration (IVCDi) and expiration (IVCDe), serum albumin, and serum C-reactive protein (CRP) were measured. RESULTS: All patients on peritoneal dialysis (PD) had at least one sign or symptom of increased extracellular fluid volume, hypertension being the most common. Patients also had higher TBW (C, 60.7 +/- 7.2; APD, 62.6 +/- 8.7; CAPD, 66.1 +/- 8.3, as percentage of body weight, p <0.02), higher BV (C, 7.9 +/- 1.6; APD, 9.8 +/- 2.3; CAPD, 9.6 +/- 2.3, as percentage of body weight, p <0.02), higher DIVCi (C, 2.9 +/- 1.2; APD, 4.6 +/- 2.5; CAPD, 4.5 +/- 2.4 mm/m2 BSA, p <0.02), and higher DIVCe (C, 6.2 +/- 1.7; APD, 8.3 +/- 3.4; CAPD, 8.0 +/- 2.8 mm/m2 BSA, p <0.05). PD patients also had hypoalbuminemia and higher CRP levels. There was significant positive correlation between CRP and DIVCi (r=0.43, p <0.05) and IVCe (r=0.45, p <0.05) and between serum albumin and creatinine dialysate-to-plasma ratio (D/P Cr, r=0.57, p <0.01). Serum albumin and CRP were negatively correlated (r= -0.54, p <0.02). CONCLUSIONS: Patients on PD have increased extracellular fluid volume as compared with healthy controls. Hyperhydration is related to inflammation and to higher peritoneal transport types.

Adult↗

PubMedDate not supplied

The role of plasma high molecular weight kininogen in experimental intestinal and systemic inflammation.

Inflammation is accompanied by activation of the plasma kallikrein-kinin system (KKS). KKS activation has been demonstrated in a variety of inflammatory human diseases. To further explore the participation of KKS in arthritis and inflammatory bowel disease, we used two experimental animal models in arthritis and enterocolitis. We found that activation of KKS is associated with arthritis induced by intraperitoneal injection of peptidoglycan-polysaccharide polymers (PG-PS) as well as the enterocolitis and systemic inflammation induced also by PG-PS when injected into the intestinal wall of genetically susceptible Lewis rats. We postulated that KKS participates in the pathogenesis of inflammatory reactions involved in cellular injury, coagulation, fibrinolysis, kinin formation, complement activation, cytokine secretion, and release of proteases. We demonstrated that therapy with a specific plasma kallikrein inhibitor modulated the experimental enterocolitis, arthritis, and systemic inflammation. The fact that deficiency of plasma high molecular weight kininogen in the genetically susceptible Lewis rat results in decreased chronic enterocolitis and systemic inflammation also supports our hypothesis. We suggest that KKS plays a similar role in idiopathic human intestinal inflammatory disease and arthritis, making kallikrein-kinin system proteins appealing targets for drug therapy in chronic inflammatory diseases such as rheumatoid arthritis and Crohn's disease.

Amino Acid Sequence↗

PubMed2007

Inflammation and oxidative stress markers by pentoxifylline treatment in rats with chronic renal failure and high sodium intake.

BACKGROUND: Inflammation is a risk factor for mortality in patients with chronic renal failure (CRF). Prevention of extracellular fluid volume expansion and the use of certain drugs such as pentoxifylline (PF) may reduce inflammation and oxidative stress. The aim of this study is to analyze the effect of dietary sodium and PF treatment on the levels of inflammation and oxidative stress markers in rats with CRF. METHODS: CRF was induced in rats by 5/6 nephrectomy. Different groups of rats with CRF received low sodium (LNa, 0.01% sodium chloride [NaCl] in the diet), normal sodium (NNa, 0.05% NaCl in the diet), or high sodium diet (HNa, as in NNa plus 0.015% NaCl in the drinking water). An additional group received HNa plus PF treatment (25 mg/kg in the drinking water) for 60 days. Circulating creatinine, tumor necrosis factor alpha (TNF-alpha), nitrites, thiols, malondialdehyde (MDA), and advanced oxidation protein products (AOPP) were measured. RESULTS: Higher sodium intake was associated with higher serum creatinine levels (median; interquartile range), LNa, 1.255; 0.715, NNa, 1.305; 0.495, HNa, 2.015; 1.115 mg/dL (p < 0.05), TNF-alpha levels, LNa, 2.7; 23.6, NNa, 36.7; 47.7, HNa, 263.7; 126.5 pg/mL, and AOPP, LNa, 31.72; 7.55, NNa, 45.89; 9.38, HNa, 60.41; 37.42 microg/mL. MDA was not modified by sodium intake. PF treatment decreased serum TNF-alpha (151.7 pg/mL, p < 0.5) and AOPP (49.83 micromol/L, p < 0.03), and increased nitrites and thiols levels when compared with HNa rats. CONCLUSIONS: High sodium intake increases the serum concentration of inflammation and oxidative stress markers; these changes are prevented by PF treatment.

Animals↗

PubMed2026

Targeted Epigenetic Silencing of Jumonji Domain-Containing Protein 3 Alleviates Nuclear Factor-Kappa B-Mediated Inflammation in Familial Mediterranean Fever.

BACKGROUND: Familial Mediterranean fever (FMF) is an inherited autoinflammatory condition caused by variants in the MEFV gene encoding pyrin, the essential component of the NLRP3/NF-κB complex of inflammasomes. Deregulation of nuclear factor-kappa B (NF-κB), a key proinflammatory mediator, leads to chronic inflammation in autoinflammatory/autoimmune diseases. Epigenetic modulation offers a new approach to regulate inflammasome activity, with Jumonji domain-containing protein 3 (JMJD3) being a promising target for managing inflammatory illnesses. GSK-J4 is a selective inhibitor of JMJD3, restricting pro-inflammatory cytokines and inflammation. AIM: Our research aimed to elucidate the role of JMJD3 and the NF-κB-JMJD3 signaling pathways in regulating inflammation in an in vitro model, and to investigate GSK-J4's effect in inhibiting inflammasome activation in primed peripheral blood mononuclear cells (PBMCs) isolated from FMF cases. METHODS: PBMCs were cultured and primed with LPS, and then treated with GSK-J4. JMJD3 knockdown was achieved using siRNA interference. Cellular inflammatory dynamics were assessed by Western blotting (WB) and ELISA. The qRT-PCR was used for gene expression quantification. Untreated cells served as a negative control. RESULTS: Our results showed significantly downregulated gene expression of NF-κB, NLRP3, and inflammatory cytokines in GSK-J4-treated cells compared to untreated cells, as confirmed by ELISA. WB reported a reduction of NF-κB in induced cells following GSK-J4 treatment. Knocking down JMJD3 also showed decreased levels of JMJD3, NF-κB, and inflammatory cytokines, indicating its proinflammatory role. CONCLUSION: The study showed that selective inhibition or silencing of JMJD3 significantly suppressed the inflammasome in FMF cases, suggesting its role as a therapeutic target for alleviating inflammation in various autoinflammatory diseases.

Humans↗

PubMed2005

Peroxisome proliferator-activated receptor gamma polymorphisms affect systemic inflammation and survival in end-stage renal disease patients starting renal replacement therapy.

BACKGROUND: Inflammation may contribute to the markedly increased cardiovascular morbidity and mortality in end-stage renal disease (ESRD). However, the prevalence of inflammation varies in different ESRD populations. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is an important nuclear signaling protein that may regulate inflammatory response, and recent studies have revealed genetic polymorphisms that have significant effect on PPAR-gamma signaling. The aim of this study was to clarify whether the PPAR-gamma 161C/T and PPAR-gamma2 Pro12Ala single-nucleotide polymorphisms (SNPs) influence the inter-individual variance of inflammation and mortality in ESRD patients. METHODS: The present prospective study included 229 incident Caucasian ESRD patients (62% males) just prior to starting renal replacement therapy and 207 healthy controls (62% males). Blood samples were taken for measuring systemic inflammatory (CRP, TNF-alpha, IL-6) and nutritional (S-albumin) parameters. The presence of diabetes mellitus, malnutrition (subjective global assessment (SGA)) and cardiovascular disease (CVD) were also assessed. Genotyping of the two PPAR-gamma SNPs was performed using Pyrosequencing. During follow-up (1621+/-63 days), both all-cause and CVD-mortality were investigated. RESULTS: ESRD patients had a higher prevalence of both the PPAR-gamma 161 CC and PPAR-gamma2 Pro12Pro genotypes than the general population (p<0.01). Whereas the Pro12Pro genotype was associated with higher median serum levels of both hs-CRP (p<0.05) and TNF-alpha (p<0.01) the 161CC genotype was associated with a significantly higher (6.6 mg/L versus 3.3 mg/L; p<0.01) median hs-CRP level. Following adjustment for age, gender, SGA and CVD a significantly higher mortality rate was observed in patients with the Pro12Pro genotype. CONCLUSION: This study demonstrates significant differences in PPAR-gamma genotype distribution between ESRD patients and healthy controls. Furthermore, as the PPAR-gamma2 Pro12Pro genotype was associated with both higher levels of biomarkers of inflammation as well as shorter survival, genetic polymorphisms seem to play a role in determining systemic inflammatory status and outcome in this patient group.

Adult↗

PubMed2005

Sex differences in the relation of body composition to markers of inflammation.

OBJECTIVE: It has been suggested that low-grade systemic inflammation is associated with obesity and that this association might be modified by sex. METHODS AND RESULTS: We performed a cross-sectional analysis among 641 men and 597 women aged 55-74 years who participated in the population-based KORA Survey 2000, conducted in the area of Augsburg, Germany. Measures of both total (fat mass, body mass index) and abdominal adiposity (waist circumference (WC), waist to hip ratio (WHR)) were highly correlated with markers of systemic inflammation (C-reactive protein (CRP), serum amyloid A (SAA), fibrinogen (FIB), interleukin-6 (IL-6)) in men and in women. Significant associations persisted when the effect of lifestyle factors was taken into account. In multivariable linear regression analysis, a considerably higher percentage of variability in inflammatory markers was explained by body composition in women compared to men. Furthermore, the relevance of single body composition variables varied by sex. In women, fat mass in % explained the highest percentage of the variability of circulating acute-phase proteins (18.2% for CRP, 7.2% for SAA, 6.1% for FIB, all p-values < 0.001), whereas in men, WHR explained the highest percentage of the variability (6.2% for CRP, 2.3% for SAA, 1.8% for FIB, all p-values < 0.001). For IL-6, WC explained the highest percentage of the variability in women (3.7%, p < 0.001) and in men (1.8%, p < 0.001). CONCLUSION: Adiposity is strongly associated with low-grade systemic inflammation in men and in women but the association is considerably stronger in women, especially for CRP. Thus, weight reduction as a means to prevent a state of subclinical inflammation might be particularly effective in women.

Adiposity↗

PubMed2005

Miniaturized cardiopulmonary bypass in coronary artery bypass surgery: marginal impact on inflammation and coagulation but loss of safety margins.

PURPOSE: Inflammation and coagulation disturbances are common consequences of cardiopulmonary bypass (CPB). Recently, miniaturized closed CPB circuits without cardiotomy suction and venous reservoir have been proposed to reduce complication rates. We compared outcomes with conventional (CCPB) and miniaturized cardiopulmonary bypass (MCPB) after coronary artery bypass operations (CABG) with respect to inflammation and coagulation. DESCRIPTION: Thirty patients (23% female; aged 67.9 +/- 9.0 years) were prospectively randomly assigned to undergo isolated CABG with CCPB or MCPB. Conventional CPB had a pump prime of 1, 600 mL. Miniaturized CPB consisted of a centrifugal pump, arterial filter, heparinized tubing, and oxygenator with a priming volume of 800 mL. Shed blood was removed by a cell-saving device and reinfused. Measurements included interleukin (IL)-2 receptor, IL-6, IL-10, tumor necrosis factor receptor 55 and 75, C reactive protein, leukocyte differentiation, d-dimers, fibrinogen, and thrombocytes at six time points. EVALUATION: In both groups no major complication occurred. However, two dangerous air leaks occurred in the closed MCPB circuit, demonstrating the narrow safety margins. Operative handling was also more difficult owing to limitations in venting and fluid management. International normalized ratio (p = 0.03) and antithrombin III (p = 0.04) levels were elevated during CPB in the CCPB group, most likely owing to differences of the intraoperative anticoagulation management. Repeated measures analysis revealed that not a single parameter of inflammation or clinical outcome showed significant differences among groups. CONCLUSIONS: Use of a MCPB affected inflammation and coagulation variables only marginally and did not lead to clinical relevant changes as assessed by blood loss, need for blood products, and intensive care unit and clinical stays. However, safety margins for volume loss, air emboli, and weaning from CPB decrease, because of the closed MCPB circuit.

Adult↗

PubMed2003

Phagocytosis of apoptotic cells and the resolution of inflammation.

Clearance of apoptotic cells by phagocytic cells plays a significant role in the resolution of inflammation, protecting tissue from harmful exposure to the inflammatory and immunogenic contents of dying cells. Apoptosis induces cell surface changes that are important for recognition and engulfment of cells by phagocytes. These changes include alterations in surface sugars, externalization of phosphatidylserine and qualitative changes in the adhesion molecule ICAM-3. Several studies have contributed to clarify the role of the receptors on the surface of phagocytes that are involved in apoptotic cell clearance. The phagocytic removal of apoptotic cells does not elicit pro-inflammatory responses; in contrast, apoptotic cell engulfment appears to activate signals that suppress release of pro-inflammatory cytokines. Therefore, clearance of apoptotic leucocytes is implicated in the resolution of inflammation and mounting evidence suggests that defective clearance of apoptotic cells contributes to inflammatory and autoimmune diseases. Defining the ligands on apoptotic cells and the corresponding receptors on phagocytes with which they engage, is likely to lead to the development of novel anti-inflammatory pro-resolution drugs. In this article, we will review the recognition and signaling mechanisms involved in the phagocytosis of apoptotic cells as well as the role of endogenous compounds that play a relevant role in the modulation of inflammation. We will also discuss what is currently known about diseases that may reflect impaired phagocytosis and the consequences on inflammation and immune responses.

Apoptosis↗

PubMed2006

Hostility and pain are related to inflammation in older adults.

Chronically elevated systemic inflammation has a dramatic impact on health for older individuals. As stress-related responses, both hostility and pain perception may contribute to inflammation which in turn may maintain negative emotion and pain over time. We used structural equation modeling to examine the degree to which trait hostility and pain were uniquely associated with C-reactive protein (CRP) and serum IL-6 levels over a 6-year span in a sample of older adults. The sample included 113 present or former caregivers of a spouse with dementia and 101 non-caregivers. After accounting for depression, health behaviours, and other risk factors, which were also assessed longitudinally, pain and, to a lesser extent, hostility were uniquely associated with plasma levels of CRP but not IL-6. When examined separately, the association between pain and CRP was significant only for caregivers, while the association between hostility and CRP was comparable for the two groups. These findings suggest that hostility may play a role in a cycle of inflammation among older adults, and that pain may be particularly problematic for those under chronic stress. Our results also shed light on inflammation as a mechanism underlying the effects of hostility on cardiovascular disease morbidity and mortality.

Age Factors↗

PubMed2006

Inflammation and the pathophysiology of work-related musculoskeletal disorders.

Work-related musculoskeletal disorders (MSDs) have accounted for a significant proportion of work injuries and workers' compensation claims in industrialized nations since the late 1980s. Despite epidemiological evidence for the role of repetition and force in the onset and progression of work-related MSDs, complete understanding of these important occupational health problems requires further elucidation of pathophysiological mechanisms of the tissue response, particularly in the early stage of these disorders. Results from several clinical and experimental studies indicate that tissue microtraumas occur as a consequence of performing repetitive and/or forceful tasks, and that this mechanical tissue injury leads to local and perhaps even systemic inflammation, followed by fibrotic and structural tissue changes. Here we review work linking inflammation and the development of work-related MSDs. We also propose a conceptual framework suggesting the potential roles that inflammation may play in these disorders, and how inflammation may contribute to pain, motor dysfunction, and to puzzling psychological symptoms that are often characteristic of patients with work-related MSDs.

Cumulative Trauma Disorders↗

PubMed2004

Tart cherry anthocyanins suppress inflammation-induced pain behavior in rat.

The use of complementary and alternative medicine (CAM) has increased in the United States and more patients are seeking CAM therapies for control of pain. The present investigation tested the efficacy of orally administered anthocyanins extracted from tart cherries on inflammation-induced pain behavior in rats. Paw withdrawal latency to radiant heat and paw withdrawal threshold to von Frey probes were measured. The first set of experiments examined the effects of tart cherry anthocyanins (400 mg/kg) on the nociceptive behaviors and edema associated with inflammation induced by intraplantar injection of 1% carrageenan. These studies also included tests of motor coordination. The second set of experiments determined if tart cherry anthocyanins (15, 85, and 400 mg/kg) dose-dependently affected the inflammation induced by intraplantar injection of 25% complete Freund's adjuvant. We found that tart cherry extracts reduce inflammation-induced thermal hyperalgesia, mechanical hyperalgesia and paw edema. The suppression of thermal hyperalgesia was dose-dependent and the efficacy of highest dose (400 mg/kg) was similar to indomethacin (5 mg/kg). The highest dose anthocyanin (400 mg/kg) had no effects on motor function. These data suggest that tart cherry anthocyanins may have a beneficial role in the treatment of inflammatory pain. The antihyperalgesic effects may be related to the anti-inflammatory and antioxidant properties of anthocyanins. A better understanding of the modulatory role of dietary constituents and phytonutrients on pain will offer further therapeutic options for treating patients with persistent and chronic pain conditions.

Administration, Oral↗

PubMed2006

Macrophage-secreted factors induce adipocyte inflammation and insulin resistance.

Macrophage infiltration into adipose tissue increases with obesity, a condition associated with low-grade inflammation and insulin resistance. We investigated the direct effects of macrophage-secreted factors on adipocyte inflammation and insulin resistance. 3T3-L1 adipocytes incubated with media conditioned by RAW264.7 macrophages (RAW-CM) showed dramatically increased transcription of several inflammation-related genes, greater nuclear factor kappa B (NF-kappaB) activity, and enhanced binding of U937 monocytes. All of these effects were prevented by co-incubation with pyrrolidinedithiocarbamate, an NF-kappaB inhibitor. Adipocytes incubated with RAW-CM also released more non-esterified fatty acids and this increased lipolysis was not suppressed by insulin. In addition, RAW-CM treatment decreased insulin-stimulated glucose uptake in adipocytes. Taken together, these results indicate that macrophage-secreted factors induce inflammatory responses and reduce insulin responsiveness in adipocytes. These effects of macrophage-secreted factors on adipocytes may contribute significantly to the systemic inflammation and insulin resistance associated with obesity.

3T3-L1 Cells↗

PubMed2006

Inflammation and cancer: how hot is the link?

Although inflammation has long been known as a localized protective reaction of tissue to irritation, injury, or infection, characterized by pain, redness, swelling, and sometimes loss of function, there has been a new realization about its role in a wide variety of diseases, including cancer. While acute inflammation is a part of the defense response, chronic inflammation can lead to cancer, diabetes, cardiovascular, pulmonary, and neurological diseases. Several pro-inflammatory gene products have been identified that mediate a critical role in suppression of apoptosis, proliferation, angiogenesis, invasion, and metastasis. Among these gene products are TNF and members of its superfamily, IL-1alpha, IL-1beta, IL-6, IL-8, IL-18, chemokines, MMP-9, VEGF, COX-2, and 5-LOX. The expression of all these genes are mainly regulated by the transcription factor NF-kappaB, which is constitutively active in most tumors and is induced by carcinogens (such as cigarette smoke), tumor promoters, carcinogenic viral proteins (HIV-tat, HIV-nef, HIV-vpr, KHSV, EBV-LMP1, HTLV1-tax, HPV, HCV, and HBV), chemotherapeutic agents, and gamma-irradiation. These observations imply that anti-inflammatory agents that suppress NF-kappaB or NF-kappaB-regulated products should have a potential in both the prevention and treatment of cancer. The current review describes in detail the critical link between inflammation and cancer.

Anti-Inflammatory Agents↗

PubMed2006

NF-kappaB and inflammation in genetic disease.

By responding to pro-inflammatory cytokines, such as IL-1beta and TNF-alpha, and controlling itself the expression of numerous mediators of inflammation, NF-kappaB plays a pivotal role in controlling the proper sequence of events characterizing the inflammation process. Although excessive NF-kappaB activation is often associated with inflammatory signs in many different tissues, impaired NF-kappaB activation can also generate inflammation. This is the case in humans suffering from the genetic disease incontinentia pigmenti that exhibit severe skin inflammation. Identifying the molecular basis of this pathology, mutations affecting the gene coding for NEMO, has allowed production of mouse models for investigating the disease. Their characterization supports the view that a very tight positive and negative regulation of the NF-kappaB signaling pathway is required in vivo to ensure not only a fine-tuned response to injury or infection but also to maintain tissue homeostasis.

Animals↗

PubMed2005

Transgenic AD model mice, effects of potential anti-AD treatments on inflammation and pathology.

The extracellular deposition of amyloid (A) peptides in plaques, and neurofibrillary tangles are the two characteristic pathological features of Alzheimer's disease (AD). Plaques are surrounded by activated astrocytes and microglia, to study the relation between amyloid neuropathology and inflammation, we examined the changes in amyloid pathology in the hippocampus following three different treatments aimed at reducing the amyloid burden. (1) To investigate the effects of long-term cholinergic deafferentation, we lesioned the fimbria-fornix pathway in our AD-model mice at 7 months of age, and 11 months post-lesion the mice were sacrificed for histopathological analysis. The fimbria-fornix transection resulted in a substantial depletion of cholinergic markers in the hippocampus, but the lesion did not result in an alteration in hippocampal A deposition and inflammation (i.e., numbers or staining density of astrocytes and microglia). (2) To investigate the effects of estrogen, we ovariectomized mice and treated them with estrogen (sham-lesion, zero dose, low dose, and high dose) and studied the pathology at different postsurgery intervals. Estrogen depletion (i.e., ovariectomy) or estrogen replacement did not affect A deposition or inflammation at any time point. (3) In the final studies, we treated mice with flurbiprofen and an NO-donating derivative of flurbiprofen (HCT 1026) for several months (from 6 till 14 months of age), and studied the A pathology and inflammation in the brain. Sham treatment, flurbiprofen, and the low-dose HCT 1026 did not affect pathology; however, a higher dose of HCT 1026 reduced both A load and amount of microglial activation surrounding plaques.

Acetylcholinesterase↗

PubMed2005

Autoimmune hepatic inflammation by vaccination of mice with dendritic cells loaded with well-differentiated hepatocellular carcinoma cells and administration of interleukin-12.

Vaccination of mice with dendritic cells loaded with Hepa1-6, well-differentiated hepatocellular carcinoma cell line (DC/Hepa1-6), induced cytotoxic T lymphocytes against Hepa1-6. Liver-specific inflammation was generated by vaccination of mice with DC/Hepa1-6 and subsequent administration of interleukin (IL)-12. Vaccination with DCs loaded with MC38 or B16 and administration of IL-12 did not generate significant liver-specific inflammation. Splenic T cells from DC/Hepa1-6-vaccinated mice showed proliferative response by stimulation with S-100 protein of the liver and showed cytotoxic activity to hepatocytes. Hepatic mononuclear cells from DC/Hepa1-6 + IL-12-treated mice also showed cytotoxic activity to hepatocytes. Adoptive transfer of splenocytes from DC/Hepa1-6-vaccinated mice produced hepatic inflammation in recipient mice that had been pretreated with IL-12. IL-12 upregulated the expression of adhesion molecules and chemokines in the liver. In conclusion, CTLs responsive to hepatocytes induced by DC/Hepa1-6 and enhanced expression of adhesion molecules and chemokines in the liver by IL-12 would produce autoimmune hepatic inflammation.

Animals↗

PubMed2006

The influence of the time course of inflammation and spinalization on the antinociceptive activity of the alpha2-adrenoceptor agonist medetomidine.

The purpose of the present study was to investigate the influence of the time course of inflammation and the implication of spinal and supraspinal sites on the antihyperalgesic effects of the alpha(2)-adrenoceptor agonist medetomidine. Behavioral experiments showed a more intense antihyperalgesia in the phase of maintenance of inflammation than in the early or resolution stages. Maximum effect, without sedation, was observed with a dose of 40 microg/kg (66+/-12% and 76+/-15% reduction of mechanical and thermal hyperalgesia). No change was observed in the paw swelling, indicating that its effects were not secondary to a reduction of inflammation. In electrophysiological experiments, the effect was more pronounced in animals with an intact spinal cord than in spinalized animals (max. effects of 2+/-0.7% vs. 48+/-11% of control, noxious mechanical stimulation). We conclude that the antihyperalgesic effect of medetomidine depends on the time course of inflammation and that it is mainly located supraspinally.

Adrenergic alpha-2 Receptor Agonists↗

PubMed2006

Effects of NO-1886 on inflammation-associated cytokines in high-fat/high-sucrose/high-cholesterol diet-fed miniature pigs.

Inflammation, closely associated with obesity, is emerging as an important risk factor for the pathophysiological development of atherosclerosis and diabetes mellitus. Fat balance is critical in the aetiology of obesity. Lipoprotein lipase is an important enzyme in lipid metabolism. The aim of this study was to investigate the long-term effect of the lipoprotein lipase activator, NO-1886, on inflammation cytokines, adiposity and related diseases in miniature pigs fed a high-fat/high-sucrose/high-cholesterol diet (HFSC diet). Chinese Bama-miniature pigs were fed a control diet or HFSC diet with or without NO-1886 for 5 months. The levels of inflammation-associated cytokines were determined using the antibody arrays. Feeding of the HFSC diet to miniature pigs markedly increased the expression of inflammatory cytokines. On the other hand, supplementation of NO-1886 to HFSC diet decreased the expression of inflammatory cytokines significantly, protecting against the development of atherosclerosis and diabetes mellitus. NO-1886 may have a beneficial effect on the most inflammation-associated cytokines, and this effect may contribute to improving atherosclerosis and diabetes mellitus.

Animals↗