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PubMed2004

The influence of systemic inflammation on inflammation in the brain: implications for chronic neurodegenerative disease.

Systemic inflammation is associated with sickness behaviour and signals pass from the blood to the brain via macrophage populations associated with the brain, the perivascular macrophages and the microglia. The amplitude, or gain, of this transduction process is critically dependent on the state of activation of these macrophages. In chronic neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, or prion disease the pathology is associated with a highly atypical inflammatory response, characterised by the activation of the macrophage populations in the brain: the cells are primed. Recent evidence suggests that systemic inflammation may impact on local inflammation in the diseased brain leading to exaggerated synthesis of inflammatory cytokines and other mediators in the brain, which may in turn influence behaviour. These interactions suggest that systemic infections, or indeed any systemic challenge that promotes a systemic inflammatory response, may contribute to the outcome or progression of chronic neurodegenerative disease.

Alzheimer Disease↗

PubMed1998

A double-masked, placebo-controlled evaluation of 0.5% loteprednol etabonate in the treatment of postoperative inflammation. The Loteprednol Etabonate Postoperative Inflammation Study Group 2.

OBJECTIVE: This study aimed to compare the efficacy and safety of loteprednol etabonate (LE) 0.5% to placebo (vehicle) in controlling the anterior chamber cell and flare reaction in patients undergoing cataract surgery with intraocular lens (IOL) implantation. DESIGN: Randomized, double-masked, placebo-controlled, parallel group multicenter study. PARTICIPANTS: A total of 203 patients undergoing elective cataract removal and posterior chamber intraocular lens implantation who, on the day after surgery, exhibited a minimum anterior chamber inflammation score (ACI, sum of cell and flare reaction) rating of 3 (0-9 scale). INTERVENTION: All patients received either LE 0.5% or placebo (vehicle) four times daily in the eye that was operated on for up to 14 days after surgery. MAIN OUTCOME MEASURES: Resolution of ACI by final, on-treatment visit was measured. RESULTS: The proportion of patients with ACI resolved by the final visit was 56 (55%) of 102 in the LE group and 28 (28%) of 100 in the placebo group (P < 0.001). For all the individual components of ACI (cell and flare), as well as other signs and symptoms, the resolution rate and mean change from baseline favored LE. Expanding the efficacy criterion to include patients with mild inflammation at final visit, the efficacy of LE was 95 (93%) of 102 in contrast to 65 (65%) of 100 for placebo. Among the 39 patients who did not complete the study, the majority were discontinued for inadequate anti-inflammatory effect: 25 (25%) of 101 placebo patients and 5 (5%) of 102 of LE patients. The difference in the treatment failure rates, as well the difference in the time course of failures, was both clinically meaningful and statistically significant in favor of LE (P < 0.001). Both treatments were well-tolerated. No clinically significant elevations in intraocular pressure (> or = 10 mmHg) were seen in the LE treatment group. One patient in the placebo treatment group met this criterion. CONCLUSIONS: Loteprednol etabonate showed a clinically meaningful reduction in the signs and symptoms of postoperative anterior chamber inflammation when compared with that of placebo and had an acceptable safety profile compared with placebo.

Adult↗

PubMed1997

Factor Xa as an interface between coagulation and inflammation. Molecular mimicry of factor Xa association with effector cell protease receptor-1 induces acute inflammation in vivo.

Coagulation proteases were tested in a rat model of acute inflammation. Subplantar injection of Factor Xa (10-30 microg) produced a time- and dose-dependent edema in the rat paw, and potentiated carrageenin-induced edema. In contrast, the homologous protease Factor IXa was ineffective. This inflammatory response was recapitulated by the Factor Xa sequence L83FTRKL88(G), which mediates ligand binding to effector cell protease receptor-1 (EPR-1), while a control scrambled peptide did not induce edema in vivo. Conversely, injection of the EPR-1-derived peptide S123PGKPGNQNSKNEPP137 (corresponding to the receptor binding site for Factor Xa) inhibited carrageenin-induced rat paw edema, while the adjacent EPR-1 sequence P136PKKRERERSSHCYP150 was without effect. EPR-1-Factor Xa-induced inflammation was characterized by fast onset and prominent perivascular accumulation of activated and degranulated mast cells, was inhibited by the histamine/serotonin antagonists cyproheptadine and methysergide, but was unaffected by the thrombin-specific inhibitor, Hirulog. These findings suggest that through its interaction with EPR-1, Factor Xa may function as a mediator of acute inflammation in vivo. This pathway may amplify both coagulation and inflammatory cascades, thus contributing to the pathogenesis of tissue injury in vivo.

Amino Acid Sequence↗

PubMed2001

[Inflammation-allergy and prostanoids. (2). The role of prostanoids in allergic inflammation].

Allergic inflammation is orchestrated by mainly antigen-specific CD4+ T cells, eosinophils and mast cells, which is a characteristic feature of bronchial asthma, rhinitis and atopic dermatitis. Prostanoids are one of the arachidonic metabolites, which are produced by a variety of inflammatory cells upon stimulation and are thought to be involved in the pathogenesis of diseases as well as the regulation of homeostasis. We investigated the role of a prostanoid, prostaglandin D2 (PGD2), in the pathogenesis of allergic bronchial asthma using its receptor, DP, gene-deficient mice. We found that the disruption of the DP gene attenuated the allergen-induced airway eosinophilic inflammation, Th2 type cytokine production and bronchial hyperresponsiveness to cholinergic stimuli, suggesting that PGD2 is an important mediator of allergic asthma. In contrast, the treatment of non-steroidal anti-inflammatory agents, which are known to be inhibitors of cyclooxygenases, did not inhibit or instead exaggerated these responses in asthmatics or experimental animal models, indicating that there are regulatory prostanoids in allergic inflammation. Recently, strategies of gene manipulation such as the "knockout" or "transgenic" techniques are important means to understand the role of a certain functional molecule. These approaches and the development of their antagonists/inhibitors could help us to understand the function of prostanoids in the pathophysiology of allergic disorders.

Animals↗

PubMed1985

Fibronectin in chronic inflammation: studies using the rat air pouch model of chronic allergic inflammation.

Fibronectin is a large glycoprotein of plasma, tissue fluids and tissues. The rat air pouch model of mesenchymal inflammation was used to examine changes in fibronectin levels during inflammation within a mesenchymal cavity. Rat plasma fibronectin levels showed a rapid and significant rise in relation to the induction of an air pouch. In contrast pouch fluid fibronectin levels were initially low and gradually increased with chronicity. They were unrelated to plasma levels. Pouch fluid fibronectin showed no relationship to cell content of the fluid, its volume, nor the weight of granulation tissue. Two-dimensional immuno-electrophoresis showed pouch fluid fibronectin was partially complexed but plasma fibronectin was not. These results show plasma and tissue fluid fibronectin have different patterns of response to inflammation. In rats plasma fibronectin is an acute-phase reactant, although this is not the case in humans.

Air↗

PubMedDate not supplied

[Thermometry in experimental inflammation. II. Studies of the effect of local cold application on the skin temperature of the rat's paw in experimental inflammation].

In continuation of earlier thermometric investigations on experimental inflammations in rats we studied the effect of a single local cold application on paw skin temperature after injection of caolin , carrageenan and dextran. In all cooling experiments a highly significant drop of skin temperature of the inflamed paw could be demonstrated which came up to an average of 17 degrees C. However, the further course of skin temperature was very different. In caolin edema, the skin of the inflamed paw rewarmed quickly; after injection of carrageenan and dextran the skin temperature was significantly low after 60 min, but it exceeded the values later on. These results demonstrate that local cooling significantly influences experimental inflammations. Depending on different etiology and pathogenesis, however, the reaction of inflammation on cooling is very different.

Animals↗

PubMed1994

[Experimental study of differentiation between tumor and inflammation using MR imaging: correlation between VX2 tumors and croton oil induced inflammation in the rabbit's femoral muscle].

We evaluated the various Magnetic Resonance (MR) sequences for differentiation between tumors and inflammation. Experimental models of rabbit's tumors (VX2) and inflammation induced by croton oil in the femoral muscle were used for this evaluation. Both types of lesions presented a high intensity area on T2-weighted and heavy T2-weighted images. An inflammatory lesion was revealed with iso-/low intensity area and tumors were defined as high signal lesions on Sinc saturation fat suppression T1-weighted, standard T1-weighted and fat suppression T1-weighted images by the 3 Point dixon method. T1, T2 values of tumor and inflammatory lesions were also measured. The T1 value of the tumors was 1186 +/- 58 msec (n = 5) and that of the inflammatory lesion was 1097 +/- 40 msec (n = 3). The T2 value of the tumors was 71 +/- 13 msec (n = 5) and that of the inflammatory lesions was 70 +/- 5.5 msec (n = 3). There were no significant differences between both the T1 and T2 values. Calculated relative proton density was 0.69 +/- 0.14 (n = 4) in the tumors, and 0.42 +/- 0.12 (n = 3) in the inflammatory lesions. A statistical difference (p < 0.05) was found in both value. These results suggest that a T2-weighted image is not useful for differentiation between tumors and inflammation, and a T1-weighted image might be useful for such differentiation. This phenomenon is related to the difference of the proton density.

Animals↗

PubMed1993

Prostaglandin E2 administered by subcutaneous pellets causes local inflammation and systemic bone loss: a model for inflammation-induced bone disease.

The effects of prostaglandin E2 (PGE2) given in controlled-release pellets or by daily sc injection for 21 days on mineral homeostasis and bone histomorphometry were compared in 7-week-old female rats. Sham operation and ovariectomy were performed at the beginning of the studies. In experiment 1, 7.5 mg PGE2 or drug-free, controlled-release pellets were implanted sc at the back of the neck on day 7. In experiment 2, 3 mg/kg body weight of PGE2 or vehicle was injected sc daily beginning on day 7. The animals were sacrificed on day 28 of the two experiments, and the tibiae were removed for histomorphometric analysis of the diaphysis and metaphysis. When administered by pellets in experiment 1, PGE2 lowered serum 1,25-dihydroxyvitamin D and did not influence weight gain, serum calcium, phosphorus, or magnesium, cross-sectional or medullary areas, periosteal bone formation and apposition rates, endosteal bone formation and apposition rates, or endosteal tetracycline-labeled perimeter. PGE2 lowered cancellous bone area and cancellous bone perimeter in both the sham-operated and ovariectomized rats. In contrast, when administered by sc injection in experiment 2, PGE2 reduced weight gain, increased serum magnesium, increased cortical area, and reduced medullary area without changing cross-sectional area, increased periosteal bone formation and apposition rates and endosteal bone and apposition rates, did not alter endosteal tetracycline-labeled perimeter, and increased cancellous bone area and cancellous bone perimeter in both sham-operated and ovariectomized animals. PGE2 produced local inflammation when given by pellets, and the serum concentration of 13,14-dihydro-15-ketoprostaglandin E2, the major metabolite of PGE2, increased when PGE2 was given by sc injection but not when administered by pellets. Thus, PGE2 given sc by controlled-release pellets (1) produces local inflammation and systemic bone loss without increasing PGE2 systemically and (2) provides a model for inflammation-induced loss of cancellous bone. The results also indicate that the pellet is not a valid means for the delivery of PGE2 to the general circulation.

Analysis of Variance↗

PubMed1997

Central inflammation is more important than peripheral inflammation.

Inflammation is present in the airways of asthma patients even during stable periods of the disease. In post-mortem samples of the proximal airways, inflammation can be visualised as T-cell infiltration of the bronchial wall. Lymphocyte accumulation is also evident around the small airways, indicating that inflammation is present in the peripheral regions of the lungs. However, the major inflammatory events associated with asthma appear to occur in the proximal airways.

Asthma↗

PubMed2005

Modulating bladder neuro-inflammation: RDP58, a novel anti-inflammatory peptide, decreases inflammation and nerve growth factor production in experimental cystitis.

PURPOSE: In interstitial cystitis (IC) inflammation induces and perpetuates neurotrophic changes in the bladder, resulting in the symptoms of frequency, urgency and pain. RDP58 (NH2-arg-norleucine (nle)-nle-arg-nle-nle-nle-gly-tyr-CONH2) (Sangstat Corp., Fremont, California) is a novel synthetic peptide that inhibits early signal transduction pathways for the expression of inflammatory cytokines. In this study we evaluated the effects of intravesical RDP58 on an established model of cystitis. MATERIALS AND METHODS: Mice were catheterized and equal volumes of Escherichia coli lipopolysaccharide (LPS) or saline were instilled into the bladder. After 45 minutes the bladders were drained and distilled water or RDP58 (1 mg/ml) was instilled for 30 minutes. At 24 hours later the bladders were excised and cultured for analysis of tumor necrosis factor-alpha (TNF-alpha), substance P (SP) and nerve growth factor (NGF) production, as quantified by enzyme-linked immunosorbent assay. RESULTS: LPS caused severe inflammation in mouse bladders compared with controls. Exposure to LPS increased the levels of TNF-alpha, SP and NGF production compared with controls (each p <0.05). In LPS exposed mice RDP58 significantly decreased inflammatory parameters by 82% 24 hours after treatment (p <0.05). Within 4 hours RDP58 abolished TNF-alpha production and at 24 hours TNF-alpha remained undetectable. RDP58 also significantly decreased SP and NGF production in LPS exposed bladders by more than 40% and 85%, respectively (each p <0.05). CONCLUSIONS: Inflammatory models of cystitis result in increased levels of TNF-alpha, SP and NGF production in the bladder, paralleling the hypothesized neuro-inflammatory etiology of IC. RDP58 decreases inflammation and neurotrophic factors in vivo and it may potentially treat bladder disorders with an inflammatory component, such as IC.

Animals↗

PubMed2004

Inflammation and cancer IV. Colorectal cancer in inflammatory bowel disease: the role of inflammation.

Patients with ulcerative colitis and Crohn's disease are at increased risk for developing colorectal cancer. To date, no known genetic basis has been identified to explain colorectal cancer predisposition in these inflammatory bowel diseases. Instead, it is assumed that chronic inflammation is what causes cancer. This is supported by the fact that colon cancer risk increases with longer duration of colitis, greater anatomic extent of colitis, the concomitant presence of other inflammatory manifestations such as primary sclerosing cholangitis, and the fact that certain drugs used to treat inflammation, such as 5-aminosalicylates and steroids, may prevent the development of colorectal cancer. The major carcinogenic pathways that lead to sporadic colorectal cancer, namely chromosomal instability, microsatellite instability, and hypermethylation, also occur in colitis-associated colorectal cancers. Unlike normal colonic mucosa, however, inflamed colonic mucosa demonstrates abnormalities in these molecular pathways even before any histological evidence of dysplasia or cancer. Whereas the reasons for this are unknown, oxidative stress likely plays a role. Reactive oxygen and nitrogen species produced by inflammatory cells can interact with key genes involved in carcinogenic pathways such as p53, DNA mismatch repair genes, and even DNA base excision-repair genes. Other factors such as NF-kappaB and cyclooxygenases may also contribute. Administering agents that cause colitis in healthy rodents or genetically engineered cancer-prone mice accelerates the development of colorectal cancer. Mice genetically prone to inflammatory bowel disease also develop colorectal cancer especially in the presence of bacterial colonization. These observations offer compelling support for the role of inflammation in colon carcinogenesis.

Animals↗

PubMed2003

Mild hypothermia inhibits inflammation after experimental stroke and brain inflammation.

BACKGROUND AND PURPOSE: We previously showed that mild hypothermia protects against experimental stroke, even when cooling was delayed by 2 hours. Protection may be due in part to inhibiting inflammation. To clarify, we examined leukocyte infiltration, microglial activation, and adhesion molecule expression in models of stroke and pure brain inflammation. METHODS: Rats underwent 2-hour middle cerebral artery occlusion (MCAO; n=36) or intravenous injection with 5 mg/kg lipopolysaccharide (LPS; n=22). Temperature was lowered to 33 degrees C for 2 hours or kept at 37 degrees C. In MCAO, cooling was applied intraischemically or on reperfusion (delayed). In the LPS model, cooling began after injection. One and 3 days later, brains were assessed for neutrophils, monocytes/microglia, major histocompatibility complex class II antigen, and intercellular adhesion molecule-1 (ICAM-1). RESULTS: One day after MCAO, both intraischemic and delayed hypothermia decreased ICAM-1 (51% and 60%, respectively, versus normothermia; P<0.001), monocytes (63% and 57%; P<0.01), and microglia (55% and 53%; P<0.001). Similar decreases were seen at 3 days for ICAM-1 (91% and 93%; P<0.001), monocytes (62% and 54%; P<0.01), and microglia (55% and 53%; P<0.001). In the LPS model, ED-1-positive cells were not observed in the brain, but hypothermia decreased ICAM-1 (26%; P<0.05), OX6 (56%; P<0.01), and microglia (47%; P<0.01) at 1 day. CONCLUSIONS: Mild hypothermia decreases inflammatory responses in both brain inflammation and stroke, implicating a direct anti-inflammatory effect of cooling. This suggests that hypothermia can attenuate factors contributing to delayed ischemic injury.

Animals↗

PubMed1984

Quantitative assay for acute intestinal inflammation based on myeloperoxidase activity. Assessment of inflammation in rat and hamster models.

An assay was devised to quantitate acute intestinal inflammation based on the assessment of myeloperoxidase activity. Myeloperoxidase is an enzyme found in neutrophils and, in much smaller quantities, in monocytes and macrophages. Myeloperoxidase was solubilized with hexadecyltrimethylammonium bromide and myeloperoxidase activity was measured with a dianisidine-H2O2 assay. In neutrophil suspensions, myeloperoxidase activity was directly related to cell number down to as few as 500 cells. Myeloperoxidase activity was assayed in two animal models of inflammation: acetic acid-induced colitis in rats and Clostridium difficile enterotoxin-induced enteritis in hamsters. In both models, the activity of myeloperoxidase solubilized from the inflamed tissue was directly proportional to the number of neutrophils seen in histologic sections. Histologic evaluation of neutrophil accumulation was performed by counting the number of neutrophils in a histologic section 0.18 mm long and 5 micron thick. In both animal models, myeloperoxidase activity was linearly related to neutrophil number from 400 and 4000 cells/mm. Myeloperoxidase activity from chronically inflamed colon, in which both neutrophils and histiocytes were present, was directly related to neutrophil content. Histiocytes did not contribute significantly to myeloperoxidase activity. The determination of myeloperoxidase activity in the intestine is a simple biochemical assay that can be used to quantitate inflammation.

Acetates↗

PubMed1980

Effects of various pharmacologic agents on allergic inflammation of the eye. The roles of chemical mediators in ocular inflammation.

Effects of pharmacologic agents on experimental ocular inflammation induced by reverse passive Arthus reactions were investigated by a slit-lamp technique utilizing fluorescein-labeled rabbet serum albumin as an indicator. Cobra venom factor completely eliminated inflammatory responses, indicating that the complement system is a trigger for this type of ocular inflammation. Antihistamines mainly suppressed the early vascular response. Reserpine and indomethacin remarkably inhibited the increase of the permeability of the blood-aqueous barrier over the first 5 hr. Epinephrine and steroid hormone were also effective. Neither diethylcarbamazine nor isonicotinic acid showed effects on the permeability changes induced in this type of inflammation.

Animals↗

PubMed2002

Effects of eprosartan versus hydrochlorothiazide on markers of vascular oxidation and inflammation and blood pressure (renin-angiotensin system antagonists, oxidation, and inflammation).

Antagonists of the renin-angiotensin system, such as angiotensin type 1 (AT(1)) receptor inhibitors and angiotensin-converting enzyme inhibitors, are becoming increasingly popular agents in treating patients with systemic hypertension and minimizing organ damage. In the present study, we compared the effects of eprosartan, an AT(1) receptor inhibitor, with the diuretic hydrochlorothiazide in a group of newly diagnosed hypertensive patients with multiple risk factors for atherosclerosis. The subjects were monitored and tested at 0 and 4 weeks to determine their individual effects on vascular and inflammatory markers. Although blood pressure reduction was comparable between the 2 agents, there were notable differences in their effects on markers of inflammation and oxidation. We observed a 28% reduction in neutrophil superoxide anion generating capacity, a 34% reduction in soluble monocyte chemotactic protein-1, and a 35% reduction in soluble vascular cell adhesion molecule with eprosartan therapy (all p <0.05 from the start of therapy). In addition, eprosartan showed further benefit in its ability to increase low-density lipoprotein oxidation lag time, suggesting an increased resistance to oxidation and/or modification of low-density lipoprotein. Although hydrochlorothiazide was effective in blood pressure reduction, there were no significant changes in any of the above parameters after 4 weeks of treatment. These findings suggest that eprosartan, an AT(1) receptor inhibitor, effectively reduces systemic blood pressure and, compared with hydrochlorothiazide, suggests additional benefits in the vasculature by inhibiting mechanisms of inflammation and oxidation.

Acrylates↗

PubMed2002

Genomic scale profiling of autoimmune inflammation in the central nervous system: the nervous response to inflammation.

Using gene microarray technology, we found that inflammation in the central nervous system (CNS) not only induced the expression of many immune-related genes, but also significantly altered the gene expression profile of neural cells. Two unique groups of CNS genes were identified. The first group includes genes encoding ion channels, neural transmitters and growth factors. The second group includes genes that are important for nervous tissue regeneration. Additionally, a distinct pattern of gene expression was also identified in recovering animals. Thus, during autoimmune inflammation, the CNS actively responds to immune attacks by activating its own defense and repair genes.

Animals↗

PubMed2000

Role of neutrophils in induction of acute inflammation in T-cell-mediated immune dermatosis, psoriasis: a neutrophil-associated inflammation-boosting loop.

A growing body of evidence has indicated that T-cell-mediated immunity plays an important role in triggering and maintenance of psoriatic lesions. In this review we present our own experimental results as well as those from the literature related to the pathomechanism of the development of inflammatory changes in psoriatic lesions. First of all it is important to acknowledge the fact that psoriatic lesions are not uniform as assumed by many authors but that they are actually rather heterogeneous both clinically and histologically even within the same plaques. Lymphokines produced by activated T cells in psoriatic lesions have a strong influence on the proliferation of the epidermis, whose stimulated kertinocytes released several cytokines, which in turn enhance the activation state of T cells. Thus, they form a vicious cycle, a T-cell-mediated inflammation-sustaining loop. Although the interaction between T-cell-mediated immunity and epidermal keratinocytes may well explain the maintenance of background "chronic" inflammatory changes diffusely observed throughout psoriatic lesions, it is not enough to explain the island-like, "acute" inflammatory changes observed within and at the border of the plaque lesions. Characteristic neutrophil accumulation under the stratum corneum can be observed in the highly inflamed and therapeutically recalcitrant areas of psoriatic lesions. They are chemotactically attracted and activated there by synergistic action of chemokines, IL-8 and Gro-a released by the stimulated keratinocytes, and particularly C5a/C5a des arg produced via the alternative complement pathway activation possibly on the surface of corneocytes. In this review, we emphasize that the accumulation of neurophils is not simply a passive event. We think that those stimulated neutrophils are able to influence not only the growth and differentiation of epidermal keratinocytes but also the activation-state of T cells by aberrant expression of HLA-DR on their surfaces as well as by their effects. These T cells in turn influence the transepidermal neutrophil migration through the effect of their lymphokines on the keratinocyte production of pro-inflammatory mediators including C3. Therefore, we propose a neutrophil-associated inflammation-boosting loop that may well explain the localized "acute" inflammatory changes scattered over the "chronic" psoriatic plaques as well as in the acutely inflamed lesions of pustular psoriasis.

Acute Disease↗

PubMed2001

Mast cell regulation of inflammation and gene expression during antigen-induced bladder inflammation in mice.

Mast cell numbers are significantly increased in bladder disorders including malignancy and interstitial cystitis, but their precise role has been difficult to determine. We characterized the role of mast cells on gene regulation associated with antigen-induced bladder inflammation in mice. For this purpose, we examined the responses in mast cell-deficient (Kit(W)/Kit(W-v)), congenic normal (+/+), and Kit(W)/Kit(W-v) mice that were reconstituted with bone marrow stem cells (BMR) to restore mast cells. All mice were actively sensitized and challenged intravesically with either saline or specific antigen. Bladder inflammation occurred in +/+ and BMR but not the Kit(W)/Kit(W-v) mice. Gene expression was determined using mouse cDNA expression arrays. Self-organizing maps, performed without preconditions, indicated gene expression changes dependent on the presence of mast cells. These genes were upregulated in bladders isolated from antigen challenge of +/+, not altered in Kit(W)/Kit(W-v), and were upregulated in BMR mice. Taken together these results demonstrate an important role for mast cells in allergic cystitis and indicate that mast cells can alter their environment by regulating tissue gene expression.

2,4-Dinitrophenol↗