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At least 883 records · Page 49Linked to original sources
PubMed2005

Experimental inflammation of the rat distal colon inhibits ion secretion in the proximal colon by affecting the enteric nervous system.

Intestinal inflammation causes hyporesponsiveness of the inflamed tissue to secretagogues but little is known about the behaviour of the areas proximal to the site of inflammation. We studied the responses of the proximal segment of the colon to carbachol, histamine, isobutylmethylxanthine (IBMX) and vasoactive intestinal peptide (VIP) in rats with trinitrobenzenesulphonic acid (TNBS)-induced, chronic inflammation of the distal colon. Macroscopic and biochemical analysis ruled out the presence of inflammation in the proximal colon. When mounted in Ussing chambers under voltage-clamp conditions, basal transport and conductance were not affected. However, the maximum response in the concentration/response curves (short-circuit current) for carbachol and histamine was reduced in TNBS-treated rats, without changes in the EC(50). This effect corresponded to reduced chloride secretion, as demonstrated by ion substitution experiments. The responses to IBMX and VIP were virtually unaffected. The inhibitory effect was abolished by pretreatment with the neural blockers tetrodotoxin and lidocaine but not indomethacin, suggesting that the enteric nervous system is responsible for the inhibition. In conclusion, chronic distal inflammation of the distal colon results in inhibition of calcium-dependent secretion in the proximal colon via a reduction of the contribution of the enteric nervous system.

1-Methyl-3-isobutylxanthine↗
PubMed2005

Interrelationship among neutrophil efficiency, inflammation, antioxidant activity and zinc pool in very old age.

Neutrophils are the first barrier against infections. Aged neutrophils display impaired oxidative burst and phagocytosis with subsequent less capability to destroy bacteria. In successful ageing (nonagenarians), neutrophil efficiency (phagocytosis) increases. After ingested microbes, aged neutrophils are less prone to undergo apoptosis favouring chronic inflammation. Moreover, the superoxide dismutase (SOD) activity, which is necessary in avoiding ROS produced by oxidative burst, is limited in ageing. The mechanisms of age-related changes in neutrophil function are not fully understood, taking also into account that nonagenarians escape infections in comparison with elderly. Zinc pool may be involved because it is pivotal for neutrophil efficiency and SOD activity. Since zinc also controls the inflammation, via IL-6 and soluble factor of gp130 (sgp130), we have assessed the possible interrelationship among oxidative burst, apoptosis, inflammation, SOD, adhesion molecule Mac-1 and zinc pool in elderly and in nonagenarians. The oxidative burst and the capacity to increase Mac-1 after PMA stimulation decrease both in elderly and nonagenarians, but the latter display a slight increased neutrophil induced apoptosis, decreased sgp130, increased SOD, and more neutrophil zinc content, as it occurs in young-adults. Significant correlation exists between sgp130 and zinc pool in very old age. These findings suggest lower chronic inflammation in nonagenarians, via more zinc available, with subsequent long-life survival. Therefore, a more correct interrelationship among neutrophil efficiency, inflammation, antioxidant activity and zinc pool exists in successful ageing with subsequent more effectiveness to control the inflammatory response to pathogens.

Adult↗
PubMed2005

Novel -209A/G MT2A polymorphism in old patients with type 2 diabetes and atherosclerosis: relationship with inflammation (IL-6) and zinc.

Vascular complications, including ischaemic cardiomyopathy, are the major causes of death in old diabetic patients. Chronic inflammation due to high IL-6 production occurs in type 2 diabetes (NIDDM) and atherosclerosis. High levels of IL-6 are associated with hyperglycaemia, dyslipidemia and provoke insulin resistance. In ageing and inflammation, IL-6 affects Metallothionein (MT) homeostasis, which in turn is involved in zinc turnover. Zinc deficiency is an usual event in ageing, inflammation, type 2 diabetes and atherosclerosis. No genetic study exists on MT polymorphisms in NIDDM-atherosclerotic patients. The aim of the present study is to screen a single nucleotide polymorphism in the promoter region of the MT2A gene in relation to inflammation (IL-6) and plasma zinc in NIDDM-atherosclerotic patients. The -209 A/G MT2A polymorphism is associated with chronic inflammation (higher plasma levels of IL-6), hyperglycaemia, enhanced HbA1c and more marked zinc deficiency in AA than AG genotype carrying patients. Analysing patients and controls subdivided in AA and AG genotypes, significant interactions existed between disease status and genotypes for glucose and zinc. AA patients are more at risk of developing NIDDM in association with atherosclerosis (p=0.0015 odds ratio=2.617) and its complications, such as ischaemic cardiomyopathy (p=0.0050 odds ratio=12.6). In conclusion, high levels of IL-6 unmask the phenotypes (higher insulin resistance and zinc deficiency) in relation to the genotypes with subsequent risk of developing ischaemic cardiomyopathy in NIDDM-atherosclerotic patients carrying AA genotype. Hence, the novel -209A/G MT2A polymorphism may be a further useful tool for the prevention, diagnosis and therapy of these combined pathologies in the elderly.

Aged↗
PubMed2004

Inflammation and atherosclerosis.

Inflammation plays a pivotal role in all stages of atherogenesis, from foam cell to plaque formation to rupture and ultimately to thrombosis. Insight gained from recent basic and clinical data linking inflammation to atherosclerosis has yielded important diagnostic and prognostic information. Low-grade chronic inflammation as measured by high sensitivity C-reactive protein predicts future risk of acute coronary syndrome independent of traditional cardiovascular risk factors. In addition, individuals with higher "inflammatory burden" gain the largest absolute risk reduction with aggressive risk-lowering therapy. The link between inflammation and atherosclerosis provides a new venue for future pharmacologic agents that may slow the progression of atherosclerosis by inhibiting inflammation.

Animals↗
PubMed2006

The effect of weight loss and dietary fatty acids on inflammation.

Inflammation plays a pivotal role in all stages of atherosclerosis. Weight loss appears to be the best nonpharmacologic modality to reduce inflammation. Intervention trials convincingly demonstrate that weight loss reduces biomarkers of inflammation, such as C-reactive protein. Limited studies have shown that certain dietary fatty acids (ie, oleic acid and alpha-linolenic acid) reduce biomarkers of inflammation. Most of the studies with fish oil supplementation have shown null effects, and conflicting results have been reported with saturated and trans fatty acids. Much further research is needed to define the role of individual dietary factors on the biomarkers of inflammation and the mechanism of the anti-inflammatory effects of weight loss.

Atherosclerosis↗
PubMed1989

Abnormal fetal heart rate patterns and placental inflammation.

Can acute inflammation in the placental membranes, amniotic fluid, or both, predispose to the development of abnormal fetal heart rate patterns? One hundred cases in which bradycardia was noted were compared with 48 cases in which abnormal fetal heart rate patterns did not occur. Case and control subjects were matched to provide an equivalent risk of developing ascending infection in the two groups. Fetoplacental weight ratio and the presence of other placental diseases were also considered. The presence of acute inflammation in the umbilical cord (p = 0.03), amnion (p = 0.01), and choriodecidua (p = 0.03), and higher grades of inflammation in chorionic plate (p = 0.03) were linked to the presence of abnormal fetal heart rate patterns. No other placental factors were associated with increased risk of fetal bradycardia. The association of abnormal fetal heart rate patterns with acute inflammation suggests that intra-amniotic inflammation is important in the genesis of fetal bradycardias. The inflamed amniotic fluid could alter fetal metabolism via effects on the pulmonary or gastrointestinal systems or effects on umbilical and chorionic vessels.

Acute Disease↗
PubMed1990

Apolipoprotein A-I and apolipoprotein SAA half-lives during acute inflammation and amyloidogenesis.

The half-lives of two apolipoproteins of mouse high-density lipoproteins, apo A-I and apo SAA, were determined in normal animals and compared with those having an inflammatory condition, or inflammation leading to AA amyloid deposition. The apo A-I half-life was considerably shorter in animals with inflammation and in those that were preamyloidotic, than in controls (t1/2 of 3-3.5 h vs. 10-12 h). The average loss of apo A-I in controls over the first 10 h was 31.1 micrograms/ml per h, while that in inflamed animals was 58.7 micrograms/ml per h a 2-fold increase in apo A-I clearance. The apo SAA half-life was similar in all groups of animals and was of the order of 1.5 h. The concentration of apo SAA during inflammation is however considerably higher (500-1000-fold) than in controls, which implies a much greater clearance rate during inflammation and involving a process which is apparently not saturable. In addition to hypertriglyceridemia and Tangier's disease, ordinary acute inflammation can now be added to those pathological conditions which lead to a significant decrease in apo A-I half-life.

Amyloid↗
PubMed1994

Suppression of acute inflammation with liposome associated prostaglandin E1.

Prostaglandin E1 (PGE1) suppresses leucocyte effector function and reduces inflammation in several animal models of acute and chronic inflammation. A drawback to its use as a therapeutic agent is the relatively high doses needed to suppress inflammation. We present evidence in this report that liposome associated PGE1 (LAP) reduces markedly acute inflammation induced in a subcutaneous air pouch by monosodium urate crystals, and by the polypeptide mediators, interleukin 1-beta (IL-1 beta) and tumor necrosis factor alpha (TNF alpha). A single dose of 12 micrograms/kg LAP given intravenously 2 hr after inflammation was induced, reduced accumulation of cells and exudate by 31-49%.

Acute Disease↗
PubMed1992

Activity-dependent neuronal plasticity following tissue injury and inflammation.

Increases in neuronal activity in response to tissue injury lead to changes in gene expression and prolonged changes in the nervous system. These functional changes appear to contribute to the hyperalgesia and spontaneous pain associated with tissue injury. This activity-dependent plasticity involves neuropeptides, such as dynorphin, substance P and calcitonin gene-related peptide, and excitatory amino acids, such as NMDA, which are chemical mediators involved in nociceptive processing. Unilateral inflammation in the hindpaw of the rat results in an increase in the expression of preprodynorphin and preproenkephalin mRNA in the spinal cord, which parallels the behavioral hyperalgesia associated with the inflammation. Cellular intermediate-early genes, such as c-fos, are also expressed in spinal cord neurons following inflammation and activation of nociceptors. Peripheral inflammation results in an enlargement of the receptive fields of many of these neurons. Dynorphin applied to the spinal cord also induces an enlargement of receptive fields. NMDA antagonists block the hyperexcitability produced by inflammation. A model has been proposed in which dynorphin, substance P and calcitonin gene-related peptide enhance excitability at NMDA receptor sites, leading first to dorsal horn hyperexcitability and then to excessive depolarization and excitotoxicity.

Animals↗
PubMed1986

Inhibition of complement dependent experimental inflammation in human skin by different heparin fractions.

The anticoagulant activity of heparin is dependent on its affinity for antithrombin III (AT III) and on its molecular weight. In contrast, heparin fractions differing in these respects are equally effective inhibitors of the human complement system in vitro. In this study we designed and evaluated a model to investigate the effects of different heparin fractions on a complement dependent inflammation. Locally administered heparin, in a dose-dependent manner, inhibited the flare, itch and wheal responses induced by intradermal injection of heat-aggregated human IgG (HAGG). These reactions were also inhibited by the antihistamine mepyramine, favouring the view that HAGG activates complement and that the observed inflammatory response is mediated by anaphylatoxin liberation of histamine. Similar cutaneous reactions induced by trypsin, which can generate C3a and C5a by proteolysis of C3 and C5, the histamine liberator compound 48/80 or histamine were inhibited by mepyramine but not by heparin. Thus it is strongly suggested that heparin inhibits the HAGG induced reactions by modulating the early pre-C3 steps of complement activation. On a weight basis heparin fractions differing in AT III-affinity or in average molecular weight (5,000 and 16,000 D) were equally potent modulators of the HAGG-induced inflammation. We conclude that heparin can inhibit an apparently complement-dependent inflammation irrespective of its AT III-affinity or of its size, and suggest that a heparin with low anticoagulant activity could be of value as a modulator of inflammation and should be useful in investigating the consequences of complement inhibition in inflammation.

Animals↗
PubMed1986

Studies on the effect of experimental inflammation on sialyltransferase in the mouse and guinea pig.

The effect of inflammation on sialyltransferase was studied in the mouse and guinea pig. There was a three-fold increase in mouse liver sialyltransferase activity reaching a maximum at 72 hr after inflammation; serum levels were increased by five-fold at 72 hr after inflammation. The response of guinea pig sialyltransferase was slower and of lower magnitude compared with the response of the mouse enzyme; liver and serum sialyltransferase increased by about 50% reaching a maximum at 96 hr after inflammation. The specificity of the enzyme that responded to inflammation in the mouse and guinea pig was found to be Gal beta 1----4GlcNAc alpha 2----6 sialyltransferase, the same enzyme activity that was shown to be an acute phase reactant in earlier studies in the rat (Kaplan et al., 1983).

Animals↗
PubMed1993

Inhibition of IL-1 beta-induced peripheral inflammation by peripheral and central administration of analogs of the neuropeptide alpha-MSH.

Interleukin-1 (IL-1) is a proinflammatory cytokine, alpha-MSH(1-13) molecules inhibit inflammation induced by cytokines, other mediators of inflammation, and by peripheral irritants. D-valine substitution in the antiinflammatory/antipyretic message sequence [alpha-MSH(11-13), Lys-Pro-Val] of alpha-MSH(1-13) increases the activity of the tripeptide. Our aim was to learn if D-valine substitution also enhances the antiinflammatory activity of the entire alpha-MSH(1-13) molecule and to determine if an antipyretic D-valine-substituted alpha-MSH(8-13) molecule is also antiinflammatory. Intraperitoneal injection of alpha-MSH(1-13) and of (D-Val13)alpha-MSH(1-13) caused dose-related suppression of ear edema induced in mice by intradermal injection of IL-1 beta; the two molecules were equipotent. (D-Val13)alpha-MSH(8-13) likewise inhibited inflammation, but the potency was less than that of the larger molecules. Intracerebroventricular injections of (D-Val13)alpha-MSH(1-13) and of the unsubstituted molecule were equipotent in reducing inflammation; the (D-Val13)alpha-MSH(8-13) molecule was less effective. The results support the idea that the alpha-MSH(1-13) molecule inhibits inflammation and suggest that the L-conformation of alpha-MSH(1-13) is maximally effective with regard to its antiinflammatory activity. The results with alpha-MSH(8-13) are consistent with previous findings of lesser antihost response activity of alpha-MSH fragments that contain the COOH-terminal tripeptide Lys-Pro-Val.

Animals↗
PubMed2005

The implication of obesity and central fat on markers of chronic inflammation: The ATTICA study.

OBJECTIVE: We evaluated the association of obesity with various markers of chronic inflammation, in a population-based sample of 3,042 adults. METHODS: During 2001-2002, we randomly enrolled 1,514 men (18-87 years old) and 1,528 women (18-89 years old), from the Attica area, Greece; the sampling was stratified by the age-sex distribution of the region (census 2001). Among several variables, we also measured various inflammatory markers (C-reactive protein, tumor necrosis factor alpha, amyloid A, white blood cells and interleukin-6) and anthropometric variables (weight, height, waist and hip circumferences). Central fat was defined as waist-to-hip ratio>or=0.95 in men and>or=0.8 in women, while obesity as body mass index (BMI)>29.9 kg/m(2). RESULTS: Central fat prevailed in 36% of men and 43% of women (p<0.001), while obesity prevailed in 20% of men and 15% of women, respectively. Compared to participants with normal body fat distribution, those with central fat exhibited 53% higher C-reactive protein levels, 30% higher tumor necrosis factor, alpha levels, 26% higher amyloid A levels, 17% higher white blood cell counts and 42% higher interleukin-6 levels (all p<0.05). We observed that all inflammation markers were related to BMI (index for obesity), waist and to waist-to-hip ratio (indices for central fat), in both genders. Moreover, the models that included waist or waist-to-hip ratio as independent variable had higher explanatory ability (i.e. R(2)) than the models included BMI, especially in women, even after adjusting for age and various other potential confounders. CONCLUSION: Our results suggest a relationship between central adiposity and inflammation process, irrespective of age and other potential confounders. This association was more prominent than the relationship between total obesity and inflammation. It could be hypothesized that a disproportionate accumulation of visceral fat mass could be partially associated with increased coronary risk, through inflammation process.

Adolescent↗
PubMed2004

Is damage in central nervous system due to inflammation?

The aim of this work was to review the inflammatory factors involved in central nervous system (CNS) inflammation and the damage associated to their participation in an inflammatory disease of CNS, multiple sclerosis in humans and experimental allergic encephalomyelitis in the murine model. Inflammation has an important repairing function, nevertheless frequently in the CNS inflammation is the cause of damage and it does not fulfill this repairing function as it happens in other compartments of the body. The inflammatory response in the CNS involves the participation of different cellular types of the immune system (macrophages, mast cells, T and B lymphocytes, dendritic cells) and resident cells of the CNS (microglia, astrocytes, neurons), adhesion molecules, cytokines and chemokines among other proteic components. During neuroinflammation chemotaxis is an important event in the recruitment of cells to the CNS. The lymphocyte recruitment implies the presence of chemokines and chemokine receptors, the expression of adhesion molecules, the interaction between lymphocytes and the bloodbrain barrier (BBB) endothelium, and finally their passage through the BBB to arrive at the site of inflammation. If this process is not controlled, is prolonged, inflammation loses its repairing function and can be the cause of damage. Usually neuroinflammation has the tendency to decline to damage, which would explain most of the CNS pathologies.

Animals↗
PubMed2006

Inflammation: a pivotal link between autoimmune diseases and atherosclerosis.

Premature coronary heart disease has emerged as a major cause of morbidity and mortality in systemic autoimmune diseases. Recent epidemiologic and pathogenesis studies have suggested a great deal in common between the pathogenesis of prototypic autoimmune disease such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and that of atherosclerosis. Some of the most remarkable data in support of a link between autoimmunity and atherosclerosis comes from epidemiological studies of patients with autoimmune disorders (RA and SLE). Many epidemiologic observations have linked systemic inflammation with the cardiovascular events in autoimmune disease such as RA and SLE. Inflammation is increasingly being considered central to the pathogenesis of atherosclerosis and an important risk factor for vascular disease. Systemic inflammation may be regarded as accelerating the atherosclerotic process. Systemic levels of soluble inflammatory mediators such as C-reactive protein (CRP) have been associated with cardiovascular risk in the general population. CRP, or more specifically high sensitivity-hsCRP, is a marker of systemic inflammation that has been identified as a valid biomarker of cardiovascular risk. Furthermore, the immunomodulatory and anti-inflammatory actions of statins may affect their utility in the context of chronic inflammatory autoimmune disease. Thus, effective control or dampening of inflammation, with such agents, should be included in the therapeutic armamentarium of autoimmune diseases with the aim of protecting against cardiovascular disease.

Animals↗
PubMed2005

Glycosylation of site-specific glycans of alpha1-acid glycoprotein and alterations in acute and chronic inflammation.

BACKGROUND: alpha(1)-Acid glycoprotein (AGP), an acute phase reactant, is extensively glycosylated at five Asn-linked glycosylation sites. In a number of pathophysiological states, including inflammation, rheumatoid arthritis, and cancer, alterations of Asn-linked glycans (N-glycans) have been reported. We investigated alteration of N-glycans at each of glycosylation sites of AGP in the sera of patients with acute and chronic inflammation. METHODS: AGP purified from sera was digested with Glu-C and the liberated glycopeptides were isolated by reverse phase HPLC. N-glycans released with peptide N-glycosidase F and followed by neuraminidase treatment were analyzed by matrix-assisted laser desorption ionization-time of flight mass spectrometry. RESULTS: Site-specific differences in branching structures were observed among N-glycosylation sites 1, 3, 4 and 5. Within the sera of patients with acute inflammation, increases in bi-antennary and decreases in tri- and tetra-antennary structures were observed, as well as increases in alpha1,3-fucosylation, at most glycosylation sites. In the sera of patients with chronic inflammation, increased rates of tri-antennary alpha1,3-fucosylation at sites 3 and 4 and tetra-antennary alpha1,3-fucosylation at sites 3, 4 and 5 were detected. Although there were no significant differences between acute and chronic sera in site directed branching structures, significant differences of alpha1,3-fucosylation were detected in tri-antennary at sites 2, 4 and 5 and in tetra-antennary at sites 3 and 4. CONCLUSION: Little variation in the N-glycan composition of the glycosylation sites of AGP was observed among healthy individuals, while the sera of patients with acute inflammation demonstrated increased numbers of bi-antennary and alpha1,3-fucosylated N-glycan structures at each glycosylation site.

Acute Disease↗
PubMed2005

Sequential induction of prostaglandin E and D synthases in inflammation.

Enhanced biosynthesis of prostaglandin (PG)D(2) and subsequent formation of 15-deoxy-Delta(12,14)-PGJ(2) has been suggested to contribute to resolution of inflammation. The primary aim of the present study in mouse heart was, therefore, to determine at the transcriptional level if there is sequential induction of PGE and PGD synthases (S) during inflammation. Expression of interleukin (IL)-1beta in heart was enhanced 4h after systemic inflammation and declined thereafter within 3-5 days to basal levels. In contrast to cyclooxygenase-2 and membrane-bound (m)-PGES-1, which both peaked 4h after endotoxin administration, hematopoietic (H)-PGDS expression was enhanced only >or=48h after endotoxin. The expression of lipocalin-type (L)-PGDS was not significantly influenced. mRNA encoding the putative target of 15-deoxy-Delta(12,14)-PGJ(2), peroxisome proliferator-activated receptor gamma, was enhanced between 4 and 24h after induction of inflammation. Treatment of mice with acetylsalicylic acid or indomethacin at doses effective to cause near-complete inhibition of PGE(2) and PGD(2) biosynthesis in heart ex vivo resulted in enhanced expression of IL-1beta 24h after endotoxin administration. These results provide additional support for the hypothesis of a shift towards PGD(2) biosynthesis during resolution of inflammation.

Animals↗
PubMed2005

Effects of peripheral inflammation on activation of ERK in the rostral ventromedial medulla.

In the present study, the activation of extracellular signal-regulated kinase (ERK) in the rostral ventromedial medulla (RVM) following the injection of complete Freund's adjuvant (CFA) into the rat hindpaw was examined in order to clarify the mechanisms underlying the dynamic changes in the descending pain modulatory system after peripheral inflammation. Phospho-extracellular signal-regulated kinase-immunoreactive (p-ERK-IR) neurons were observed in the nucleus raphe magnus (NRM) and nucleus reticularis gigantocellularis pars alpha (GiA). Inflammation induced the activation of ERK in the RVM, with a peak at 7 h after the injection of CFA into the hindpaw and a duration of 24 h. In the RVM, the number of p-ERK-IR neurons per section in rats killed at 7 h after CFA injection (14.2 +/- 1.7) was significantly higher than that in the control group (4.5 +/- 0.9) [P < 0.01]. At 7 h after CFA injection, about 60% of p-ERK-IR neurons in the RVM were serotonergic neurons. The percentage of RVM serotonergic neurons that are also p-ERK positive in the rats with inflammation (20.5% +/- 2.3%) was seven times higher than that in control rats (2.7% +/- 1.4%) [P < 0.01]. These findings suggest that inflammation-induced activation of ERK in the RVM may be involved in the plasticity in the descending pain modulatory system following inflammation.

Adjuvants, Immunologic↗