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At least 1,603 records · Page 89Linked to original sources
PubMed2006

Beta-endorphin differentially affects inflammation in two inbred rat strains.

It has been shown that inflammation of rat paws elicits accumulation of opioid peptide beta-endorphin-containing immune cells in the inflamed subcutaneous tissue, contributing to immunocyte-produced pain suppression. However, the possible mechanisms involved in the pharmacological application of beta-endorphin in rat paw inflammation have not been investigated. The present study was set up to explore the effects of intraplantar injection of beta-endorphin on Concanavalin A-induced paw edema in two inbred rat strains, Albino Oxford (AO) and Dark Agouti (DA). Both high dose-induced suppression and low dose-induced potentiation of edema development in AO and DA rats, respectively, were blocked with antagonists specific for delta (naltrindole) and kappa (nor-binaltorphimine) opioid receptors. beta-endorphin in vitro decreased phagocytosis and increased nitric oxide (NO) production in air pouch granulocytes obtained from AO rats. However, in cells from DA rat strain beta-endorphin modulated both phagocytosis and NO production in a concentration-dependent manner. It could be concluded that the strain-dependent opposing effects of beta-endorphin on paw inflammation are mediated through delta and kappa opioid receptors and probably involve changes in the production of reactive oxygen species by inflammatory cells. Our results point to the importance of genotype for pharmacological manipulations and the development of inflammation.

Animals↗
PubMed2004

Plasma homocysteine and inflammation in elderly patients with cardiovascular disease and dementia.

Increased levels of plasma total homocysteine (tHcy) may play a role in both cardiovascular diseases (CVD) and old-age dementias via enhancement of vascular inflammation. However, the association between plasma tHcy and serum C-reactive protein (sCRP), taken as a marker of low-grade inflammation, is still uncertain. We investigated this association in normal aging, CVD, and dementia, and examined whether it was modified by the presence of two major comorbid diseases of older age: chronic obstructive pulmonary disease (CPOD) and peptic ulcer (PU). Six hundred-twenty-seven individuals aged > or = 65 yr (74+/-7 yr) were selected for this study: 373 healthy controls; 160 patients with CVD but no evidence of comorbid diseases (CVD+/comorbidity-); 46 patients with CVD and concurrent CPOD and/or PU (CVD+/comorbidity+); and 48 patients with dementia. A positive association between plasma tHcy and serum CRP, independent of several confounders (socio-demographic status, known tHcy and sCRP determinants, inflammation markers, traditional vascular risk factors), was found for CVD+/comorbidity+ (p=0.001; not affected by dementia type) and dementia (p=0.001; not affected by dementia type), but not for CVD+/comorbidity- and controls. The results suggest that the association between plasma tHcy and sCRP is more an aspecific reflection of poor health than a specific correlate of vascular inflammation.

Aged↗
PubMed2005

CD4+CD25+ suppressor T cells regulate pathogen induced inflammation and disease.

A key suppressor role has recently been ascribed to the natural CD4+CD25+ regulatory T cells (Treg), the removal of which leads to the development of autoimmune disease and aggravated pathogen-induced inflammation in otherwise normal hosts. The repertoire of antigen specificities of Treg is as broad as that of naive T cells, recognizing both self and non-self antigens, enabling Treg to control a broad range of immune responses. Although widely acknowledged to play a role in the maintenance of self-tolerance, recent studies indicate that Treg can be activated and expanded against bacterial, viral and parasite antigens in vivo. Such pathogen-specific Treg can prevent infection-induced immunopathology but may also increase the load of infection and prolong pathogen persistence by suppressing protective immune responses. This review discusses the role of Treg in the prevention of exaggerated inflammation favoring chronicity in bacterial or fungal infections and latency in viral infections. Special attention is given to the role of Treg in the modulation of gastric inflammation induced by Helicobacter pylori infection. Findings in both experimentally infected mice and humans with natural infection indicate that Treg are important in protecting the H. pylori-infected host against excessive gastric inflammation and disease symptoms but on the negative side promote bacterial colonization at the gastric and duodenal mucosa which may increase the risk in H. pylori-infected individuals to develop duodenal ulcers.

Animals↗
PubMed2005

C-reactive protein and atrial fibrillation: "evidence for the presence of inflammation in the perpetuation of the arrhythmia".

BACKGROUND: Atrial fibrillation (AF) is associated to a high risk of systemic embolism. The mechanisms that contribute to thrombogenesis in these patients are still poorly understood. Systemic and/or local inflammation could be involved in the process of thrombogenesis and contribute to the perpetuation of the arrhythmia. The purpose of the study was to evaluate the role of inflammation and its relation to thrombogenesis and cardiac rhythm in AF. METHODS: We prospectively studied 130 patients with newly diagnosed non-valvular AF in absence of antithrombotic therapy. Determinations of C-reactive protein (CRP) and thrombin-antithrombin complex (TAT) plasma levels, along with a transesophageal echocardiogram were performed in all the patients at admission. RESULTS: Mean age of the group was 67+/-14 years. CRP levels were significantly elevated in AF patients versus controls (matched by age, gender and cardiovascular risk factors) (1.0+/-1.8 versus 0.3+/-0.4 mg/dl, respectively, p<0.01). Baseline TAT levels were also significantly elevated in AF patients but no correlation was found between CRP and TAT. At 1-year of follow-up, mean CRP levels were still elevated in patients that remained in AF compared to those who converted to sinus rhythm (1.2+/-1.8 compared to 0.5+/-1.5 mg/dl, p=0.03). CRP was the only biochemical predictor of sinus rhythm maintenance at 1-year follow-up independently of clinical (including adjustment for risk factors and antiarrhythmic drugs), biochemical and echo parameters. CONCLUSIONS: There is evidence for the presence of inflammation in patients with non-valvular AF, which is not related to activation of the coagulation cascade. The persistence of inflammation is associated with chronic AF at 1-year follow up.

Aged↗
PubMed2004

Therapeutic efficacy of sustained drug release from chitosan gel on local inflammation.

The model anti-inflammatory drug prednisolone (PS) was retained in chitosan (CS) gel beads, which were prepared in a 10% aqueous amino acid solution (pH 9.0). Sustained release of PS from the CS gel beads was observed. Carrageenan solution was injected into air pouches (AP), which were prepared subcutaneously on the dorsal surface of mice, in order to induce local inflammation. CS gel beads retaining PS were then implanted into the AP to investigate the therapeutic efficacy of sustained PS release against local inflammation. In vivo PS release from CS gel beads was governed by both diffusion of the drug and degradation of the gel matrix. Sustained drug release by CS gel beads allowed the supply of the minimum effective dose and facilitated prolonged periods of local drug presence. Inflammation indexes were significantly reduced after implantation of CS gel beads when compared with injection of PS suspension. Thus, extension of the duration of drug activity by CS gel beads resulted in improved therapeutic efficacy. These observations indicate that CS gel beads are a promising biocompatible and biodegradable vehicle for treatment of local inflammation.

Adjuvants, Pharmaceutic↗
PubMed2004

Accumulation of radiolabelled low molecular peptides and proteins in experimental inflammation.

This study focuses on evaluating accumulation of the low molecular peptides and proteins labelled with 99mTc in rat inflammatory/infection foci. Peptides (human leukocyte dialysate, HLD; thymosin fraction 5, TF5; aprotinin, APT), and proteins (human IgG, HIG) were labelled with 99mTc using redox polymer. The labelling efficiency was evaluated using paper, TLC and/or column chromatography. Biodistribution of labelled substances was evaluated in rats with Staphylococcus aureus infection or with sterile kaolin suspension inflammation 24 h after abscess induction. Accumulation of 99mTc activity was determinated both by external gamma camera imaging and by counting dissected tissues 4 h after administration. The evaluated peptides and proteins show high labelling efficiency (99mTc-HLD>98%, 99mTc-TF5>95%, 99mTc-APT>98%, 99mTc-HIG>95%). Usage of redox polymer for labelling increases the stability of 99mTc-labelled substances. The labelling efficiency stays nearly the same (95-98%) after 8 h at least. In experimentally induced inflammation the amount of 99mTc-peptides and 99mTc-HIG activity accumulated is 2.5-6.5 and 5.3-10.6 times higher than in a control tissue. When comparing two types of model inflammations (kaolin- and Staphylococcus-induced ones), the values measured with 99mTc-peptides are more than double than those of kaolin suspension inflammation. The studied low molecular peptides labelled with 99mTc allow rapid localisation of infection foci. 99mTc labelled HIG proved useful for detection of infections and inflammatory lesions.

Animals↗
PubMed2005

Basophils play a critical role in the development of IgE-mediated chronic allergic inflammation independently of T cells and mast cells.

The recruitment of basophils into the sites of allergic inflammation is often observed. However, no definitive evidence has been provided that basophils are crucially involved in the pathogenesis of chronic allergic disorders. Here, we show that basophils are responsible for the development of IgE-mediated chronic allergic inflammation independently of T cells and mast cells. A single subcutaneous injection of multivalent antigens elicited not only immediate- and late-phase ear swelling but also delayed-onset ear swelling with massive eosinophil infiltration in mice sensitized with antigen-specific IgE. Mast cells were essential for the immediate- and late-phase ear swelling but dispensable for the delayed one. T cells were also dispensable for the latter. Transfer of FcRI-expressing basophils into FcRI-deficient mice restored the development of the delayed-onset allergic inflammation. These findings indicate a novel mechanism of development of chronic allergic inflammation that is induced by basophils through the interaction of antigen, IgE, and FcRI.

Animals↗
PubMed2004

Angiogenesis as an immunopharmacologic target in inflammation and cancer.

Many pathological processes including wound healing, chronic inflammation and cancer require angiogenesis, i.e., the formation of new vasculature in the lesions. Accumulating evidence indicates that angiogenesis is crucial for both chronic inflammation and the growth of malignant tumors with the participation of diverse cytokines, chemokines and growth factors. It is nevertheless believed that differences exist in angiogenesis between cancer and chronic inflammatory diseases. The aim of this review is to outline the characteristics of angiogenesis in chronic inflammation and cancer. A better understanding of the angiogenic processes may facilitate the design of more effective therapies for chronic inflammation and cancer.

Angiogenesis Inhibitors↗
PubMed2004

Smad7 in TGF-beta-mediated negative regulation of gut inflammation.

Mice with targeted disruptions of the transforming growth factor-beta1 (TGF-beta1) gene or TGF-beta1 intracellular signalling pathways develop intestinal inflammation. Conversely, TGF-beta1-producing regulatory T cells protect against experimental colitis. Paradoxically, however, TGF-beta1 production is high in the gut of patients with chronic inflammatory intestinal disease, and yet inflammation proceeds unchecked. Here we discuss the functional role of Smad7, an intracellular inhibitor of TGF-beta1 signalling, in the control of gut inflammation by TGF-beta1. In particular, we delineate a scenario in which the high expression of Smad7 in inflammatory cells renders them unresponsive to TGF-beta1 and propose that control of Smad7, not TGF-beta1 production, is a key determinant in understanding how TGF-beta1 negatively regulates gut inflammation.

Animals↗
PubMed2005

Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree: a histopathologic study of patients dying of acute myocardial infarction.

OBJECTIVES: This study was undertaken to define and compare geographic coronary artery inflammation in patients who were dying of acute myocardial infarction (AMI), chronic stable angina (SA), and noncardiac causes (CTRL). BACKGROUND: Biochemical markers and flow cytometry provide indirect evidence of diffuse coronary inflammation in patients dying of acute coronary syndromes. Yet no histopathologic studies have corroborated these findings. A key unanswered question is whether the inflammatory burden involves the entire coronary tree or is limited to a few plaques. METHODS: We examined 544 coronary artery segments from 16 patients with AMI, 109 segments from 5 patients with SA, and 304 coronary segments from 9 patients with CTRL. RESULTS: An average of 6.8 +/- 0.5 vulnerable segments per patient were found in the AMI group (in addition to culprit lesions) compared with an average of 0.8 +/- 0.3 and 1.4 +/- 0.3 vulnerable lesions/patient in the SA and CTRL groups, respectively. The AMI group, independent of the type of plaque observed, showed significantly more inflammatory infiltrates compared with the SA and CTRL groups (121.6 +/- 12.4 cell x mm2 vs. 37.3 +/- 11.9 cell x mm2 vs. 26.6 +/- 6.8 cell x mm2, p = 0.0001). In AMI patients, active inflammation was not only evident within the culprit lesion and vulnerable plaques but also involved stable plaques. These showed a three- to four-fold higher inflammation than vulnerable and stable plaques from the SA and CTRL groups, respectively. CONCLUSIONS: This histopathologic study found that both vulnerable and stable coronary plaques of patients dying of AMI are diffusely infiltrated by inflammatory cells.

Aged↗
PubMed2005

Inflammation, as measured by the erythrocyte sedimentation rate, is an independent predictor for the development of heart failure.

OBJECTIVES: Our objective was to explore inflammation, measured as erythrocyte sedimentation rate (ESR), as a predictor for the development of heart failure (HF). BACKGROUND: In recent years, evidence of the importance of inflammation in the pathophysiology of HF has emerged, and various inflammatory markers have been found to predict future HF. Erythrocyte sedimentation rate is an inexpensive and easily accessible marker of systemic inflammation, but to this date it is unknown whether ESR predicts subsequent HF. METHODS: In a community-based prospective study of 2,314 middle-aged men free from HF, myocardial infarction, and valvular disease at baseline, ESR was analyzed in multivariable models together with established risk factors for HF (hypertension, diabetes, electrocardiographic left ventricular hypertrophy, smoking, obesity, and serum cholesterol) and hematocrit. RESULTS: A total of 282 men developed HF during a median follow-up time of 30 years. In Cox proportional hazards analyses, ESR was an independent predictor of HF (hazard ratio 1.46 for highest quartile vs. the lowest, 95% confidence interval 1.04 to 2.06). This observation remained significant when also adjusting for interim myocardial infarction during follow-up. CONCLUSIONS: Erythrocyte sedimentation rate was a significant predictor of HF, independent of established risk factors for HF, and interim myocardial infarction after three decades of follow-up in a population-based sample of middle-aged men. Our findings indicate that inflammation occurs early in the process leading to HF and that ESR could be used to evaluate this process.

Blood Sedimentation↗
PubMed2006

The effects of diet on inflammation: emphasis on the metabolic syndrome.

Reducing the incidence of coronary heart disease with diet is possible. The main dietary strategies include adequate omega-3 fatty acids intake, reduction of saturated and trans-fats, and consumption of a diet high in fruits, vegetables, nuts, and whole grains and low in refined grains. Each of these strategies may be associated with lower generation of inflammation. This review examines the epidemiologic and clinical evidence concerning diet and inflammation. Dietary patterns high in refined starches, sugar, and saturated and trans-fatty acids, poor in natural antioxidants and fiber from fruits, vegetables, and whole grains, and poor in omega-3 fatty acids may cause an activation of the innate immune system, most likely by an excessive production of proinflammatory cytokines associated with a reduced production of anti-inflammatory cytokines. The whole diet approach seems particularly promising to reduce the inflammation associated with the metabolic syndrome. The choice of healthy sources of carbohydrate, fat, and protein, associated with regular physical activity and avoidance of smoking, is critical to fighting the war against chronic disease. Western dietary patterns warm up inflammation, while prudent dietary patterns cool it down.

Antioxidants↗
PubMed2004

Both inflammation and remodeling influence nitric oxide output in children with refractory asthma.

BACKGROUND: Exhaled nitric oxide can be used to monitor airway inflammation in asthma. We hypothesized that the strong link between nitric oxide and inflammation may obscure a weaker link with airway remodeling. OBJECTIVE: The aim of this study was to determine whether airway remodeling influenced exhaled nitric oxide in 28 asthmatic children (median age [25th-75th], 11 [10-14] years old) with refractory asthma defined as airflow limitation and/or exacerbations despite high-dose inhaled steroids. METHODS: Multiple-flow analysis of exhaled nitric oxide was used to correlate alveolar nitric oxide concentration and maximal conducting airway nitric oxide output to pulmonary function tests, bronchoalveolar lavage, and bronchial biopsy findings. RESULTS: Nitric oxide measurements were related to inflammation and T(H)1/T(H)2 balance, that is, subepithelial eosinophilic infiltration and eosinophilic cationic protein and IFN-gamma/IL-4 ratio in bronchoalveolar lavage fluids. Nitric oxide measurements were also correlated with several parameters of airway remodeling: alveolar nitric oxide concentration with TGF-beta in bronchoalveolar lavage fluid (r = 0.42, P =.03) and maximal conducting airway nitric oxide output with reticular basement membrane thickness (r = 0.61, P =.0007) and tissue inhibitor of matrix metalloproteinases 1/matrix metalloproteinase 9 ratio in bronchoalveolar lavage fluid (r = 0.43, P =.04). Moreover, alveolar nitric oxide concentration was correlated with MEF(25-75) (r = 0.60, P =.02). CONCLUSIONS: These findings suggest that both subacute inflammation and remodeling influence nitric oxide output in refractory asthma.

Adolescent↗
PubMed2004

Lung eosinophilic inflammation and airway hyperreactivity are enhanced by murine anaphylactic, but not nonanaphylactic, IgG1 antibodies.

BACKGROUND: Chronic airway inflammation is a fundamental feature of bronchial asthma, which is characterized by the accumulation and activation of inflammatory cells, such as mast cells and eosinophils, that are tightly regulated by TH2 cytokines and chemokines. Recently, we demonstrated, in a murine model of asthma with immunosuppressed mice reconstituted with antigen-specific IgE or IgG1 antibodies, that IgE, but not IgG1, participates in potentiation of airway inflammation and induction of airway hyperreactivity (AHR). The IgG1 antibody, however, did not elicit passive cutaneous anaphylactic reactions, which was in contrast to IgE. OBJECTIVES: Because 2 types of murine IgG1 have been demonstrated with regard to anaphylactic activity, the present experiments were undertaken to determine the role of anaphylactic and nonanaphylactic IgG1 antibodies in the development of antigen-induced eosinophilia and AHR in this model. METHODS: Dinitrophenyl-conjugated, heat-coagulated hen's egg white was implanted in immunosuppressed mice reconstituted with anaphylactic or nonanaphylactic IgG1. Intratracheal challenge with aggregated dinitrophenyl-ovalbumin was performed on day 14, and lung inflammatory and mechanical parameters were evaluated after 48 hours. RESULTS: Our results demonstrated that reconstitution of immunosuppressed mice with anaphylactic IgG1 antibodies in contrast to nonanaphylactic IgG1 antibodies potentiates their ability to have pulmonary eosinophilic inflammation and AHR. IL-5 and eotaxin levels in bronchoalveolar lavage fluid from anaphylactic IgG1-reconstituted mice were also higher than those in nonanaphylactic IgG1-reconstituted mice. CONCLUSIONS: These results indicate that the anaphylactic property of murine IgG1 molecules is essential for their capacity to enhance lung eosinophilic inflammation and to induce AHR.

Anaphylaxis↗
PubMed2005

TNF-alpha induces the late-phase airway hyperresponsiveness and airway inflammation through cytosolic phospholipase A(2) activation.

BACKGROUND: Late-phase airway hyperresponsiveness (AHR) in asthma is considered the event leading to persistent inflammation in the lungs, but the molecular mechanisms involved in this process are poorly understood. OBJECTIVE: To examine the role of TNF-alpha in the development of a late AHR and airway inflammation in asthma. METHODS: We established a murine model of asthma with not only biphasic AHR to methacholine but also airway eosinophilia. The effect of TNF-alpha blockade was determined by using anti-TNF-alpha antibody and TNF-alpha knockout mice. Cytosolic phospholipase A(2) (cPLA(2)) mRNA expression and activity were assessed by using RT-PCR and 1-stearoyl-2-[1-(14)C] arachidonyl-sn-glycero-3-phosphocholine as the substrate, respectively. RESULTS: TNF-alpha blockade resulted in significant inhibition of the late AHR without affecting the early AHR, and reduction in airway eosinophilia and inflammation. cPLA(2) activity was increased in asthmatic lungs in a TNF-alpha-dependent way, and cPLA(2) inhibitor blocked late AHR and airway eosinophilia. TNF-alpha also stimulated the synthesis of cPLA(2) metabolites such as leukotriene B(4) and platelet-activating factor in the airway. Specific inhibitors of cPLA(2) metabolites inhibited the late AHR and airway eosinophilia. CONCLUSIONS: TNF-alpha is the proximal key cytokine capable of developing late-phase AHR and subsequent airway inflammation through expression/activation of cPLA(2).

Animals↗
PubMed2005

Prevention of IL-1 signaling attenuates airway hyperresponsiveness and inflammation in a murine model of toluene diisocyanate-induced asthma.

BACKGROUND: IL-1 is a pleotropic cytokine that has been shown to play a prominent role in asthma induced by large-molecular-weight proteins. Increased IL-1 immunostaining in the submucosa of patients with toluene diisocyanate (TDI)-induced asthma has also been observed, suggesting that this cytokine might also be important in asthma associated with low-molecular-weight chemicals. OBJECTIVE: We sought to determine the role of IL-1 signaling in airway reactivity and inflammation by using a murine model of TDI-induced asthma. METHODS: C57BL/6 mice were exposed to TDI by means of vapor inhalation (20 ppb; 4 hours per day, 5 days per week, for 6 weeks) and then challenged 2 weeks later by inhalation with 20 ppb TDI vapor for 1 hour. RESULTS: Sensitized-challenged mice showed increased airway hyperresponsiveness (AHR), increased levels of TDI-specific IgG1 antibodies, airway epithelial thickening, inflammation consisting of infiltrating lymphocytes and eosinophils, and increased mRNA expression of IL-4, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 in the lung. Prevention of IL-1 signaling through deletion of the IL-1 receptor type I or administration of neutralizing antibodies to both IL-1beta and IL-1alpha abrogated the development of TDI-induced asthma. A partial reduction in AHR and TDI-specific IgG1 levels was observed in mice administered anti-IL-1beta, whereas anti-IL-1alpha had no effect on either parameter. Antibodies to IL-1beta or IL-1alpha alone blocked airway inflammation and the expression of IL-4 and adhesion molecules in the lung. CONCLUSIONS: These results suggest that IL-1 signaling is critical for AHR and airway inflammation, with IL-1beta and IL-1alpha having unique and overlapping roles in TDI-induced occupational asthma.

Animals↗
PubMed2006

Update on the role of prostaglandins in allergic lung inflammation: separating friends from foes, harder than you might think.

Prostaglandins (PGs), small lipid molecules derived from arachidonic acid by COX enzymes, are critical mediators of allergic inflammation. Our understanding of the role of PGs in allergic lung inflammation has been hampered by the very short biologic half-life of these mediators, which has made mechanistic studies difficult in human subjects. However, advances in molecular biology and pharmacology have given investigators the opportunity to examine the role of specific prostanoids in the development of allergic inflammation in animal models. Studies investigating specific PG receptors are also elucidating the mechanisms by which PGs regulate the pulmonary allergic phenotype. This review summarizes the current literature on the role of PGs and PG receptors in allergic lung inflammation.

Animals↗
PubMed2006

Reversal of airway inflammation and remodeling in asthma by a bispecific antibody fragment linking CCR3 to CD300a.

BACKGROUND: Mast cells (MCs) and eosinophils are critically involved in asthma-associated airway damage and remodeling. However, molecular pathways that inhibit their functions in this process have been scarcely characterized. Recently we established that cross-linking of CD300a inhibits MC and eosinophil activation. OBJECTIVE: To inhibit effector cell functions in a chronic model of experimental asthma by coaggregation of CD300a with CC chemokine receptor 3 (CCR3) using a bispecific antibody fragment (LC1). METHODS: Mast cells and eosinophils were treated with LC1 before their activation. Mediator release, survival, and intracellular signaling were assessed. Furthermore, chronic experimental asthma was induced, and starting on day 30, the mice were challenged (3 challenges/wk) for an additional 38 days. With each challenge, the mice received LC1 intranasally. RESULTS: LC1 inhibited MCs and eosinophil activation in vitro and in vivo. Mice that displayed airway inflammation on day 28 and were treated with LC1 completely recovered from the disease process. In the bronchoalveolar lavage fluid of these mice, cellular inflammation cytokine expression was comparable to that of saline-treated mice. Bronchoalveolar lavage fluid levels of TGF-beta1 correlated significantly with reduced eosinophilia. Histologic analysis revealed significant reduction in lung inflammation, mucus production, collagen deposition, and peribronchial smooth-muscle thickening. CONCLUSION: CD300a is a critical modulator of MCs and eosinophil functions in allergic settings. CLINICAL IMPLICATIONS: Specific targeting of CD300a in CCR3(+) cells may be a potent tool for treating airway inflammation and tissue remodeling in asthma.

Administration, Intranasal↗