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PubMed2002

Cocoa products decrease low density lipoprotein oxidative susceptibility but do not affect biomarkers of inflammation in humans.

Flavonoids and related polyphenolics with antioxidant and anti-inflammatory activities may play a role in the prevention of cardiovascular disease by decreasing oxidative stress and inflammation. We wished to determine the effects of cocoa extract supplementation on markers of oxidative stress and inflammation. Healthy subjects (n = 25) were studied at baseline, after cocoa supplementation (36.9 g of dark chocolate bar and 30.95 g of cocoa powder drink) for 6 wk and after a 6-wk washout period. Fasting blood and early morning urine were collected at the three time points. Two indices of flavonoid intake, total phenols and oxygen radical absorbance capacity of plasma, were measured after an overnight fast. Neither was affected by supplementation. Measures of oxidative stress included copper-catalyzed LDL oxidation kinetics and urinary F(2) isoprostanes. LDL oxidizability was lower after chocolate supplementation as evidenced by a longer lag time (P < 0.05) of conjugated diene formation (101.0 +/- 20.7 min) compared with baseline (91.3 +/- 18.0 min) and washout (96.4 +/- 7.5 min) phases. There was no effect of chocolate on urinary F(2) isoprostane levels or on markers of inflammation including the whole-blood cytokines, interleukin-1 beta, interleukin-6 and tumor necrosis factor-alpha, high sensitivity C-reactive protein and P-selectin. In conclusion, cocoa products supplementation in humans affects LDL oxidizability, but not urinary F(2) isoprostanes or markers of inflammation.

Antioxidants↗
PubMed2005

Breast milk retinol concentrations are not associated with systemic inflammation among breast-feeding women in Malawi.

The acute phase response and inflammation are associated with lower plasma retinol concentrations, but their effect on breast milk retinol concentrations is unclear. We measured plasma retinol concentrations, acute phase proteins, and breast milk retinol concentrations in 237 breast-feeding women at 2 wk postpartum in Blantyre, Malawi; 16.5% of the women had plasma retinol < 0.70 micromol/L and 14.8% had breast milk retinol < 1.05 micromol/L. Among women with and without inflammation [alpha(1)-acid glycoprotein (AGP) > 1 g/L and/or C-reactive protein (CRP) > 5 mg/L], geometric mean (95% CI) plasma retinol was 0.89 (0.84, 0.94) and 1.05 (1.01, 1.17) mumol/L, respectively (P < 0.0001). Among women with and without inflammation, geometric mean (95% CI) breast milk retinol was 2.12 (1.89, 2.36) and 2.05 (1.75, 2.39) micromol/L, respectively (P = 0.74). In multiple linear regression models adjusting for age, parity, education, BMI, and days postpartum, plasma retinol concentrations were associated with plasma AGP and CRP concentrations (P < 0.0001 and P = 0.01, respectively), whereas breast milk retinol concentrations were unaffected by plasma AGP and CRP concentrations (P = 0.22 and P = 0.86, respectively). These findings suggest that breast milk retinol concentrations are not affected by systemic inflammation.

Adult↗
PubMed2001

Procalcitonin: a new marker of inflammation in haemodialysis patients?

BACKGROUND: Although procalcitonin (PCT) has been described as a new marker of infection and inflammation, it has not been extensively studied in dialysis patients. METHODS: We measured plasma PCT levels in 62 patients on maintenance haemodialysis (30 M/32 F, age 61.8+/-17.1 years, on dialysis for 75+/-93 months, 12 h/week, with a Kt/V of 1.53+/-0.31, high-flux membrane being used in 25 patients and low-flux in 37 patients, without reuse). PCT levels were compared with other markers of inflammation and nutritional status, including C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), leukocytes, urea, creatinine, albumin, prealbumin, normalized protein catabolic rate (nPCR), haemoglobin (Hb), and epoetin (Epo) doses. Patients were divided into different groups according to their infectious and vascular status. RESULTS: PCT plasma levels before dialysis were 0.69+/-0.81 ng/ml. Fifty-seven per cent of PCT values were higher than the upper normal limit of 0.5 ng/ml. CRP and PCT concentrations were high in patients with a current infection, while IL-6 values were elevated in all patients regardless of infection status. Plasma CRP concentrations before dialysis were 21.2+/-31.4 mg/l, and 70% of these values were higher than the upper normal limit. CRP, PCT, IL-6, and fibrinogen were positively correlated with each other and were all negatively correlated with albumin. Prealbumin was negatively correlated with CRP and IL-6. In the 43 patients treated with Epo, haemoglobin was negatively correlated with IL-6 and Epo doses, while Epo doses were positively correlated with IL-6 but not with CRP or PCT. The 23 patients with both elevated PCT and CRP plasma levels had the lowest Hb, albumin, and prealbumin concentrations, and the highest fibrinogen concentrations and Epo doses. CONCLUSION: PCT in haemodialysis patients is positively correlated with currently used markers of inflammation such as CRP and fibrinogen, and negatively correlated with markers of nutritional status such as albumin. The concomitant elevations in PCT and CRP could be more sensitive in the evaluation of inflammation than each marker separately.

Aged↗
PubMed2006

The reverse epidemiology of plasma total homocysteine as a mortality risk factor is related to the impact of wasting and inflammation.

BACKGROUND: The reason(s) for the apparently paradoxical 'reverse' association in end-stage renal disease (ESRD) patients in whom a low, rather than a high, total plasma total homocysteine (tHcy) level is an indicator of poor outcome remains unclear. The aim of this study was to examine whether the inverse association maintains, mitigates or reverses after comprehensive multivariate adjustment for the presence of wasting and inflammation as well as other potential confounders. METHODS: We studied 317 ESRD patients starting dialysis therapy. Fasting blood samples were taken for the analyses of tHcy, serum albumin, C-reactive protein (CRP), serum creatinine and plasma folate. Nutritional status was assessed by subjective global assessment (SGA). Survival was followed for up to 66 months; 105 patients died. RESULTS: Using Kaplan-Meier analysis, a low tHcy concentration (< or =30 micromol/l) was associated with higher all-cause and cardiovascular (CV) mortality (P < 0.05). Using Cox proportional analysis adjusting for age, gender, glomerular filtration rate = GFR, cardiovascular disease = CVD, plasma folate, total cholesterol and diabetes mellitus, the all-cause and CV mortality still tended to be high for patients with low tHcy. Adding nutritional and inflammation markers (Body mass index = BMI, SGA, serum creatinine, serum albumin and CRP), a low tHcy level was no longer associated with higher mortality but a trend for high tHcy was observed. CONCLUSIONS: The link between wasting inflammation and a low tHcy appears to be responsible for the reverse association between plasma tHcy and clinical outcome in ESRD patients. After adjustment for confounders including nutritional and inflammation markers, a trend towards increased death risk for high, rather than low, tHcy levels was apparent after adjustment.

Adult↗
PubMed2006

Subclinical hypothyroidism is linked to micro-inflammation and predicts death in continuous ambulatory peritoneal dialysis.

BACKGROUND: Low T3 is a frequent alteration in patients with ESRD. This derangement has been recently linked to inflammation in haemodialysis patients. Whether this association holds true in peritoneal dialysis patients has not been studied. METHODS: We investigated the relationship between low-grade inflammation [IL-6, C-reactive protein (CRP) and serum albumin levels] and free tri-iodothyronine (fT3) in a cohort of 41 CAPD patients (mean age, 66 years; M, 26; F, 15) without heart failure and inter-current illnesses. RESULTS: CAPD patients had lower fT3 levels (2.7 +/- 0.8 pg/ml) than healthy subjects (3.7 +/- 1.0 pg/ml, P < 0.001) of similar age. Free T3 levels were directly related to those of serum albumin (r = 0.52, P = 0.001) and inversely to IL-6 (r = -0.30, P = 0.05) and CRP (r = -0.54, P < 0.001). Age (r = -0.61, P < 0.001), haemoglobin levels (r = 0.32, P = 0.05) and diastolic blood pressure (r = 0.50, P = 0.001) were also related to fT3. In multiple regression models adjusting for all variables related to fT3, CRP and albumin were retained as independent correlates of fT3. During the follow-up (2.8 +/- 1.7 years) 27 patients died. Plasma fT3 levels were lower in patients who died (2.5 +/- 0.8 pg/ml) compared with survivors (3.3 +/- 0.5 pg/ml P = 0.001). In Cox analyses, fT3 was a significant predictor of mortality independent of the main traditional as well as non-traditional risk factors. CONCLUSIONS: The relationship between fT3, CRP and serum albumin suggests that inflammation-malnutrition might be involved in the low T3 syndrome in CAPD patients. Thyroid dysfunction might be implicated in the pathogenic pathway which links micro-inflammation to survival in PD patients.

Aged↗
PubMed2005

RvE1 protects from local inflammation and osteoclast- mediated bone destruction in periodontitis.

Periodontitis is a well-appreciated example of leukocyte-mediated bone loss and inflammation that has pathogenic features similar to those observed in other inflammatory diseases such as arthritis. Resolvins are a new family of bioactive products of omega-3 fatty acid transformation circuits initiated by aspirin treatment that counter proinflammatory signals. Because it is now increasingly apparent that local inflammation plays a critical role in many diseases, including cardiovascular disease, atherosclerosis, and asthma, experiments were undertaken to evaluate the actions of the newly described EPA-derived Resolvin E1 (RvE1) in regulation of neutrophil tissue destruction and resolution of inflammation. The actions of an aspirin-triggered lipoxin (LX) analog and RvE1 in a human disease, localized aggressive periodontitis (LAP), were determined. Results indicate that neutrophils from LAP are refractory to anti-inflammatory molecules of the LX series, whereas LAP neutrophils respond to RvE1. In addition, RvE1 specifically binds to human neutrophils at a site that is functionally distinct from the LX receptor. Consistent with these potent actions, topical application of RvE1 in rabbit periodontitis conferred dramatic protection against inflammation induced tissue and bone loss associated with periodontitis.

Administration, Topical↗
PubMed2003

Systemic inflammation leads to resistance to atracurium without increasing membrane expression of acetylcholine receptors.

BACKGROUND: Systemic inflammation may be associated with resistance to nondepolarizing neuromuscular blocking drugs, the mechanisms of which are, however, uncharacterized. The authors therefore investigated the pharmacodynamics of atracurium and its relation to the expression of nicotinic acetylcholine receptors and alpha1 -acid glycoprotein in a rat model of systemic inflammation. METHODS: To induce a systemic inflammation, male CD rats received 56 mg/kg corynebacterium parvum intravenously. On days 2, 4, 6, 8, 10, 12, 14, or 16 after infection, neuromuscular transmission was measured. The individual effective dose of atracurium was determined, followed by an atracurium infusion at a rate to establish a steady state neuromuscular block of 50%. Total and unbound plasma concentrations of atracurium for 50% paralysis were measured using high-performance liquid chromatography. Acetylcholine receptors were quantitated using 125I-alpha-bungarotoxin. alpha1 -Acid glycoprotein concentrations in the serum were measured using a competitive chemiluminescence immunoassay. RESULTS: The effective dose of atracurium was increased on days 4, 6, and 8. Total atracurium plasma concentrations at 50% neuromuscular paralysis were increased on days 4, 6, 8, and 10, with a peak at day 8 (8.0 +/- 1.3 micro g/ml) compared with control rats (4.23 +/- 0.82 micro g/ml). The alpha1 -acid glycoprotein concentrations were increased between days 2 and 10, with a peak on day 4 (6.52 +/- 1.45 mg/ml), and recovered to control values (0.61 +/- 0.33 mg/ml) on day 12. Unbound plasma concentrations of atracurium to achieve 50% depression, as well as the expression of acetylcholine receptors, did not differ between groups. CONCLUSION: Resistance to atracurium during corynebacterium parvum-induced systemic inflammation is due to increased drug binding to alpha1 -acid glycoprotein and is unrelated to changes in acetylcholine receptor expression.

Anesthesia↗
PubMed1996

Descending modulation of Fos expression after persistent peripheral inflammation.

The effects of spinal transection on Fos protein expression following complete Freund's adjuvant-induced hindpaw inflammation and hyperalgesia were studied. Fos-like immunoreactivity (LI) was used as a measure of neuronal activity in dorsal horn nociceptive pathways. Induction of Fos-LI in spinally transected rats with 3 days of hindpaw inflammation was significantly increased in ipsilateral lumbar (L 4,5) spinal cord, when compared with control animals with similar inflammation but an intact spinal cord. The contralateral side of spinally transected rats also showed significant induction of Fos-LI compared to the non-inflamed side of control rats. Since Fos induction provides an indication of the level of neuronal activity in response to a given stimulus, these results suggest that the net effect of brain stem descending pathways is to dampen central hyper-excitability in the spinal cord induced by tissue inflammation and hyperalgesia.

Animals↗
PubMed1998

Pituitary adenylate cyclase-activating peptide is upregulated in sensory neurons by inflammation.

The neuropeptide pituitary adenylate cyclase-activating peptide (PACAP) is expressed in sensory neurons. Expression of several neuropeptides is up-regulated in sensory neurons following inflammation. To examine whether also PACAP expression is regulated by inflammation, PACAP expression in L5 dorsal root ganglion (DRG) was determined, using in situ hybridization, after unilateral adjuvant-induced inflammation in the rat paw. At 12 h and day 3, but not day 21, the percentage of neurons expressing PACAP mRNA was greater in the innervating L5 DRG. Similarly, PACAP mRNA expression in individual neurons was higher in the innervating L5 DRG at 12 h and day 3, but not day 21. Up-regulated PACAP expression following adjuvant injection suggests a role for PACAP in inflammation.

Animals↗
PubMed2001

Increased Fos induction in adult rats that experienced neonatal peripheral inflammation.

The response to noxious stimulation was compared in adult rats that had peripheral inflammation as neonates and untreated rats. On postnatal day 1, rat pups experienced complete Freund's adjuvant (CFA)-induced inflammation of the left hind paw. At 8 weeks of age, these rats and neonatal untreated rats received a bilateral injection of CFA into their hind paws. Fos-like immunoreactivity (Fos-LI) was used as a measure of neuronal activity in dorsal horn nociceptive pathways. A significant increase in Fos-LI was found on the left side of the lumbar spinal cord of neonatal treated rats as compared to neonatal untreated rats. These results suggest that the experience of neonatal peripheral inflammation may result in an increase in the response of spinal cord neurons to peripheral inflammation as adults.

Animals↗
PubMed1996

Scintiscan demonstration of localized bowel loop inflammation. Comparison of Tc-99m dextran, Tc-99m citrate, and Tc-99m human immunoglobulin G.

A 60-year-old man with localized small bowel inflammation underwent abdominal scintigraphy with Tc-99m human polyclonal immunoglobulin G and two experimental inflammation-seeking agents, Tc-99m dextran and Tc-99m citrate. The abnormal loop was visualized in all the three studies. Additionally, the Tc-99m dextran study revealed exudation and luminal transit of the tracer suggestive of regional protein-losing enteropathy. The authors conclude that Tc-99 dextran and Tc-99 citrate are clinically suitable inflammation-seeking agents that need further evaluation, especially for locating abdominal inflammations.

Citrates↗
PubMed2002

Endothelium: interface between coagulation and inflammation.

OBJECTIVE: To review the involvement of endothelial cells in the pathogenesis of coagulation abnormalities during severe infection, the differential role of proinflammatory cytokines in these mechanisms, and the cross talk between coagulation and inflammation. DATA SOURCES: Published articles on experimental studies of coagulation activation during inflammation and clinical studies of patients with sepsis and associated hemostatic abnormalities. DATA SYNTHESIS AND CONCLUSION: The endothelium plays a central role in all major pathways involved in the pathogenesis of the hemostatic derangement observed during severe inflammation (i.e., initiation and regulation of thrombin generation and inhibition of fibrinolysis). Rather than being a unidirectional relationship, the interaction between inflammation and coagulation involves significant cross talk in which the endothelium seems to play a pivotal role.

Animals↗
PubMed2003

Inflammation is involved in the organ damage induced by sinoaortic denervation in rats.

OBJECTIVE: The present study was designed to test the hypothesis that inflammation is involved in the end-organ damage (EOD) induced by sinoaortic denervation (SAD) in rats. METHOD: SAD was performed in male Sprague-Dawley rats at the age of 10 weeks. Under anaesthesia, aortic nerves were cut and the sinus region of the carotid artery was stripped and painted with 10% phenol. Pathological evaluation of EOD and the determination of plasma or tissue levels of the factors related to inflammation, including thromboxane B2 (TXB2) interleukin-1 (IL-1), tumour necrosis factor alpha (TNF-alpha) and reactive oxygen species (ROS) were performed at 16 weeks after SAD. Pathological evaluation of EOD included heart weight ratio, myocardial and blood vessel hydroxyproline and collagen volume fraction, glomerular injury score and number of infiltrating inflammatory cells. Indomethacin (20 mg/kg per day, orally) or vitamin E (100 mg/kg per day, orally) was administered for 12 weeks, beginning from 4 weeks after SAD, to observe their effects on SAD-induced EOD. RESULTS: There were significant fibrosis and inflammatory infiltration in the myocardium and blood vessels, represented by higher hydroxyproline and collagen volume fraction, and a large amount of inflammatory cells in the tissues of SAD rats. Heart weight and kidney glomerular injury score were significantly higher in SAD than in sham-operated rats. Plasma TXB2, TNF-alpha, IL-1 and tissue ROS increased significantly after SAD. Indomethacin and vitamin E significantly decreased the contents of some factors related to inflammation in SAD rats. Both drugs also alleviated myocardial and vessel fibrosis, inflammatory infiltration and kidney damage. CONCLUSION: Inflammation is involved in the organ damage induced by SAD in rats.

Animals↗
PubMed1996

Imaging inflammation with 99Tcm-labeled chemotactic peptides: analogues with reduced neutropenia.

Two 99Tcm-labelled analogues of the chemotactic peptide ForMLF were evaluated as potential agents for imaging inflammation and infection, in the hope that they would be simple to use and would give diagnostically useful images shortly after injection. The peptides differed in the chelation site for 99Tcm and the presence of a hydrophilic spacer. The sequences of RP050 and RP056 were ForNleLFNleYK(G)G-C(Acm)-GPic and ForNleLFNleYKK(DG)GC(Acm)SPic respectively, where Pic is picolinic acid. In in vitro tests of binding to the ForMLF receptor on polymorphonuclear neutrophils and potency for release of myeloperoxidase, RP056 was similar in potency to ForMLF, whereas RP050 was 10 times more potent. When administered in 5-nmol doses to rats, RP050 produced less extensive neutropenia than ForMLF, whereas RP056 produced very little neutropenia. Following labelling by ligand exchange from tartrate or glucoheptonate at 100 degrees C and purification using a C-18 solid-phase extraction cartridge, 4-MBq doses were administered to rats bearing infectious (Escherichia coli) or sterile (zymosan) inflammation sites in the thigh. The inflammation-to-normal muscle ratios at 30 min after injection were 3.9 +/- 0.4 for RP050 and 4.7 +/- 0.3 for RP056 (mean +/- S.E.M., n = 4), and the ratios were maintained for up to 3 h. These peptides are promising agents for imaging inflammation and infection.

Amino Acid Sequence↗
PubMed1996

Scintigraphic evaluation of the severity of inflammation of the joints with 99TCm-HIG in rheumatoid arthritis.

A prospective study was carried out to determine the usefulness of 99TCm-human immunoglobulin G (HIG) scintigraphy in the assessment of the severity of joint inflammation. Twenty-four patients with rheumatoid arthritis were studied. The presence or absence of pain and/or swelling was evaluated in 34 joints and a clinical index taking into account the surface area of each joint was calculated. We measured the following biological markers of inflammation activity: erythrocyte sedimentation rate, C-reactive protein, haemoglobin, platelet count, serum levels of IL-6, TNF-alpha and soluble receptors of IL-2. Scintigraphic was performed 4 h after the injection of 740 MBq 99Tcm-HIG. The scans were evaluated by visual and quantitative analysis and the scores in each joint were weighted for joint size. Pathological uptake of the radiopharmaceutical was noted in 46% (24/52) of joints evaluated as painful, 89% (146/164) of swollen joints and 94% (78/83) of both painful and swollen joints. Both the visual and the quantitative scintigraphic indices correlated significantly with the clinical index, the number of painful joints, the number of swollen joints and several biological markers of inflammation. A very high correlation was also found between the visual and the quantitative scintigraphic indices (r = 0.91, P < 0.0001). In conclusion, 99Tcm-HIG scintigraphy is an objective test to detect synovitis and to assess the severity of inflammation. A careful visual analysis of scans is good enough for routine evaluations and computer quantitative analysis should be used when more accurate intra-individual variation is required.

Adult↗
PubMed1998

The kinetics of radiolabelled interleukin-8 in infection and sterile inflammation.

Radiolabelled interleukin-8 (IL-8) is a promising agent for the imaging of infection and inflammation. Several experiments were performed to explore further the imaging potential of radiolabelled IL-8. IL-8 was radioiodinated via the Bolton-Hunter method. Rabbits with focal infection (Escherichia coli, Staphylococcus aureus) or sterile inflammation (zymosan) were injected intravenously with 18.5 MBq (0.5 mCi) of 123I-IL-8. In separate studies, rabbits were injected intravenously with 111In-granulocytes with or without 125I-IL-8. Gamma camera images were obtained at 5 min, 1, 4 and 8 h post-injection (p.i.). Biodistribution was determined at 8 h p.i. In all models, the biodistribution of 123I-IL-8 was characterized by rapid blood clearance and high uptake in infection and sterile inflammation. All foci could be clearly visualized within 4 h p.i. Ex vivo abscess-to-contralateral muscle ratios increased to 114.7+/-23.0 (E. coli), 52.3+/-24.5 (S. aureus) and 49.8+/-8.3 (zymosan) at 8 h p.i. In the circulation, most 123I-IL-8 was bound to erythrocytes. The abscess uptake of 125I-IL-8 reached high levels despite reduced migration of granulocytes towards the site of infection due to the anti-inflammatory activity of intravenously injected IL-8. IL-8 could be injected without induction of neutropenia at a dosage of 2 ng kg(-1). In conclusion, the characteristics of radiolabelled IL-8 for imaging of infection and sterile inflammation are highly encouraging and warrant further optimization for clinical application.

Animals↗
PubMed2000

Exhaled nitric oxide as an indicator of severity of asthmatic inflammation.

Traditional assessment of severity of asthma relies on an evaluation of signs and symptoms and pulmonary function tests. These pulmonary function tests, such as peak expiratory flow rates, forced vital capacity, and forced expiratory flow rates, are indirect measures of airway caliber only, and not inflammation. Since asthma is an inflammatory disease, a measure of the degree of inflammation would be helpful in quantitating severity and titrating of anti-inflammatory therapy. A noninvasive method for measuring pulmonary inflammation would therefore be helpful to assist the emergency physician in initial treatment and assist in titration of anti-inflammatory therapy during repeat visits. Exhaled nitric oxide (NO) assays are convenient and practical and may fulfill this role. In this review, we discuss the role of NO in asthmatic inflammation and the role that exhaled NO values may play in the emergency management of asthma.

Asthma↗
PubMed1989

Inflammation-induced endothelial cell adhesion to lymphocytes, neutrophils, and monocytes. Role of homing receptors and other adhesion molecules.

Adhesion to the vascular endothelium precedes or is a necessary prelude to leukocyte migration into the underlying tissue. Constitutive lymphocyte trafficking through lymphoid organs is controlled by tissue-specific interactions between molecules expressed on the surface of the lymphocyte (homing receptors) and ligands (vascular addressins) expressed on endothelial cells (HEV) within lymphoid tissues. Preliminary evidence suggests that lymphocytes may employ related but distinct interactions in their entry into some chronic sites of inflammation. Other leukocytes, such as neutrophils and monocytes, express molecules related or identical to lymphocyte homing receptors, and these molecules are exquisitely regulated by chemotactic factors and appear to be involved in the homing of these cells to inflamed tissues. In addition, inflammation in vivo induces increased endothelial cell adhesiveness for leukocytes that undoubtedly plays a key role in regulating leukocyte extravasation. Tissue- and inflammation-specific leukocyte/endothelial cell adhesion molecules constitute attractive targets for suppression or manipulation of the early stages of tissue inflammation.

Animals↗

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