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PubMed2000

Consumption of black and green tea had no effect on inflammation, haemostasis and endothelial markers in smoking healthy individuals.

OBJECTIVE: Firstly, to study the effect of tea and tea polyphenols on cardiovascular risk indicators of the inflammatory system (IL6, IL1beta and TNF-alpha, CRP), and on haemostasis and endothelial proteins with an acute phase behaviour (fibrinogen, vWF, PAI-1, FVIIa and u-PA). Secondly, to study the relationship between plasma levels of antioxidants (alpha-tocopherol, beta-carotene and vitamin C) and these acute-phase, cardiovascular risk indicators. DESIGN: Randomized study. SUBJECTS: Sixty-four smoking healthy volunteers were recruited by newspaper advertisements; there were five dropouts. INTERVENTION: Four-week administration of black tea, green tea, green tea polyphenol isolate and mineral water ( 13-16 per group). MEASURES: Plasma levels of the inflammatory markers IL6, IL1beta, TNF-alpha, CRP, fibrinogen, vWF, PAI-1, FVIIa and u-PA and of the antioxidants alpha-tocopherol, beta-carotene and vitamin C. RESULTS: Different dosages of tea polyphenols had no effect on inflammation, haemostasis and endothelial markers. There was a significant negative correlation between the levels of the antioxidant beta-carotene and the inflammation markers IL6 and fibrinogen (r = -0.35 and r = -0.37, respectively, P<0.01) in this group of smokers. Remarkably, there was a significant positive correlation between the levels of the antioxidant alpha-tocopherol and the inflammation marker IL6 (r = 0.28, P<0.05). CONCLUSIONS: Tea drinking had no effect on the levels of the inflammation, haemostasis and endothelial cardiovascular risk factors measured. We did observe a relationship between the antioxidant variables alpha-tocopherol and beta-carotene and inflammation markers in this group of healthy smoking subjects.

Acute-Phase Reaction↗
PubMed2003

Emerging relationships of inflammation, cardiovascular disease and chronic diseases of aging.

The last 10 y have seen an enormous surge in research focused on inflammation and atherosclerotic heart disease. In parallel, inflammation (used as a term to represent a broad array of response systems) has become a topic of interest in a number of different areas of chronic disease including type II diabetes, cognitive decline and frailty, among others. These discoveries are opening up many new opportunities for risk assessment. For example, markers of inflammation such as C-reactive protein are becoming established as important additions in helping to define those at the greatest risk of progressive vascular disease. These discoveries are also important in the area of risk management. Older medications now in wide use are being found to have previously unknown anti-inflammatory effects (eg, statins); these effects are now viewed as being important to the overall effectiveness of these compounds. In addition, the many different aspects of inflammation provide a wealth of targets for new therapeutics, which will be increasingly important as the population continues to age. Although daunting in complexity, studies on the relation of inflammation to disease have already proven useful, and hold promise for providing fundamental advances in both basic biology and clinical medicine.

Aged↗
PubMed1992

Resolution of acute inflammation and the role of apoptosis in the tissue fate of granulocytes.

We have identified a pathway for granulocyte removal in tissues which is controlled by apoptosis. This process can be modulated by agents in the inflammatory microenvironment and leads to loss of neutrophil secretory function and its phagocytosis by macrophages which utilize a novel recognition mechanism such that the macrophage does not release pro-inflammatory mediators. It is hypothesized that this represents an alternative fate to necrosis, and one which would tend to limit tissue injury and promote inflammatory resolution. This is not to suggest that granulocyte necrosis does not occur; even at sites of 'beneficial inflammation' some necrotic neutrophils may be seen. However, since the development of inflammatory disease is currently thought to result from a multifactoral, quantitative imbalance between potentially injurious inflammatory influences and tissue defences, it is reasonable to suggest that the balance between neutrophil apoptosis and necrosis could represent one of several possible pivotal points in the control of inflammation. Finally, as the specific trigger and induction processes which permit closely related cells to undergo apoptosis at markedly different rates are uncovered, it may be possible to design new anti-inflammatory therapeutic strategies directed towards causing specific cell types to 'commit suicide' and to be cleared by the mechanisms which 'nature intended'. Thus we have begun to dissect the cellular events occurring in the resolution of acute inflammation. We believe that the rapid cessation of neutrophil emigration which occurs remarkably early in the evolution of the acute inflammatory response represents one of the earliest events in the resolution process. Clearly there is much work to be done on the underlying mechanisms. These are likely to be more accessible with the recent molecular characterization of chemotactic cytokines and surface molecules involved in neutrophil-endothelial adhesion transmigration events. It is also clear that apoptosis, which represents an alternative tissue injury-limiting fate to necrosis in situ, may be important in limiting tissue injury and determining whether inflammation persists or resolves. It is also possible that there are circumstances in which the macrophage recognition and clearance of apoptotic neutrophils is impaired. However, a second glance at the events which must occur during the resolution of even the simplest model of acute inflammation (Fig. 1) is sufficient reminder that the 'surface has barely been scratched'. There remain many obscure areas, not the least of which is the fate of the inflammatory macrophage after it has completed its scavenging functions.

Animals↗
PubMed1999

Review article: the role of inflammation in the pathogenesis of gastric cancer.

Helicobacter pylori induces infiltration of the gastric mucosa by polymorphonuclear cells and macrophages, as well as T and B lymphocytes. Paradoxically, this robust immune/inflammatory response cannot clear the infection, and thus leaves the host prone to complications resulting from chronic inflammation. One adverse consequence of this inflammatory response may be gastric cancer, as inflammation has been implicated in the development of intestinal metaplasia and mutations in oncogenes that precede the development of gastric adenocarcinoma. The gastric inflammatory response is affected somewhat, by the strain of H. pylori that infects the host. Thus, the more severe clinical manifestation associated with some strains may be attributed to the higher grade of inflammation that they induce. Both H. pylori and cytokines induced during infection can stimulate the recruitment and activation of inflammatory cells including neutrophils and macrophages. When activated, these cells produce inflammatory mediators that include reactive oxygen species (ROS). These mediators impart an oxidative stress on the cells in the immediate vicinity, in this case, the gastric epithelium. Normally, oxidative stress is neutralized by natural antioxidants such as vitamin C, however, levels of this antioxidant in the gastric juice are decreased during infection. The increased levels of oxidants and decreased antioxidants create a stress that can change many processes in the gastric epithelium. For example, an accumulation of intracellular ROS regulates the expression of many genes and can induce DNA damage. Point mutations in the DNA that disrupt the expression and function of genes that inhibit cell growth (i.e. p53) are believed to contribute to the pathogenesis of gastric cancer. Several studies suggest that epithelial cell turnover is affected by the inflammatory response to H. pylori. This notion is supported by studies describing an increase in both epithelial cell proliferation, as well as cell death by apoptosis, in response to infection. Apoptosis is a regulated process of cell death that is triggered by H. pylori as well as various inflammatory mediators, including tumour necrosis factor and interferon-gamma. Activated T-cells also kill gastric epithelial cells directly. Moreover, the host response increases the expression of receptors for H. pylori and thus increases bacterial binding and the induction of apoptosis by the bacteria. There are several other immune/inflammatory responses that contribute to epithelial cell damage mucosa and the pathogenesis of gastric cancer. For example, gastric B cells produce autoreactive antibodies that bind to gastric epithelial cells. As a consequence of this antigen-antibody complex formation, complement becomes activated suggesting that some of the inflammation and epithelial cell damage is attributable to immune-complex formation. Epithelial cell death can then stimulate the proliferative response of epithelial cell precursors. In summary, the proposed model may explain how the gastric inflammatory response contributes to the pathogenesis of cancer. This model raises the possibility that it could be preferable to identify the patients at highest risk of developing gastric cancer and then apply an intervention that eliminates the infection and inflammatory response. Alternatively, clinical interventions should at least attenuate the oxidative stress that is directly attributed to inflammation. These mechanisms have to be examined in the paediatric population.

Antigen-Antibody Complex↗
PubMed1999

Airway inflammation and altered alveolar macrophage phenotype pattern after repeated low-dose allergen exposure of atopic asthmatic subjects.

BACKGROUND: The alveolar macrophage (AM) constitutes an important link between pulmonary innate and adaptive immunity due to its antigen-presenting capacity and ability to express different immunomodulating mediators. The role of AMs in the pathogenesis of allergic inflammation has yet to be fully determined. OBJECTIVE: To investigate clinical effects and any change in the AM phenotype pattern after inhalation of sub-clinical doses of allergen by asthmatic patients. METHODS: Eight subjects with allergic asthma underwent repeated low-dose allergen provocations equivalent to 10% of PD20. AMs recovered with bronchoalveolar lavage (BAL) were characterized by flow cytometric analysis of adhesion molecules, co-stimulatory molecules and markers for AM population activation and heterogeneity. RESULTS: An allergic airway inflammation, sub-clinical in six out of eight subjects, was obtained after low-dose allergen provocations, as determined by increased airway methacholine reactivity, increased BAL fluid total cell and eosinophil counts and increased serum ECP levels. The AMs showed a post-challenge altered phenotype pattern with a decreased expression of CD11a, CD16, CD71 and HLA class I and an increased expression of CD11b and CD14. The AMs were positive for CD83 and a weak post-challenge increase in the CD83 expression was found. CONCLUSION: Repeated low-dose allergen exposure induces an allergic airway inflammation in asthmatic subjects. The inflammation is associated with an altered AM phenotype pattern, consistent with an influx of monocytes and a hypothetical increased accessory cell function in the airways, possibly contributing to the development and sustenance of airway inflammation in asthma.

Adult↗
PubMed2000

Endogenous interleukin-10 suppresses allergen-induced airway inflammation and nonspecific airway responsiveness.

BACKGROUND: The airway inflammation observed in asthma is orchestrated by activated Th-2 lymphocytes relevant for the induction of altered airway responsiveness. An increasing body of evidence is accumulating that not only the pro-inflammatory cytokines interleukin (IL)-4 and IL-5 but also the immunomodulating cytokines IL-12 and possibly IL-10 are crucial for regulating the allergic airway inflammation. OBJECTIVE: Since IL-10 is capable of downregulating a broad spectrum of pro-inflammatory cytokines, we wanted to address the role of endogenously produced IL-10 in vivo in allergic asthma. METHODS: Knockout (IL-10(-/-)) mice (C57BL/6-IL10tm1Cgn) and wild-type (WT) counterparts were immunized (day 0) and exposed (day 14-21) to ovalbumin (OVA). Airway inflammation and reactivity (AR), serum allergen-specific IgE responses and cytokine profiles in the bronchoalveolar lavage fluid (BALF) were studied. RESULTS: The IL-10(-/-) mice had more eosinophilic airway inflammation but comparable levels of allergen-specific serum IgE compared to the WT mice after allergen challenge. The AR was comparably increased in the OVA challenged WT and IL-10(-/-) mice vs sham-exposed WT, but not vs sham-exposed IL-10(-/-)mice since these showed a higher baseline AR. IFN gamma, IL-4 and IL-13 were comparable and IL-5 was even lower in the BALF of the in IL-10(-/-) mice compared to the similarly exposed WT mice. CONCLUSION: These results indicate that IL-10 plays an important and possibly direct role in the control of airway inflammation and responsiveness in an in vivo mouse model of allergy.

Allergens↗
PubMed2002

Effect of ozone exposure on allergic sensitization and airway inflammation induced by dendritic cells.

BACKGROUND: Epidemiological studies suggest that ozone exposure is related to increased asthma symptoms. Dendritic cells (DCs) are the principal antigen-presenting cells in the airways. OBJECTIVE: We have examined whether ambient doses of ozone (100 ppb for 2 h) enhance allergic sensitization and/or airway inflammation in a mouse model. METHODS: C57BL/6 mice were sensitized to inhaled ovalbumin (OVA) by intratracheal instillation of OVA-pulsed DCs on day 0. Daily exposure to OVA aerosol on days 14-20 resulted in an eosinophilic airway inflammation, as reflected in bronchoalveolar lavage fluid and lung histology. In a first experiment, mice were exposed to ozone or room air immediately prior to and following sensitization. Subsequently, we tested the effect of ozone exposure during antigen challenge in DC-sensitized mice. RESULTS: Exposure to ozone during sensitization did not influence airway inflammation after subsequent allergen challenge. In contrast, in sensitized mice, challenge with OVA together with ozone (days 14-20) resulted in enhanced airway eosinophilia and lymphocytosis, as compared with mice exposed to OVA and room air (1.91 x 106 +/- 0.46 x 106 vs. 0.16 x 106 +/- 0.06 x 106 eosinophils/mL lavage fluid; P = 0.015; 0.49 x 106 +/- 0.11 x 106 vs. 0.08 x 106 +/- 0.03 x 106 lymphocytes/mL lavage fluid; P = 0.004). Ozone exposure without subsequent OVA exposure did not cause airway inflammation. CONCLUSION: Ozone exposure does not increase allergic sensitization but enhances antigen-induced airway inflammation in mice that are sensitized via the airways.

Air Pollutants↗
PubMed2000

The effect of inflammation on spiral ganglion cell density measurements in the cat cochlea.

The quantitative analysis of spiral ganglion cells is important in assessing the biological safety of cochlear implants. Quantitative analysis of ganglion cells in a histological section is conventionally expressed as cell density, the number of ganglion cells within Rosenthal's canal being divided by its area. The area of Rosenthal's canal conventionally excludes the area of blood vessels within it. Previous work has shown that the blood vessel area within Rosenthal's canal increases with cochlear inflammation. Consequently, excluding this area may result in an underestimate of ganglion cell loss and a tested implant parameter may be wrongly passed as safe. This study investigates whether the increase in blood vessel area with grade of inflammation has an effect on ganglion cell density measurements made by excluding blood vessel area. Eighteen implanted and stimulated cat cochleae were serially sectioned. Using computer image analysis we measured ganglion cell number, the area of Rosenthal's canal and its blood vessels. A 'blind' histologist graded the inflammation in each cochlea. Ganglion cell densities calculated by excluding and including blood vessel area showed no divergence with increasing inflammation (B = -163, P = 0.001 and B = -160, P = 0.001). The increase in the blood vessel area with inflammation has no effect on cell density measurements made by excluding that area.

Animals↗
PubMed2000

Analysis of adrenocortical secretory responses during acute an prolonged immune stimulation in inflammation-susceptible and -resistant rat strains.

Endogenous corticosterone secreted during immune challenge restricts the inflammatory process and genetic variations in this neuroendocrine-immune dialogue have been suggested to influence an individuals sensitivity to develop chronic inflammatory disorders. We have tested inflammation-susceptible Dark Agouti (DA) rats and resistant, MHC-identical, PVG.1AV1 rats for their abilities to secrete corticosterone in response to acute challenge with bacterial lipopolysaccharide (LPS) or a prolonged activation of the nonspecific immune system with arthritogenic yeast beta-glucan. Intravenous injection of LPS triggered equipotent secretion of corticosterone in both rat strains. Interestingly, peak concentrations of corticosterone did not differ significantly between the strains. Intradermal injection of beta-glucan caused severe, monophasic, polyarthritis in DA rats while PVG.1AV1 responded with significantly milder joint inflammation. Importantly, serial sampling of plasma from glucan-injected DA and PVG.1AV1 rats did not reveal elevated concentrations of plasma corticosterone at any time from days 1-30 postinjection compared to preinjection values, in spite of the ongoing inflammatory process. Interestingly, adrenalectomized, beta-glucan-challenged DA rats responded with an aggravated arthritic process, indicating an anti-inflammatory role for the basal levels of corticosterone that were detected in intact DA rats challenged with beta-glucan. Moreover, substitution with subcutaneous corticosterone-secreting pellets, yielding moderate stress-levels, significantly attenuated the arthritic response. In contrast, adrenalectomized and glucan-challenged PVG.1AV1 rats did not respond with an elevated arthritic response, suggesting that these rats contain the arthritic process via corticosterone-independent mechanisms. In conclusion, the hypothalamic-pituitary-adrenal axis in both rat strains exhibited strong activation after challenge with LPS. This contrasted to the basal corticosterone levels observed strains during a prolonged arthritic process. No correlation between ability to secrete corticosterone and susceptibility to inflammation could be demonstrated. Basal levels of endogenous corticosterone appeared to restrain inflammation in beta-glucan-challenged DA rats whereas resistance to inflammation in PVG.1AV1 rats may be mediated via corticosterone-independent mechanisms.

Adrenal Cortex↗
PubMed2003

Activation of peripheral cannabinoid CB1 receptors inhibits mechanically evoked responses of spinal neurons in noninflamed rats and rats with hindpaw inflammation.

The presence of cannabinoid1 (CB1) receptors on primary afferent fibres may provide a novel target for cannabinoid analgesics. The present study investigated the ability of peripheral CB1 receptors to modulate innocuous and noxious transmission in noninflamed rats and rats with peripheral carrageenan inflammation. Effects of peripheral injection of arachidonyl-2-choroethylamide (ACEA; 10 and 30 micro g in 50 micro L), a selective CB1 receptor agonist, on mechanically evoked responses of dorsal horn neurons were studied in noninflamed rats and rats with peripheral carrageenan inflammation. Peripheral injection of ACEA (30 micro g in 50 micro L) significantly inhibited innocuous (12 g) mechanically evoked responses of spinal neurons in noninflamed (27 +/- 4% of control; P < 0.01) and inflamed (12 +/- 8% of control; P < 0.05) rats. Similarly, noxious (80 g) mechanically evoked responses of spinal neurons were inhibited by peripheral injection of ACEA (30 micro g in 50 micro L) in noninflamed rats (51 +/- 9% of control; P < 0.01) and rats with peripheral carrageenan inflammation (21 +/- 8% of control; P < 0.01). Inhibitory effects of ACEA were significantly greater in rats with peripheral carrageenan inflammation than in noninflamed rats (P < 0.05). Inhibitory effects of ACEA were significantly blocked by coadministration of the CB1 receptor antagonist SR141716A in both groups of rats. Peripheral injection of SR141716A alone did not alter mechanically evoked responses of spinal neurons in either group of rats. These data demonstrate that activation of peripheral CB1 receptors can inhibit innocuous and noxious somatosensory processing. Furthermore, following peripheral inflammation there is an enhanced inhibitory effect of a peripherally administered CB1 receptor agonist on both innocuous and noxious mechanically evoked responses of spinal neurons.

Animals↗
PubMed2002

Peripheral blood markers of inflammation predict mortality and functional decline in high-functioning community-dwelling older persons.

OBJECTIVES: Several peripheral blood markers of inflammation have demonstrated prognostic ability, but the value of combining multiple markers as a measure of inflammatory burden remains unknown. The objective of this study was to determine the prognostic value of combining four peripheral blood measures of inflammation in healthy older persons. DESIGN: Inception cohort study with 7 years of follow-up. SETTING: Three communities. PARTICIPANTS: Eight hundred seventy high-functioning subjects aged 70 to 79 who had serum albumin, cholesterol, interleukin (IL)-6, and C-reactive protein (CRP) levels measured at baseline. MEASUREMENTS: Three- and 7-year mortality and Rosow- Breslau functional decline. RESULTS: A summary score was created that assigned one point each for the following blood levels: albumin <3.8 g/dL, cholesterol <170 mg/dL (bottom decile), IL-6>3.8 pg/mL (top tertile), and CRP>2.65 mg/L (top tertile). By 3 years, 6% of subjects had died, and, by 7 years, 23% had died. In subjects with three or four markers of inflammation, the adjusted odds ratios (AORs) for 3- and 7-year mortality were 6.6 and 3.2, respectively, compared with those who had no abnormal markers. Subjects with one or two markers were at more moderate and statistically insignificant increased risk of 3- and 7-year mortality with AORs of 1.5 and 1.3, respectively. The risks for functional decline at 3- and 7-years were generally small (AOR = 1.1-1.9) and not statistically significant. CONCLUSIONS: In high-functioning older persons, a measure of inflammation can identify those at a much higher risk of mortality and a possibly higher risk of functional decline. Whether therapies directed at reducing inflammation can attenuate such risk remains to be determined.

Aged↗
PubMed2001

Relative contributions of nutrition and inflammation to clinical outcome in dialysis patients.

Protein-energy malnutrition (PEM) is a common phenomenon in maintenance dialysis (MD) patients and a risk factor for poor quality of life and increased morbidity and mortality, including cardiovascular death, in these individuals. The association between undernutrition and adverse outcome in MD patients, which stands in contrast to that seen in the general population, has been referred to as reverse epidemiology. Measures of food intake, body composition tools, nutritional scoring systems, and laboratory values are used to assess the degree of severity of PEM, but no uniform approach is available for rating the overall severity of PEM. Epidemiologic studies suggest that inflammation is a missing link between PEM and poor clinical outcome in MD patients, and the existence of a malnutrition inflammation complex syndrome is suggested in these patients. Inflammation may be due to subclinical and clinically apparent illnesses. Some investigators suggest that PEM may predispose to illness and inflammation. There is a paucity of information concerning the effect of nutritional therapy on morbidity and mortality in MD patients. Interventional studies of the effect of nutritional support on outcome often are difficult to interpret because of small sample sizes, short duration of study, and other limitations. Large-scale, randomized, clinical trials of the effects of nutritional intake, nutritional status, and inflammation on clinical outcome are needed to define better the relationships between these factors in MD patients.

Animals↗
PubMed2002

Induction of protein oxidation by intravenous iron in hemodialysis patients: role of inflammation.

BACKGROUND: Oxidative stress and inflammation contribute to the high prevalence and severity of atherosclerosis, infections, and beta2-microglobulin amyloidosis; and thus, to reduced survival rate and quality of life in hemodialysis (HD) patients. Inflammation induces oxidative stress by production of the oxidants: superoxide anion, hydrogen peroxide, and hypochlorite. Intravenous iron (IVIR), administered in HD patients to correct anemia, can release free iron, that may react with hydrogen peroxide to produce the strong oxidant hydroxyl radical. Inflammation-induced lipid and protein oxidation and IVIR-induced lipid oxidation were shown in HD patients. However, IVIR-induced protein oxidation and a relationship between inflammation and IVIR-induced oxidative stress have not been reported to date. METHODS: We examined the effect of IVIR administration on markers of protein oxidation in HD patients (advanced oxidation protein products [AOPPs], thiol, and dityrosine) in relation to such inflammatory markers as C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-alpha). Iron saccharate, 100 mg, was administered to 19 HD patients for 1 hour after 3.5 hours of high-flux dialysis. Blood samples were drawn pre-HD, pre-IVIR, and post-IVIR for iron, transferrin, TNF-alpha, AOPP, thiol, total antioxidant capacity (TEAC), and dityrosine levels and pre-HD for ferritin and CRP levels. RESULTS: IVIR administration induced a 37% increase in AOPP level (P < 0.001), which correlated positively with pre-HD CRP level (r = 0.72; P < 0.05) and was greater in patients with a greater pre-HD TNF-alpha level (P < 0.05). IVIR administration did not affect TEAC, thiol, dityrosine, or TNF-alpha levels. CONCLUSION: IVIR administration induced an increase in protein oxidation (AOPP levels) that was related to the degree of inflammation.

Aged↗
PubMed2006

Does periodontitis reflect inflammation and malnutrition status in hemodialysis patients?

BACKGROUND: Chronic infection and inflammation, including periodontitis, is linked to an increased risk for atherosclerosis. To investigate the possible adverse effects of periodontitis in maintenance hemodialysis patients, we compared periodontal severity with malnutrition and inflammation, which are associated with poor atherosclerotic outcome in hemodialysis patients. METHODS: Two hundred fifty-three hemodialysis patients were included in this study to evaluate clinical periodontal status by using the Plaque Index, Gingival Index, and Periodontal Disease Index. Geographic, hematologic, biochemical, and dialysis-related data also were collected. Values for nutritional and inflammatory markers, such as albumin, blood urea nitrogen, creatinine, transferrin, absolute lymphocyte count, normalized protein catabolic rate, high-sensitivity C-reactive protein, and ferritin, were included for analysis with the Periodontal Index. RESULTS: Poor oral health status was shown by 80.6% of hemodialysis patients with periodontal disease. In an analysis of geographic and disease-related parameters, we found that aging, smoking, diabetes, and longer dialysis duration were associated with severity of periodontitis. Parameters of malnutrition and inflammation also were associated with poor periodontal status. We next conducted multiple regression analysis and found that age, diabetes, smoking, albumin level, and dialysis duration were associated independently with periodontitis severity in hemodialysis patients. According to the severity of periodontitis, there were higher percentiles of patients with malnutrition (chi-square = 13.055; P = 0.005) and inflammation (chi-square = 10.046; P = 0.018) in the severe group. CONCLUSION: Periodontal health is poor in hemodialysis patients and correlates with markers of malnutrition and inflammation. Its diagnosis and treatment deserve better awareness.

Aged↗
PubMed2005

The impact of inflammation on metabolic regulation in chronic kidney disease: a review.

Chronically uremic patients are characterized by a low-grade systemic inflammation that reflects the consequences of an unbalanced production of proinflammatory and anti-inflammatory cytokines and contributes to the progression of atherosclerotic vascular disease and malnutrition. The causes of inflammation in end-stage kidney disease have been studied in details. Nonetheless, the degree of activation of the systemic inflammatory response shows great interindividual variability that cannot be explained by renal disease or dialysis. The amount of cytokine that is produced on a definite stimulus varies among individuals. Single nucleotide polymorphisms in the promoter or coding regions of cytokine genes lead to high or low productions of these mediators and may genetically explain this heterogeneity. The "low-producer" genotypes for the anti-inflammatory cytokine interleukin-10 are more permissive for a greater level of systemic inflammation and for increased cardiovascular morbidity and mortality in patients on hemodialysis. Potential pharmacologic and nutritional approaches for treatment of systemic inflammation have been identified in recent years. In addition, physical exercise training may reduce the systemic inflammatory response. Definition of the relationships between different cytokine gene polymorphisms and systemic inflammation in chronically uremic patients will improve efficacy of targeted anti-inflammatory treatments.

Anti-Inflammatory Agents↗
PubMed2007

Thyroid function, endothelium, and inflammation in hemodialyzed patients: possible relations?

OBJECTIVE: Renal function affects the thyroid gland in many ways. Disturbances in hemostasis and inflammation are common complications of kidney diseases. Endothelial dysfunction may link these two processes. DESIGN AND PATIENTS: A cross-sectional study on thyroid hormones in relation to markers of endothelial damage and inflammation in 96 hemodialyzed (HD) patients and 39 healthy volunteers was performed. SETTING: The study took place in the dialysis unit at a university hospital. INTERVENTION: Thyroid hormones, markers of endothelial damage (von Willebrand factor, thrombomodulin, intracellular adhesion molecule, and CD146), markers of inflammation (high-sensitivity C-reactive protein, tumor necrosis factor alpha), other hemostatic parameters (thrombin-antithrombin complexes, prothrombin fragments 1 + 2 - F1 + 2, plasmin-antiplasmin complexes, tissue plasminogen activator and its inhibitor, tissue factor pathway inhibitor, and platelet glycoprotein V) were measured using commercially available kits. RESULTS: Free T3 and total T3 were lower in HD patients compared with controls. Markers of endothelial dysfunction and inflammation were significantly elevated in HD patients compared with controls. In multiple regression analysis T3 was independently related to time on dialyses, albumin, iron, ferritin, C-reactive protein (CRP), and F1 + 2 in HD patients. Free T3 was also independently related to total protein, total calcium, and triglycerides. In patients with CRP less than 6 mg/L in multiple regression analysis the only correlates of T3 were albumin and ferritin, whereas the only correlates of free T3 were albumin and time on dialyses. Multiple regression analysis showed that in HD patients with CRP greater than equal to 6 mg/L predictors of free T3 were CRP, F1 + 2, and dose of erythropoietin. In healthy volunteers T3 was related to tissue factor pathway inhibitor and platelet glycoprotein V was related to thyroid-stimulating hormone. CONCLUSIONS: We described novel relations between thyroid hormones and markers of endothelial dysfunction and inflammation in HD patients. Thyroid dysfunction is related to time on dialyses, endothelial damage, and inflammatory state, frequently encountered in uremia. Therefore, the relations between thyroid axis and endothelium in HD subjects merit additional studies.

Adult↗
PubMed2000

Hepatic cytochrome P450 down-regulation during aseptic inflammation in the mouse is interleukin 6 dependent.

Expression of cytochromes P450 (CYP) is markedly reduced during inflammatory processes. In vitro studies with hepatocytes have shown that cytokines generated during these processes down-regulate CYP. However, it is not clear to what extent each individual cytokine contributes to the overall reduced expression of the various CYP isoenzymes in vivo. Interleukin 6 (IL-6), a major player during inflammatory processes, is recognized as the most important cytokine modulating the hepatic expression of acute-phase protein (APP) genes. For this reason, we selected the IL-6(-/-) mouse as a model to investigate the role of IL-6 in the down-regulation of hepatic CYP during experimental inflammation. Our results show that the reduction in messenger RNA (mRNA) levels of CYP1A2, CYP2A5, and CYP3A11 during turpentine-induced inflammation was abrogated in IL-6-deficient mice, confirming that IL-6 is an indispensable player for the down-regulation of hepatic CYP during aseptic inflammation. Moreover, the different CYP isoenzymes showed a variable grade of dependence on IL-6, CYP2A5 being the most sensitive one. In the case of CYP2E1, differences between IL-6(-/-) and wild-type mice were no longer maintained after 24 hours, suggesting a delayed, rather than abrogated, CYP down-regulation in the absence of IL-6. As opposed to that, hepatic CYP repression took place in IL-6-deficient mice during lipopolysaccharide (LPS)-mediated inflammation. This contrasting behavior observed for CYP is surprisingly similar to the one seen for extracellular (serum amyloid A, beta-fibrinogen) and intracellular (metallothionein-1) APPs and points to the fact that, in the model of bacterial inflammation (LPS), the effects of IL-6 on CYP down-regulation are likely to be substituted by other cytokines or mediators.

Acute-Phase Proteins↗
PubMed2000

Surrogate markers of airway inflammation: inflammometry in paediatric respiratory medicine.

Until recently, there has not been any practical way to assess airway inflammation non-invasively in paediatrics. Surrogate markers of airway inflammation are potentially of great importance in the diagnosis and monitoring of inflammatory airways disease in children. A large number of substances in blood, urine and exhaled air or induced sputum are currently under study to evaluate their possible usefulness as markers of airway inflammation. To be useful, a marker should be valid, preferably non-invasive, quick, reproducible, repeatable and cheap. In addition, markers should be studied in relation to their specific purpose because different markers may be useful for different types of airway inflammation. Few, if any, markers will fulfill all these requirements. Most research has focused on applications of markers in asthma, some data refer to cystic fibrosis, infections and ciliary dyskinesia. Of all surrogate markers, exhaled nitric oxide has been studied the most and seems to offer information that should be evaluated for its relevance to clinical practice. Before introducing markers of inflammation into daily practice, analysis of benefits and costs are needed. There is little doubt that 'inflammometry' will be a major step forward and will be useful in differentiating airways diseases and improving treatment.

Biomarkers↗