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PubMed2002

Interleukin-2 levels are elevated in the bone marrow serum of patients with mutilans-type rheumatoid arthritis.

In order to investigate the pathogenesis of mutilans-type rheumatoid arthritis (RA), we measured cytokine levels in the bone marrow serum of patients with RA. We studied 35 patients with non-mutilans RA, 19 with mutilans RA, and 20 patients with osteoarthritis (OA) undergoing joint surgery. At the time of surgery, iliac bone marrow and peripheral blood were sampled from all 74 patients and cytokine levels measured. The serum levels of five cytokines (IL-1beta, IL-2, IL-3, IL-6 and GM-CSF) were measured by ELISA. Haematologic and inflammatory factors were also measured. Levels of IL-2, IL-6 and GM-CSF in bone marrow serum were significantly higher in all RA patients than in those with OA. Mean (+/-SD) IL-2 levels were significantly higher in patients with mutilans-type RA (309.8+/-686.3 pg/ml) than in patients with other types of RA (66.5+/-173.1 pg/ml; P<0.01). IL-2 was detected significantly more often in patients with mutilans-type RA than in patients with other types of RA (P < 0.01). Inflammatory factors were higher in all RA groups than in OA patients. However, the haematologic and immunologic variables were no different between mutilans RA and other types of RA. No correlations were observed between IL-1beta, IL-2, IL-3, IL-6 and GM-CSF levels and these laboratory variables. In patients with mutilans-type RA, IL-2 levels in the bone marrow serum were significantly higher than in patients with other types of RA or with OA. This elevation does not appear to be related to systemic inflammation, as there was no correlation with other inflammatory factors.

Aged↗
PubMed1990

Perinatal risk factors for inflammatory bowel disease: a case-control study.

To examine perinatal risk factors for Crohn's disease and ulcerative colitis, the authors analyzed birth records for 257 known case participants delivered from 1924 through 1957 at the University Hospital in Uppsala County, Sweden, and compared them with records for 514 controls delivered at the hospital. The two groups were matched by date of birth, sex, and either maternal age or parity. Eleven study variables were abstracted from standard forms that recorded health events during the pregnancy and the delivery hospitalization. Participants were more likely than controls to have a recorded health event (odds ratio (OR) = 4.4; 95% confidence interval (CI) 3.0-6.4). In a multivariate model, this increased risk was evident for infectious (OR = 3.8; 95% CI 2.6-5.8) and noninfectious (OR = 3.5; 95% CI 2.0-6.3) events. Perinatal health events may have contributed to 40% of the inflammatory bowel disease cases in our study. Infants from families with low socioeconomic status had greater risk of inflammatory bowel disease than did infants from families with high socioeconomic status (OR = 3.0, 95% CI 1.5-6.1). Perinatal health events and low socioeconomic status independently increased the risk of inflammatory bowel disease.

Analysis of Variance↗
PubMed1994

Ultrastructural studies of the blood-retina barrier after exposure to interleukin-1 beta or tumor necrosis factor-alpha.

BACKGROUND: During inflammatory conditions of the central nervous system (CNS), the protective function of the blood-brain barrier (BBB) may be compromised, resulting in CNS edema. However, it is not well understood how inflammatory cells may increase BBB permeability, since increased transendothelial transport of serum proteins is observed in CNS capillaries that are not directly in contact with inflammatory cells. One possible explanation may be that soluble inflammatory factors may cause BBB changes, since pathologic conditions that increase circulating cytokines produce detectable increases in BBB permeability. EXPERIMENTAL DESIGN: To investigate the role of inflammatory cytokines in induction of endothelial cell changes and inflammation in the CNS, we utilized the rabbit retinal system as a model. This system shows vascularization similar to the BBB, and is termed the blood-retina barrier (BRB). The rabbit visual system allows injection of cytokines, causing minimal trauma, and the contralateral eye serves as an intra-animal control. RESULTS: Ultrastructural morphometric analysis of vesicular content in BRB endothelium showed significant increase at 3 hours postintravitreal injection of interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF-alpha). Increased transport did not correlate with increased vitreal protein. However, intravascular tracer (horseradish peroxidase) revealed that pericytes, Müller cells, and perivascular microglia accumulate serum proteins, thus acting as sinks for extravasated proteins after BRB disruption. The IL-1 beta-induced inflammatory response was characterized by polymorphonuclear and mononuclear cells, whereas the TNF-alpha-induced response was less intense and comprised monocytes and occasional eosinophils. At the height of inflammation, IL-1 beta produced large gaps between endothelial cells that allowed for extensive cellular inflammation and hemorrhage. TNF-alpha induced necrotic changes on endothelial cells, being most severe at 3 hours postintravitreal injection, revascularization was noted at 24 hours postintravitreal injection. CONCLUSIONS: These results demonstrate that proinflammatory effects of IL-1 beta and TNF-alpha in the BRB initiate many of the changes associated with inflammation of the CNS vasculature, such as those induced during experimental autoimmune encephalitis and multiple sclerosis. Once the permeability of the BRB endothelium is increased, perivascular phagocytic cells such as perivascular, microglia and Müller cells may act as secondary barriers to extravasated proteins.

Animals↗
PubMed2000

Distinct roles for the NF-kappaB1 (p50) and c-Rel transcription factors in inflammatory arthritis.

Rheumatoid arthritis (RA) is a complex disease, with contributions from systemic autoimmunity and local inflammation. Persistent synovial joint inflammation and invasive synovial pannus tissue lead to joint destruction. RA is characterized by the production of inflammatory mediators, many of which are regulated by the Rel/NF-kappaB transcription factors. Although an attractive target for therapeutic intervention in inflammatory diseases, Rel/NF-kappaB is involved in normal physiology, thus global inhibition could be harmful. An alternate approach is to identify and target the Rel/NF-kappaB subunits critical for components of disease. To assess this, mice with null mutations in c-rel or nfkb1 were used to examine directly the roles of c-Rel and p50 in models of acute and chronic inflammatory arthritis. We found c-Rel-deficient mice were resistant to collagen-induced arthritis but had a normal response in an acute, destructive arthritis model (methylated BSA/IL-1 induced arthritis) suggesting c-Rel is required for systemic but not local joint disease. In contrast, p50-deficient mice were refractory to induction of both the chronic and acute arthritis models, showing this subunit is essential for local joint inflammation and destruction. Our data suggest Rel/NF-kappaB subunits play distinct roles in the pathogenesis of inflammatory arthritis and may provide a rationale for more specific therapeutic blockade of Rel/NF-kappaB in RA.

Acute Disease↗
PubMed1987

Receptor antagonist of platelet activating factor inhibits inflammatory injury induced by in situ formation of immune complexes in renal glomeruli and in the skin.

Experiments were designed to test the effect of a receptor antagonist of platelet activating factor (PAF), SRI63072, on inflammatory injury induced by in situ formation of immune complexes in two vascular districts of the rat that have different structural and hemodynamic characteristics: unilateral glomerulonephritis induced by perfusion of the left kidney of preimmunized animals with cationic human IgG, and passive reversed Arthus reaction in the skin. Three days after perfusion the left kidneys of rats not treated with SRI63072 (group I) were greatly enlarged, and pale and severe exudative and proliferative lesions were present in glomeruli. Granular deposits of human IgG, rat IgG, and rat C3 were seen by immunofluorescence microscopy, and subepithelial electron-dense deposits were visualized by electron microscopy. The right kidneys were consistently normal. The animals were severely proteinuric and had increased levels of PAF in the circulation. In contrast, rats treated with SRI63072 (group II) and studied at the same interval of time developed only mild, focal glomerulonephritis in the perfused kidneys. By immunofluorescence microscopy the glomerular deposits of human IgG and rat IgG were similar in quantity and distribution to those observed in rats of group I. Despite the fact that SRI63072 did not influence the level or the activity of the rat serum complement system, the deposits of C3 were less abundant and more focal. As in animals of group I, electron-dense deposits were present at the epithelial side of the glomerular basement membrane. Proteinuria was slight, and levels of circulating PAF were not significantly increased. These effects cannot be ascribed to interference of SRI63072 with antigen "implantation," antibody binding, or local hemodynamic conditions, because the amounts of glomerular human and rat IgG were the same in treated and untreated rats; SRI63072 did not decrease the glomerular filtration rate; and SRI63072 prevented the increase in vascular permeability and the exudative lesions in passive Arthus reaction in the skin, a model less affected by hemodynamic changes than glomerulonephritis. The beneficial effect of SRI63072 indicates that PAF is an important mediator of the inflammatory process generated either in glomeruli or in the skin by in situ immune complex formation.

Animals↗
PubMed2005

Analysis of growth factors and inflammatory cytokines in exhaled breath condensate from asthmatic children.

BACKGROUND: Vascular endothelial growth factor (VEGF), AA isoform of platelet-derived growth factor (PDGF-AA), and epidermal growth factor (EGF) are involved in the pathogenesis of airway inflammation in asthma. These molecules are closely associated with cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin (IL)-4. This study investigates the relation between childhood asthma and levels of these mediators in exhaled breath condensate (EBC). METHODS: EBC was collected from asthmatic children and controls using a disposable collection kit, and the concentrations of VEGF, PDGF-AA, EGF, TNF-alpha and IL-4 in EBC were measured using sandwich enzyme immunoassays. Exhaled nitric oxide concentration was measured by a chemiluminescence analyzer. RESULTS: Thirty-five asthmatic patients aged between 7 and 18 years and 11 controls were recruited. Sixteen patients had intermittent asthma (IA) whereas 19 of them suffered from persistent asthma (PA). A significant correlation was found between IL-4 and TNF-alpha in EBC (rho = 0.374, p = 0.010). PDGF-AA levels in EBC were higher in subjects with diminished FEV1 (p = 0.023) whereas IL-4 concentrations were increased in asthmatics (p = 0.007) as well as subjects with increased plasma total IgE (p = 0.033). Patients with PA receiving high-dose inhaled corticosteroid (ICS) had higher EBC IL-4 concentration than those on low-dose ICS (p = 0.007). Linear regression revealed that PDGF-AA levels in EBC were negatively associated with FEV1 percentage (beta = -0.459, p = 0.006) among the asthmatic patients. CONCLUSIONS: IL-4 in EBC is increased in childhood asthma, and growth factors are detectable in a significant proportion of these children. Increased PDGF-AA is found in asthmatics with more severe airflow limitation.

Adolescent↗
PubMed2005

Initial upregulation of growth factors and inflammatory mediators during nerve regeneration in the presence of cell adhesive peptide-incorporated collagen tubes.

Neurotrophic factors play an important modulatory role in axonal sprouting during nerve regeneration involving the proliferation of hematogenous and Schwann cells in damaged tissue. We have exposed lesioned sciatic nerves to a collagen prosthesis with covalently bonded small cell adhesive peptides Arg-Gly-Asp-Ser (RGDS), Lys-Arg-Asp-Ser (KRDS), and Gly-His-Lys (GHK) to study local production of growth factors and cytokines in the regenerating tissues. Western/enzyme-linked immunosorbent assay (ELISA) studies were performed after 10 days of regeneration, when the tubular prosthesis is filled with fibrous matrix infiltrated by hematogenous cells and proliferating Schwann cells with growth factors produced locally. Regeneration was also analyzed by morphometrical methods after 30 days. The quantification of growth factors and proteins by ELISA revealed that there was an enhanced expression of the neurotrophic factors nerve growth factor (NGF) and neurotrophins (NT-3 and NT-4) in the regenerating tissues. This was further established by Western blot to qualitatively analyze the presence of the antigens in the regenerating tissues. Schwann cells were localized in the regenerating tissues using antibodies against S-100 protein. Other growth factors including growth-associated protein 43 (GAP-43), apolipoprotein E (Apo E), and pro-inflammatory cytokine like interleukin-1alpha (IL-1alpha) expression in the peptide groups were evaluated by ELISA and confirmed by Western blotting. Cell adhesive integrins in the proliferating cells were localized using integrin-alpha V. The combined results suggest that the early phase of regeneration of peripheral nerves in the presence of peptide-incorporated collagen tubes results in the enhanced production of trophic factors by the recruited hematogenous cells and Schwann cells, which in turn help in the secretion of certain vital trophic and tropic factors essential for early regeneration. Furthermore, hematogenous cells recruited within the first 10 days of regeneration help in the production of inflammatory mediators like interleukins that in turn stimulate Schwann cells to produce NGF for axonal growth.

Absorbable Implants↗
PubMed2005

Risk factors for inflammatory bowel disease in the general population.

BACKGROUND: The aetiology of inflammatory bowel disease remains largely unknown. AIM: We performed a comprehensive assessment of potential risk factors associated with the occurrence of inflammatory bowel disease. METHODS: We identified a cohort of patients 20-84 years old between 1995 and 1997 registered in the General Practitioner Research Database in the UK. A total of 444 incident cases of IBD were ascertained and validated with the general practitioner. We performed a nested case-control analysis using all cases and a random sample of 10 000 frequency-matched controls. RESULTS: Incidence rates for ulcerative colitis, Crohn's disease, and indeterminate colitis were 11, 8, and 2 cases per 100 000 person-years, respectively. Among women, we found that long-term users of oral contraceptives were at increased risk of developing UC (OR: 2.35; 95% CI: 0.89-6.22) and CD (OR: 3.15; 95% CI: 1.24-7.99). Similarly, long-term users of HRT had an increased risk of CD (OR: 2.60; 95% CI: 1.04-6.49) but not UC. Current smokers experienced a reduced risk of UC along with an increased risk of CD. Prior appendectomy was associated with a decreased the risk of UC (OR: 0.37; 95% CI: 0.14-1.00). CONCLUSIONS: Our results support the hypothesis of an increased risk of inflammatory bowel disease associated with oral contraceptives use and suggest a similar effect of hormone replacement therapy on CD. We also confirmed the effects of smoking and appendectomy on inflammatory bowel disease.

Adult↗
PubMed2002

Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide inhibit CBP-NF-kappaB interaction in activated microglia.

The vasoactive intestinal peptide (VIP) and the pituitary adenylate cyclase-activating polypeptide (PACAP), two immunomodulatory neuropeptides, act as anti-inflammatory factors for activated microglia, by inhibiting the production of pro-inflammatory factors, mainly mediated through the inhibition of NF-kappaB nuclear translocation and DNA binding. An additional regulatory element in the NF-kappaB transcriptional activity is the coactivator CBP, which links p65 with components of the basal transcriptional machinery. The present report demonstrates that VIP and PACAP inhibit the formation of p65/CBP complexes and that this event is directly related to the neuropeptide inhibition of NF-kappaB transcriptional activity. Since CBP is in limiting amounts in the nucleus and is capable of interacting with several transcriptional factors, competition for CBP provides another mechanism for transcriptional regulation. VIP and PACAP increase CBP-binding to CREB, replacing p65/CBP with CREB/CBP complexes in activated microglia. This is due to VIP/PACAP-induced increases in CREB phosphorylation/activation and is mediated through the specific VPAC1 receptor and the cAMP/PKA pathway. The VIP/PACAP interference with the p65/CBP interaction in activated microglia may represent a significant element in the regulation of the inflammatory response in the CNS by the endogenous neuropeptides.

Active Transport, Cell Nucleus↗
PubMed1975

Effect of soluble plaque factors on inflammatory reactions in the dental pulp.

The present investigation was undertaken to determine whether soluble factors from human dental plaque are capable of inducing or mediating pathological alterations in the dental pulp. The experiment was performed in three monkeys and involved 40 teeth in all: 20 test and 20 control teeth. Class V cavities were prepared on the buccal surface close to the marginal gingiva. In the test cavities an extract of human dental plaque was applied once very 5 min during an 8-h period. The cavities of the contralateral teeth were treated in an identical manner but with Ringer's solution. The animals were sacrificed 10 or 32 h after the initiation of the test. Two hours prior to sacrifice the animals were injected with colloidal carbon and then perfused with 10% neutral buffered formalin. Histologic examination demonstrates that the pulp tissue response to topical application of a plaque extract was characterized by (1) increased degree of carbon retention - indicative of vascular exudation and (2) enhanced rate of emigration of neutrophils and monocytes.

Animals↗
PubMed1995

Perinatal and childhood risk factors for inflammatory bowel disease: a case-control study.

OBJECTIVE: To determine whether exposure to a measles epidemic in utero or in infancy is a risk factor for the development of Crohn's disease, and to determine whether such an association can be found in individuals with subacute sclerosing panencephalitis (SSPE), a condition in which early infection with measles is known to be of aetiological importance. METHODS: A postal questionnaire was sent to 16,875 members of two national inflammatory bowel disease patient support groups. A control group was composed of friends or neighbours. Birth data were compared with the dates of measles epidemics and six possible periods of susceptibility were examined. Birth data from a national register of patients with SSPE were analysed similarly. Previously identified risk factors were also examined. RESULTS: The answers from 2522 members and 2379 controls were analysed. We found no evidence of an association between the development of Crohn's disease and exposure to a measles epidemic. The birth dates of both groups were distributed normally throughout the year. No other early risk factor for the development of inflammatory bowel disease was detected. Exposure to a measles epidemic before the age of 1 year did not emerge as a risk factor for SSPE. CONCLUSION: These data contradict reports from a recent study in central Sweden, but relatively early exposure to measles in childhood may still be a risk factor for the development of Crohn's disease.

Adult↗
PubMed1999

[An alternative to conventional antibiotic therapy in respiratory infections--Bioparox Spray].

As the main target of influenza viral aggression, the respiratory tract is subject to easier bacterial infection superimposition. The researchers from Les Laboratoires Servier--France, managed to isolate a substance--fusafungine--from the microspore of the fungus Fusarium lateritium, which demonstrates unique anti-inflammatory and antibiotic action, and is the active ingredient of Bioparox Spray, an inhalant. The principal indications of Bioparox Spray for treatment of respiratory tract infections fall within the range from the sinuses to the finest alveolar duct, namely: rhinitis, sinusitis, tonsillitis, pharyngitis, laryngitis, tracheitis and bronchitis. In terms of technology Bioparox is unique due to the fact that 90% of the aerosol particles are less than one micron large, while generally the particles needed for penetration through the alveolar duct should be less than three microns. Due to such micronization, after inhalation Bioparox Spray reaches from the sinuses to the finest bronchial branches. Bioparox Spray possesses sound and broad antibiotic spectrum of action on the most common causative agents of respiratory infections, and more over, it acts upon Candida albicans, unlike the remaining broad-spectrum antibiotics. Bioparox Spray also has an independent anti-inflammatory effect by blocking the inflammation mediators: Bioparox Spray inhibits the synthesis of free radicals and the action of IL1 and TNF as pro-inflammatory factors, and it potentiates the action of IL2 and interferon-gamma which are anti-inflammatory factors. By its dual antibiotic and anti-inflammatory action Bioparox Spray is an excellent alternative to the conventional antibiotic therapy.

Aerosols↗
PubMed1996

Thrombotic vascular risk factors in inflammatory bowel disease.

BACKGROUND: Thrombosis may be an important effector mechanism in the pathogenesis of Crohn's disease. METHODS: This study therefore investigated the prevalence of independent thrombotic risk factors (factor VII coagulant activity, lipoprotein (a), fibrinogen, plasma triglycerides, and smoking) in patients with Crohn's disease, ulcerative colitis, and normal controls. RESULTS: In Crohn's disease (n = 75), the mean plasma VII:C, lipoprotein (a) and fibrinogen concentrations were significantly greater than in the normal population (n = 85). In ulcerative colitis (n = 35), only the mean factor VII:C concentration was significantly higher than normal. Ninety three per cent of patients with Crohn's disease and 86% of those with ulcerative colitis had at least one risk factor for thrombotic vascular disease, compared with 61% of the normal population (p < 0.001). CONCLUSIONS: In many young patients with inflammatory bowel disease, plasma concentrations of these prothrombotic factors were in excess of the limits that are regarded as posing an increased risk for the development of occlusive vascular disease.

Adult↗
PubMed1983

Putrescine--a potent endogenous anti-inflammatory substance in inflammatory exudates.

Sponge-induced exudate from the rat and saline extracts of normal rat liver and rat liver damaged in situ by dimethylnitrosamine have been assayed for putrescine, spermidine and spermine levels. The three physiological oligoamines have been examined for anti-inflammatory activity by the carrageenan-induced oedema rat model and spermidine and putrescine were found to be anti-inflammatory with putrescine being about ten times as active as spermidine. Putrescine was also anti-inflammatory in the adjuvant arthritic rat model. Thioacetamide and theophylline were also anti-inflammatory and theophylline doubled the level of putrescine in rat liver. It was concluded that putrescine was a potent anti-inflammatory factor in the inflammatory exudates and extracts examined.

Animals↗
PubMed1977

Emotional factors in inflammatory bowel disease.

Inflammatory bowel diseases are not caused by emotional conflicts, but emotional factors influence both the pathogenesis and the course of the illness. Establishing a trusting physician-patient relationship is important in helping the patient to (1) avoid denial of illness or chronic illness behavior, (2) understand symptoms and diagnostic and treatment procedures, and (3) cope with loss of a key person or the threat of lessened self-control.

Adolescent↗
PubMed2005

Interaction between tumor necrosis factor-alpha and leptin-induced inhibition of cardiac contractile function in isolated ventricular myocytes.

Pro-inflammatory factors such as the adipokine leptin and cytokine tumor necrosis factor-alpha (TNFalpha) have been implicated in the onset of myocardial dysfunction in ischemia-reperfusion injury, sepsis, heart failure, viral myocarditis and cardiac allograft rejection. Although circulating TNFalpha and leptin levels are both elevated under a variety of inflammatory conditions, it remains unknown whether TNFalpha and leptin depress cardiac contractile function independently or synergistically. We examined the effect of acute (30 min) and short-term (24h) exposure of TNFalpha, leptin or both on cardiac contractile function in adult rat ventricular myocytes. Contractile properties were evaluated using an Ionoptix Softedge system including peak shortening (PS), maximal velocity of shortening/relengthening (+/-L/t), time-to-PS (TPS) and time-to-90% relengthening (TR(90)). Both TNFalpha (0.5-500 pg/ml) and leptin (1-100 nm) exerted concentration-dependent inhibitions in PS and +/-L/t following a 30-min exposure. TNFalpha but not leptin prolonged TR(90). Interestingly, TNFalpha-induced depression of cell shortening was masked by leptin and vice versa. Following a 24-h incubation, both TNFalpha and leptin significantly inhibited PS and +/-L/t without affecting TPS and TR(90). There was no additive or synergistic response by the two pro-inflammatory factors. The nitric oxide synthase inhibitor l-NMMA abolished depression of myocyte shortening elicited by TNFalpha, leptin or both. In summary, this study demonstrated that the inhibitory effect on cardiac contraction by TNFalpha and leptin may mask each other and share a common mechanism(s), probably dependent on NO.

Animals↗
PubMed1996

Insulin-like growth factors and inflammatory bowel disease.

Hallmarks of IGF-I action include synergy with other hormones and growth factors and the ability to stimulate proliferation or differentiated cell function dependent on physiological or pathophysiologial context. A complete understanding of IGF action in IBD will require analyses of mechanisms of IGF interaction with other growth factors, hormones and cytokines. GH and IGF-I may be administered to children over prolonged periods to correct growth disorders. The definition of the benefits and problems of GH/IGF-I therapy in IBD needs to distinguish between long-term and short-term effects. Short-term administration of GH and IGF-I to animal models of IBD such as the PG-PS and TNBS models, which share features of Crohn's disease (Sartor, 1992), and a recently developed murine model of ulcerative colitis induced by ingestion of dextran sulphate (Okayasu et al, 1990; Sartor, 1992; Cooper et al, 1993) could address the beneficial or detrimental consequences of short-term GH/IGF-I therapy. Adaptation of the PG-PS, TNBS and dextran sulphate models of inflammation to available transgenic mouse lines that over-express GH and IGF-I (Behringer et al, 1990; Ulshen et al, 1993), especially if over-expression is inducible, could help to define the potential benefits and problems of long-term GH/IGF-I therapy or the effects of GH/IGF-I on immune cell function and cytokine production during intestinal inflammation. It will be useful to study intestinal inflammation and complication in animal models of GH or IGF-I deficiency. In this regard, mice with targeted ablation of the IGF-I gene could be useful (Liu et al, 1993) although neonatal mortality in these models currently poses problems for in vivo studies. Development of mesenchymal cell lines from such animals could, however, provide a useful in vitro system to study the role of IGF-I in altered cell function in response to pro-inflammatory cytokines.

Animals↗