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PubMed2002

Indinavir-associated interstitial nephritis and urothelial inflammation: clinical and cytologic findings.

The objective of the present study was to characterize the genitourinary syndromes that accompany indinavir-associated pyuria. Of 23 indinavir-treated patients with persistent pyuria, 4 had isolated interstitial nephritis, 10 had both interstitial nephritis and urothelial inflammation, 7 had isolated urothelial inflammation, and 2 had pyuria with nonspecific urinary tract inflammation. A total of 21 patients had multinucleated histiocytes identified by cytologic testing of urine specimens. Urine abnormalities resolved in all 20 patients who stopped receiving indinavir therapy. Pyuria continued in the 3 patients who continued receiving indinavir. Six patients had elevated serum creatinine levels, which returned to baseline levels when indinavir was discontinued. In conclusion, indinavir-associated pyuria was frequently associated with evidence of interstitial nephritis and/or urothelial inflammation, multinucleated histiocytes were commonly present in urine specimens, and cessation of indinavir therapy was associated with prompt resolution of urine abnormalities.

Adult↗
PubMed2004

Efficacy of low concentrations of ketorolac tromethamine in animal models of ocular inflammation.

PURPOSE: To determine if topical ophthalmic application of ketorolac tromethamine concentrations below 0.5% can block the biochemical and physiological processes associated with chemically induced ocular inflammation in rabbits. METHODS: Ocular inflammation was induced in rabbits by intravenous (i.v.) injection of endotoxin (2.5 microg/kg) isolated from Salmonella typhimurium, or by a topical application of arachidonic acid (1.0%). The effect of ketorolac (at concentrations ranging from 0.001%-0.5%) on ocular inflammation was determined by measuring changes in the blood-aqueous barrier, using fluorophotometry (dextran-isothiocyanate-fluorescein; FITC-dextran 2%) and by measuring changes in aqueous humor protein concentrations. Changes in aqueous humor prostaglandin E(2) (PGE(2)) concentrations were also measured. RESULTS: Ketorolac 0.01%-0.5% produced substantial decreases in endotoxin-induced fluorescein leakage into the aqueous humor. The decrease produced by ketorolac 0.1% was comparable to that produced by ketorolac 0.5%. Ketorolac 0.1%-0.5% produced substantial decreases in endotoxin-induced increases in prostaglandin concentrations in the aqueous humor, and in arachidonic acid-induced protein leakage into the aqueous humor. CONCLUSIONS: Topical application of ketorolac concentrations as low as 0.01%-0.1% significantly reduce chemically induced ocular inflammation in rabbits.

Animals↗
PubMed2004

Effects of hyaluronan on free-radical formation, corneal endothelium damage, and inflammation parameters after phacoemulsification in rabbits.

Free-radical formation may play a role in postoperative complications of phacoemulsification (e.g., corneal endothelium damage from mechanical injury). The present experiments were aimed at investigating whether different molecular weight ranges (2000-2600, 2600-3200, or 3200-3800 kDa) of hyaluronan may influence free radical formation, corneal endothelium damage, and inflammation parameters after phacoemulsification in the rabbit eye. The viscoelastic substance was injected in the anterior chamber of rabbits' eyes before phacoemulsification, at a 2.5% concentration. The formation of free radicals was determined by adding luminol to the irrigation media and measuring the chemoluminescence in eyes. The corneal endothelial damage was evaluated by measuring the corneal central thickness by pachimetry. The inflammation parameters were measured by calculation in aqueous humor of peak levels of leukocytes and prostaglandin E(2) (PGE(2)) and evaluation in uveal tissue of myeloperoxidase activity. Hyaluronan decreased by about 58-60% free-radical formation during phacoemulsification, reduced by about 76-80% modifications in mean corneal thickness and by about 54-61% the corneal endothelial cell loss in all molecular weight ranges used. No difference was found among various molecular weight ranges. The highest molecular weight range showed to be more potent than the lowest range for reduced number of inflammation cells and level of PGE(2) in aqueous humor. Thus, hyaluronan reduces free-radical formation, exerts protection on the corneal endothelium and exerts anti-inflammation properties after phacoemulsification in rabbits. The latter effect seems to depend on the molecular weight of the substance.

Animals↗
PubMedDate not supplied

Role of NADPH oxidases in disturbed flow- and BMP4- induced inflammation and atherosclerosis.

Atherosclerosis is an inflammatory disease, occurring preferentially in branched or curved arterial regions exposed to disturbed flow conditions including oscillatory shear stress (OS). In contrast, straight portions exposed to undisturbed laminar shear stress (LS) are relatively lesion free. The opposite effects of atheroprotective LS and proatherogenic OS are likely to be determined by differential expression of genes and proteins, including redox regulating factors. OS induces inflammation via mechanisms involving increased reactive oxygen species (ROS) production from the NADPH oxidases. Through a transcript profiling study and subsequent verification and functional studies, the authors discovered that OS induces inflammation by producing bone morphogenic protein 4 (BMP4) in endothelial cells. BMP4 stimulates expression and activity of NADPH oxidase requiring p47phox and Nox-1 in an autocrine-like manner. The NADPH oxidase activation by BMP4 then leads to ROS production, NF-kappaB activation, intercellular adhesion molecule 1 (ICAM-1) expression, and subsequent increased monocyte adhesivity of endothelial cells. It is proposed that endothelial NADPH oxidases play a critical role in disturbed flow- and BMP4-dependent inflammation, which is the critical early atherogenic response occurring in atheroprone areas. This emerging field of shear stress, BMP4, NADPH oxidases, inflammation, and atherosclerosis is reviewed.

Animals↗
PubMedDate not supplied

Elevated serum 8-oxo-dG in hemodialysis patients: a marker of systemic inflammation?

Does inflammation, as assessed by high sensitivity C-reactive protein (hs-CRP), in patients with end-stage renal disease (ESRD) tightly associate with increased serum levels of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8- oxo-dG)? Increased oxidative stress and inflammation have both been highlighted among several nontraditional risk factors for cardiovascular disease, which is the main cause of mortality in ESRD patients. In contrast to oxidative stress effects on proteins and lipids, DNA base damage has not been well demonstrated in ESRD. Two groups of hemodialysis patients were studied, one group with persistent inflammation (n = 13, with constant elevation of CRP > 10 mg/L for 6 months) and one group of noninflamed patients (n = 19, with constant CRP < 10 mg/L for 6 months). Serum 8-oxo-dG was significantly elevated in persistent inflammation in comparison to noninflamed patients. At an individual level, a significant correlation was found between serum 8-oxo-dG and hsCRP. Extracellular 8-oxo-dG leads to intracellular oxidative damage on the nucleotide pool, thus providing a sensitive marker for inflammatory response. Serum levels of 8-oxo-dG, in combination with other inflammatory markers, serve as useful diagnostic tools for identification of patients in risk for inflammatory complications.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2006

The epidemiology of low-grade chronic systemic inflammation and type 2 diabetes.

The fattening of the human species and the accompanying emergence of the metabolic syndrome and of type 2 diabetes as remarkably frequent clinical entities are among the major epidemiologic events of our time. Control of the diabetes epidemic requires a greater understanding of the pathophysiologic processes underlying these phenomena. Many epidemiologic studies have now shown associations between inflammation markers and diabetes, with the most consistent being for leukocytes and the strongest being for C-reactive protein. Consistent protective associations have also been reported for adiponectin, an adipocyte secretory protein with antiinflammatory actions. Although great variability is seen between reported associations, as a whole these studies suggest a role for inflammation linked to obesity. The variability reported is in part due to differences in model adjustment, in how diabetes was ascertained, and in the different means used to operationalize the concept of low-grade chronic systemic inflammation. It is also due, in part, to sample characterization, as findings are heterogeneous across some subgroups, such as those defined by smoking. Consistent with their association with type 2 diabetes, inflammation markers have also be shown to predict conditions present in the prediabetes state such as weight gain, hypertension, gestational diabetes, and decline in insulin sensitivity.

Chronic Disease↗
PubMed2005

Dietary pattern, inflammation, and incidence of type 2 diabetes in women.

BACKGROUND: Inflammation is considered a key mechanism leading to type 2 diabetes, but dietary exposures that lead to inflammation and diabetes are largely unknown. OBJECTIVE: Our objective was to investigate the relation between a dietary pattern associated with biomarkers of inflammation and the incidence of type 2 diabetes. DESIGN: We conducted a nested case-control study of 656 cases of type 2 diabetes and 694 controls among women in the Nurses' Health Study and 2 prospective cohort studies of 35,340 women in the Nurses' Health Study and 89,311 women in the Nurses' Health Study II who were followed for incident diabetes. RESULTS: Through the use of reduced rank regression, we identified a dietary pattern that was strongly related to inflammatory markers in the nested case-control study. This pattern, which was high in sugar-sweetened soft drinks, refined grains, diet soft drinks, and processed meat but low in wine, coffee, cruciferous vegetables, and yellow vegetables, was associated with an increased risk of diabetes (multivariate-adjusted odds ratio comparing extreme quintiles: 3.09; 95% CI: 1.99, 4.79). We identified 1517 incident cases of confirmed type 2 diabetes in the Nurses' Health Study (458,991 person-years) and 724 incident cases in the Nurses' Health Study II (701,155 person-years). After adjustment for body mass index and other potential lifestyle confounders, the relative risks comparing extreme quintiles of the pattern were 2.56 (95% CI: 2.10, 3.12; P for trend < 0.001) in the Nurses' Health Study and 2.93 (95% CI: 2.18, 3.92; P for trend < 0.001) in the Nurses' Health Study II. CONCLUSION: The dietary pattern identified may increase chronic inflammation and raise the risk of developing type 2 diabetes.

Adult↗
PubMed2004

Diet-induced weight loss, exercise, and chronic inflammation in older, obese adults: a randomized controlled clinical trial.

BACKGROUND: Persistent, low-grade inflammation is an independent predictor of several chronic diseases and all-cause mortality. OBJECTIVE: The intention of this study was to determine the independent and combined effects of diet-induced weight loss and exercise on markers of chronic inflammation. DESIGN: Three hundred sixteen community-dwelling, older (> or = 60 y), overweight or obese [body mass index (in kg/m2) > or = 28], sedentary men and women with radiographic evidence of knee osteoarthritis were randomly assigned to four 18-mo treatments: healthy lifestyle control, diet-induced weight loss, exercise, and diet plus exercise. The exercise intervention consisted of combined weight training and walking for 1 h 3 times/wk. The weight-loss intervention consisted of a weekly session with a registered dietitian to provide education and support for lowering energy intake. RESULTS: The diet-induced weight-loss intervention resulted in significantly greater reductions in concentrations of C-reactive protein (P = 0.01), interleukin 6 (P = 0.009), and soluble tumor necrosis factor alpha receptor 1 (P = 0.007) than did no weight-loss treatment. Changes in soluble tumor necrosis factor alpha receptor 1 but not in C-reactive protein or interleukin 6 correlated with changes in body weight. Exercise training did not have a significant effect on these inflammatory biomarkers, and there was no significant interaction between weight loss and exercise training. CONCLUSIONS: These findings provide evidence from a randomized controlled trial that a dietary intervention designed to elicit weight loss reduces overall inflammation in older, obese persons. Additional studies are needed to assess the effects of different modes and intensities of exercise on inflammation.

Aged↗
PubMed2004

Dietary intake of trans fatty acids and systemic inflammation in women.

BACKGROUND: trans Fatty acid (TFA) intake predicts risks of coronary artery disease and diabetes. Systemic inflammation may be involved in the pathogenesis of such conditions; however, relations between TFA intake and systemic inflammation are not well established. OBJECTIVE: We investigated the relations between TFA intake and inflammatory markers. DESIGN: In 823 generally healthy women in the Nurses' Health Study I and II, concentrations of soluble tumor necrosis factor alpha receptors 1 and 2 (sTNF-R1, sTNF-R2), interleukin 6 (IL-6), and C-reactive protein (CRP) were measured. Usual dietary intakes assessed from 2 semiquantitative food-frequency questionnaires were averaged for each subject. RESULTS: In age-adjusted analyses, TFA intake was positively associated with sTNF-R1 and sTNF-R2 (P for trend < 0.001 for each): sTNF-R1 and sTNF-R2 concentrations were 10% (+108 pg/mL; 95% CI: 50, 167 pg/mL) and 12% (+258 pg/mL; 138, 377 pg/mL) higher, respectively, in the highest intake quintile than in the lowest. These associations were not appreciably altered by adjustment for body mass index, smoking, physical activity, aspirin and nonsteroidal antiinflammatory drug use, alcohol consumption, and intakes of saturated fat, protein, n-6 and n-3 fatty acids, fiber, and total energy. Adjustment for serum lipid concentrations partly attenuated these associations, which suggests that they may be partly mediated by effects of TFAs on serum lipids. TFA intake was not associated with IL-6 or CRP concentrations overall but was positively associated with IL-6 and CRP in women with higher body mass index (P for interaction = 0.03 for each). CONCLUSIONS: TFA intake is positively associated with markers of systemic inflammation in women. Further investigation of the influences of TFAs on inflammation and of implications for coronary disease, diabetes, and other conditions is warranted.

Adult↗
PubMed2006

Whole grains, bran, and germ in relation to homocysteine and markers of glycemic control, lipids, and inflammation 1.

BACKGROUND: Intake of whole grains is inversely associated with risk of diabetes and ischemic heart disease in observational studies. The lower risk associated with high whole-grain intakes may be mediated through improvements in glycemic control, lipid profiles, or reduced inflammation. OBJECTIVE: The aim was to examine whether the intake of whole grains, bran, and germ is related to homocysteine, plasma markers of glycemic control (fasting insulin, hemoglobin A1c, C-peptide, and leptin), lipids (total cholesterol, triacylglycerol, HDL cholesterol, and LDL cholesterol), and inflammation (C-reactive protein, fibrinogen, and interleukin 6). DESIGN: This was a cross-sectional study of the relations of whole grains, bran, and germ intakes with homocysteine and markers of glycemic control, lipids, and inflammation in 938 healthy men and women. RESULTS: Whole-grain intake was inversely associated with homocysteine and markers of glycemic control. Compared with participants in the bottom quintile of whole-grain intake, participants in the highest quintile had 17%, 14%, 14%, and 11% lower concentrations of homocysteine (P < 0.01), insulin (P = 0.12), C-peptide (P = 0.03), and leptin (P = 0.03), respectively. Inverse associations were also observed with total cholesterol (P = 0.02), HDL cholesterol (P = 0.05), and LDL cholesterol (P = 0.10). Whole-grain intake was not associated with the markers of inflammation. Whole-grain intake was most strongly inversely associated with markers of glycemic control in this population. CONCLUSION: The results suggest a lower risk of diabetes and heart disease in persons who consume diets high in whole grains.

Adult↗
PubMed2000

Clustering of procoagulation, inflammation, and fibrinolysis variables with metabolic factors in insulin resistance syndrome.

The known metabolic cardiovascular disease risk factors associated with insulin resistance syndrome (IRS) do not adequately explain the excess cardiovascular disease risk attributed to this syndrome, and abnormalities in hemostatic variables may contribute to this excess risk. Using data from 322 nondiabetic elderly men and women (aged 65-100 years) participating in the Cardiovascular Health Study during 1989-1990, the authors performed factor analysis on 10 metabolic risk factors associated with IRS and 11 procoagulation, inflammation, and fibrinolysis variables to examine the clustering of the metabolic and hemostatic risk markers. Factor analysis of the metabolic variables confirmed four uncorrelated factors: body mass, insulin/glucose, lipids, and blood pressure. Adding the hemostatic variables yielded three new factors interpreted as inflammation, vitamin K-dependent proteins, and procoagulant activity. Plasminogen activator inhibitor-1 clustered with the body mass factor, supporting the hypothesis that obesity is related to impaired fibrinolysis. Fibrinogen clustered with the inflammation summary factor rather than procoagulant activity, supporting the position that fibrinogen principally reflects underlying inflammation rather than procoagulant potential. The authors conclude that should hemostatic variables be shown to contribute to IRS-related cardiovascular disease, apart from plasminogen activator inhibitor-1, they may do so independently of the established metabolic abnormalities.

Aged↗
PubMed2005

Inflammation and triglycerides partially mediate the effect of prepregnancy body mass index on the risk of preeclampsia.

The objective of this study was to quantify the mediating role of inflammation and triglycerides in the association between prepregnancy body mass index (weight (kg)/height (m)2) and preeclampsia. The authors conducted a nested case-control study of 55 preeclamptic women and 165 pregnant controls from the Pregnancy Exposures and Preeclampsia Prevention Study (Pittsburgh, Pennsylvania, 1997-2001). Serum samples collected at < or = 20 weeks' gestation were analyzed for levels of C-reactive protein and triglycerides. The adjusted odds ratio (AOR) from a multivariable conditional logistic regression model assessing the total effect of body mass index on preeclampsia risk was compared with the AOR from the same model after results were controlled for C-reactive protein, triglycerides, and confounding factors (direct-effects model). The percentage of the total effect that was mediated through inflammation and triglycerides was calculated as 100 - [ln(direct-effects AOR)/ln(total-effects AOR)]. In the total-effects model, 4- and 8-unit increases in body mass index were associated with 1.7-fold (95% confidence interval (CI): 1.3, 2.3) and 2.9-fold (95% CI: 1.6, 5.2) increases in preeclampsia risk, whereas in the direct-effects model, these AORs were 1.4 (95% CI: 1.0, 1.9) and 2.0 (95% CI: 1.0, 3.8), respectively. Inflammation was a more important mediator than triglycerides. These findings suggest that approximately one third of the total effect of body mass index on preeclampsia risk is mediated through inflammation and triglyceride levels.

Adult↗
PubMed2005

Inflammation and primary demyelination induced by the intraspinal injection of lipopolysaccharide.

Inflammation is a prominent feature of several disorders characterized by primary demyelination, but it is not clear whether a relationship exists between inflammation and myelin damage. We have found that substantial demyelination results from the focal inflammatory lesion caused by the injection of lipopolysaccharide (LPS; 200 ng) directly into the rat dorsal funiculus. Within 24 h, such injections caused a focal inflammatory response consisting of a substantial number of polymorphonuclear cells and ED1-positive and inducible nitric oxide synthase (iNOS)-positive macrophages/microglia. The number of inflammatory cells was substantially reduced by day 7. OX-52-positive T-cells were less frequently observed but were present in the meninges at 8 h, reached a maximum in the dorsal funiculus at 7 days, and were rare at 14 days. The inflammation was followed by the appearance of a large lesion of primary demyelination that encompassed up to approximately 75% of the cross-sectional area of the dorsal funiculus. Treatment with dexamethasone significantly reduced the number of cells expressing iNOS, but did not prevent the demyelination. By 28 days the lesions were largely remyelinated, usually by Schwann cells. These changes were not observed in control, saline-injected animals. We conclude that the intraspinal injection of LPS results in inflammation and subsequently in prominent demyelination. The mechanisms underlying the demyelination are not clear, but it is notable that it typically begins with disruption of the adaxonal myelin. Indeed, there is an early loss of myelin-associated glycoprotein within the lesion, despite the persistence of proteolipid protein. This combination is a feature of the pattern III lesion recently described in multiple sclerosis (Lucchinetti et al., 2000), and we therefore suggest that LPS-induced demyelination may serve as the first experimental model available for the study of this type of multiple sclerosis lesion.

Animals↗
PubMed2005

Effect of inflammation on cyclooxygenase (COX)-2 expression in benign and malignant oesophageal cells.

Chronic inflammation has been linked to carcinogenesis in various tissue sites. Barrett's oesophageal epithelium (BE) is a premalignant condition in which cyclooxygenase-2 (COX-2) levels are increased. However, it is not clear whether the primary stimulus for the high COX-2 levels is related to inflammation or malignancy. The effect of exogenous cytokines (IL-1beta, IL-10 and IL-13) on COX-2 expression was assessed by western blotting in three BE cancer cell lines (SEG-1, BIC-1 and OE33) and a squamous cancer cell line (OE21). Primary tissue was assessed from 17 patients with long BE segments, 13 oesophagitis, 30 oesophageal adenocarcinoma (EAC), and 40 normal oesophageal (NE) and duodenal (DU) controls. COX-2 protein expression was determined by western blotting and its tissue localization was examined using immunohistochemistry. COX-2 protein and the neutrophil marker myeloperoxidase (MPO) were quantified along BE segments. The leukocyte marker CD45 was used to identify any correlation between COX-2 expression and leukocyte cell distribution in EAC. IL-1beta induced COX-2 expression in SEG-1 cells (P < 0.05), whereas IL-10 and IL-13 had no effect. COX-2 protein levels were found to be increased in distal BE > proximal BE > oesophagitis > NE (P < 0.001). COX-2 expression in EAC was heterogeneous and the overall levels were not significantly increased. The increased COX-2 expression in distal BE was not associated with inflammation (MPO expression). In addition, there was no correlation between COX-2 and CD45 in AC. COX-2 protein expression in the oesophagus appears to be independent of the degree of inflammation.

Adenocarcinoma↗
PubMedDate not supplied

The complement system in host defense and inflammation.

In this discussion I have reviewed the major role of complement in host defense and inflammation. In addition, I have discussed dificiency states. Although these are rare, their clinical signs and symptoms can be predicted, at least in part, on the basis of our current understanding of the biological activities of complement and the various pathways of complement activation. This is not to say that complement plays no role in a wide variety of other illnesses. However, when complement plays a role in an illness, often this is not because it is functioning in an aberrant fashion. The usual situation is that complement is being activated and is serving its normal function in causing inflammation and damage to tissues under abnormal circumstances. Thus, for example, circulating antigen complexes may be deposited in the kidney, activate complement, and mediate tissue inflammation. In this case, complement is functioning normally but is being activated under abnormal circumstances. The same type of analysis can be made for many diseases of many different organ systems. At present, we have no drugs that are effective in humans in controlling the activation of complement and complement-mediated inflammation. We have not yet even established whether local variations in the activity of complement may affect the course of a clinical infection, but there is certainly strongly suggestive evidence to support this idea. It should be clear that under certain circumstances complement may well be a major factor in controlling the course of an infection. The near future should bring a vast expansion in our understanding of how complement contributes to specific clinical illnesses and to the defense of the host against specific microorganisms.

Angioedema↗
PubMed1998

Monocyte cytokine production in an elderly population: effect of age and inflammation.

OBJECTIVE: To determine the association among aging, inflammation, and cytokine production by peripheral blood mononuclear cells. POPULATION AND METHODS: We examined production of interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), IL-1 receptor antagonist (IL-1Ra), and IL-6 in 711 elderly participants in the Framingham Heart Study (mean age, 79 y) and 21 young healthy volunteers (mean age, 39 y). The elderly subjects were categorized by serum C-reactive protein (CRP) concentration, a marker of systemic inflammation. RESULTS: Production of IL-6 (p < .00001) and IL-1Ra (p < .00001) was higher in the elderly subjects than in the control group. IL-6 production increased with increasing CRP, whereas IL-1RA was uniformly elevated in elderly subjects regardless of CRP. However, we found no difference in the production of IL-1 beta or TNF-alpha between the young and elderly groups, regardless of CRP status. IL-6 population correlated with IL-1 beta (r = .36, p < .0001) and TNF-alpha production (r = .25, p < .0001), but IL-1Ra production did not. CONCLUSION: Production of IL-6 and IL-1Ra--but not IL-1 beta or TNF-alpha--was increased in the elderly compared to healthy, young subjects. The increase in IL-6 also correlated with increased production of CRP, a marker of inflammation. However, IL-1Ra was increased in the elderly independently of CRP production. Although limited by the small control group, these data suggest that dysregulation of some inflammatory cytokines occurs with age, but the role of inflammation in aging remains unclear.

Adult↗
PubMed2004

Inflammation-induced transcriptional regulation of Golgi transporters required for the synthesis of sulfo sLex glycan epitopes.

The de novo synthesis and expression of sulfo sLex glycan on vascular endothelial glycoproteins has a central role in the initiation of inflammatory reactions, serving as a putative ZIP code for organ-specific trafficking of leukocytes into sites of inflammation. The synthesis of sulfo sLex requires energy carrying donors, CMP-sialic acid (CMP-SA), GDP-fucose (GDP-Fuc), and adenosine 3'-phosphate 5'-phosphosulphate (PAPS) for donation of SA, Fuc, and sulfate, respectively. These donors are synthesized in the nucleus or cytosol and translocated into Golgi by specific transporters where corresponding transferase and proteins as well as enzymatic activities increase on inflammatory stimuli. Here we analyze the transcriptional coregulation of CMP-SA, GDP-Fuc, and PAPS transporters with in situ hybridization and real-time PCR in acute inflammation using kidney and heart allografts as model systems. Our results indicate that these three transporters display coordinated transcriptional regulation during the induction of the sulfo sLex glycan biosynthesis. With in silico analysis, the data generated with 230 human Affymetrix U133A gene chips indicated that the coregulated expression of CMP-SA and GDP-Fuc transporters was not common. Taken together our results suggest that inflammation-induced transcriptional regulation exists for Golgi membrane transporters required for the synthesis of the inflammation-inducible ZIP code sulfo sLex glycans.

Animals↗
PubMed1992

Rat serum osteocalcin concentration is determined by food intake and not by inflammation.

Osteocalcin, or bone gla protein, is the major noncollagenous protein in bone. Previous findings of decreased serum osteocalcin concentrations in children with Kwashiorkor led us to analyze the respective influence of nutritional status and inflammation on circulating osteocalcin in growing rats. Food deprivation for 72 h induced a significant 24% decrease in serum osteocalcin. Refeeding produced a rapid rise in serum osteocalcin, which reached control concentrations after 24 h of refeeding. Bone osteocalcin was not affected by these dietary manipulations. The changes in serum osteocalcin were not correlated with serum 1,25-dihydroxycholecalciferol, whereas they could be related to serum 25-hydroxycholecalciferol concentrations. Turpentine injection reduced serum osteocalcin concentration, but pair-feeding showed that this decrease was entirely attributable to spontaneous food restriction and not to inflammation. By contrast, the sensitive nutritional marker, serum transthyretin, was affected by both inflammation and food restriction. These results indicate that serum osteocalcin is closely related to food intake but not to inflammation, suggesting that the dramatic decrease in serum osteocalcin that we previously observed in children with Kwashiorkor is due to malnutrition per se.

Animals↗