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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various cytokines were recently found to be involved in the pathogenesis of rheumatoid arthritis (RA) and particularly, cytokines with hematopoietic activity have been detected in synovial tissues. We counted the number of myeloid precursors in terms of granulocyte/macrophage colony forming units (CFU-GM) and the number of stromal cell progenitors in terms of fibroblast colony forming units (CFU-F) in the tibial bone marrow adjacent to the joints affected by RA (n = 21), osteoarthritis (OA) (n = 10), and trauma (n = 2) using the colony formation unit assay. We also quantitated the amounts of interleukin 1 beta (IL-1 beta), IL-6, and granulocyte/macrophage colony stimulating factor (GM-CSF) in the culture supernatant of synovial tissue explants of these patients by enzyme linked immunosorbent assay (ELISA). The mean number (+/- SEM) of CFU-GM in patients with RA (7.4 +/- 4.9) was greater than that in patients with OA (0.5 +/- 0.2), while CFU-GM was not detected in trauma patients. The number of CFU-GM in the tibial bone marrow of patients with RA correlated well with the amount of IL-1 beta (r = 0.64, p < 0.01), but not with GM-CSF or with IL-6 from synovial tissues. These findings suggest that active bone marrow is present adjacent to the affected joints in patients with RA and that hematopoietic activity is influenced by IL-1 beta produced in nearby synovial tissues.
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PMID:Detection of myeloid precursors (granulocyte/macrophage colony forming units) in the bone marrow adjacent to rheumatoid arthritis joints. 146 60

New Zealand rabbits were chronically incannulated in the lateral ventricle and cisterna magna to assess the hypothesis that calcium concentration (Ca) of cerebrospinal fluid (CSF) varies during fevers of diverse origin. In normothermic and febrile animals recovering from surgery, CSF Ca was positively and significantly correlated to rectal temperature (TR). IV injection of E. coli endotoxin and ICV injection of human recombinant interleukin 1 beta (hrIL-1 beta) induced a TR rise of 1.7 +/- 0.3 degrees C (mean +/- SEM) and 1.45 +/- 0.25 degrees C, respectively, accompanied by significant increases in CSF Ca. After endotoxin administration, maximal Ca increases ranged between 0.21 and 0.48 mM above basal values in individual animals (p < 0.01), whereas after administration of hrIL-1 beta increases were 0.17 and 0.25 mM (p < 0.05). Acetylsalicylic acid (ASA) countered the fever induced by both endotoxin and hrIL-1 beta administrations and concomitantly antagonized the Ca increase in CSF. HrIL-1 beta-derived nonapeptide was characteristically devoid of pyrogenic effect and did not modify CSF Ca. Although ICV injection of prostaglandin E2 (PGE2) increased TR by 2.1 +/- 0.77 degrees C, it failed to have any effect on CSF Ca. Differently from the other Ca enhancers, PGE2, however, increased CSF protein concentration (protein). These findings suggest that brain calcium metabolism plays a role in fever development and that prostaglandin involvement is only engaged once changes in CSF calcium concentration have taken place.
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PMID:Calcium changes in rabbit CSF during endotoxin, IL-1 beta, and PGE2 fever. 147 10

Juvenile chronic myelogenous leukemia (JCML) is a rare pediatric malignancy characterized by marked hepatosplenomegaly, leukocytosis with prominent monocytosis, elevated fetal hemoglobin, no Philadelphia chromosome, and generally a poor prognosis. In vitro, JCML peripheral blood granulocyte-macrophage progenitors (granulocyte-macrophage colony-forming units, CFU-GM) demonstrate the unique characteristic of "spontaneous" proliferation at very low cell densities in the absence of exogenous growth factors. The "spontaneous" CFU-GM proliferation can be abolished by prior adherent cell (monocyte) depletion, suggesting a paracrine mode of cellular proliferation. Although previous studies using a [3H]thymidine ([3H]TdR) incorporation assay suggested an important role for granulocyte-macrophage colony-stimulating factor (GM-CSF) in JCML, many non-growth factor-related reasons for [3H]TdR incorporation and the relatively low level of inhibition of [3H]TdR uptake left those conclusions open to question. Therefore, we performed clonal CFU-GM assays, which more specifically reflect cytokine effects on CFU-GM, using JCML peripheral blood mononuclear cells (PBMNC) and neutralizing antibodies against GM-CSF, granulocyte colony-stimulating factor (G-CSF), macrophage colony-stimulating (M-CSF), interleukin 3 (IL-3), interleukin 1 alpha (IL-1 alpha), interleukin 1 beta (IL-1 beta), interleukin 4 (IL-4), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF alpha), and interferon gamma (IFN gamma). Cultures containing anti-GM-CSF alone inhibited "spontaneous" JCML CFU-GM by 87% +/- 9% (mean +/- standard error of the mean [SEM]). No other anti-cytokine antibody produced a significant inhibition of CFU-GM growth. Various combinations of antibodies, excluding anti-GM-CSF, failed to demonstrate any synergistic inhibitory effects upon CFU-GM. Because this apparent paracrine cellular stimulation could be due to excessive cytokine production, by monocytes or other accessory cells, we examined cytokine levels in conditioned media from various JCML cell populations using enzyme-linked immunosorbent assays (ELISAs). Monocytes from only a minority of JCML patients produced higher than normal quantities of GM-CSF, G-CSF, IL-1 beta, IL-6, and/or TNF alpha, but no obvious pattern could be discerned. Further, only 7 of 15 JCML monocyte-conditioned media (MCM) had elevated GM-CSF, and 6 of 15 JCML patients had normal levels of all nine cytokines tested. The monocyte depletion experiments and the inhibition experiments with anti-cytokine antibodies taken together demonstrate clearly that the "spontaneous" growth of JCML CFU-GM in vitro critically depends on at least one monocyte-derived growth factor, GM-CSF.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of monocyte-derived hemopoietic growth factors in the regulation of myeloproliferation in juvenile chronic myelogenous leukemia. 191 2

Prostaglandins (PGs), interleukin 1 beta (IL-1 beta), and tumor necrosis factor alpha (TNF alpha) are likely mediators of local inflammatory reactions. We measured PGE2, PGI2, IL-1 beta, and TNF concentrations in paired cerebrospinal fluid (CSF) samples (on admission, CSF1, and 18 to 30 hours later, CSF2) from 80 infants and children with bacterial meningitis. Forty patients received dexamethasone sodium (0.6 mg/kg per day in four intravenous doses) and 40 received an intravenous saline placebo. In CSF1, PGE2, PGI2, IL-1 beta, and TNF were detected in 90%, 56%, 98%, and 71% of specimens with mean (+/- SEM) concentrations of 462 +/- 65, 377 +/- 62, 1266 +/- 242, and 799 +/- 227 pg/mL, respectively. Concentrations of PGE2 correlated significantly with PGI2, IL-1 beta, TNF, and lactate and inversely correlated with glucose concentrations in the first CSF specimens. The PGE2, PGI2, IL-1 beta, and TNF were still detected in 40%, 18%, 97%, and 60%, respectively, of second CSF specimens obtained from placebo-treated patients. Compared with patients who had detectable PGI2 or TNF alpha concentrations in CSF2 specimens, those placebo-treated patients with no detectable PGI2 or TNF alpha activity in CSF2 had a lower incidence of neurological sequelae. Dexamethasone-treated patients had significantly lower PGE2, IL-1 beta, and lactate concentrations and higher glucose concentrations in CSF 18 to 30 hours later, shorter duration of fever, and a lower incidence of neurological sequelae than did placebo-treated patients.
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PMID:Cerebrospinal fluid prostaglandins, interleukin 1 beta, and tumor necrosis factor in bacterial meningitis. Clinical and laboratory correlations in placebo-treated and dexamethasone-treated patients. 211 86

Tumor necrosis factor-alpha and interleukin 1 beta have been shown to be mediators of meningeal inflammation in animal models of bacterial meningitis. The presence of both cytokines in cerebrospinal fluid (CSF) of patients with bacterial meningitis has been documented recently. In this study, we measured concentrations of interleukin 1 beta and tumor necrosis factor-alpha in CSF samples from 36 patients with nonbacterial (aseptic) meningitis, 13 of whom had culture-proved enteroviral meningitis, and from 14 control patients. None of the samples from patients with aseptic meningitis and from the controls had detectable tumor necrosis factor activity in CSF. Thirty-two (89%) of 36 patients with aseptic meningitis had detectable interleukin 1 beta in CSF (mean +/- SEM, 48 +/- 11 pg/mL). These concentrations were significantly smaller than those previously reported in patients with bacterial meningitis (944 +/- 128 pg/mL). Only 2 of the 14 control patients had detectable CSF interleukin 1 beta concentrations of 21 and 42 pg/mL. A significant correlation was evident between interleukin-1 beta concentrations and white blood cell counts in the CSF of patients with aseptic meningitis. Our data suggest that the initial events of CSF inflammation in children with aseptic meningitis are different than those in patients with bacterial meningitis, and the participation of these two cytokines, especially tumor necrosis factor-alpha, is less critical to the process.
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PMID:Detection of interleukin 1 beta but not tumor necrosis factor-alpha in cerebrospinal fluid of children with aseptic meningitis. 230 44

Previous investigations have demonstrated a decrease of the number of beta 2-adrenergic receptors (beta 2R) on peripheral blood mononuclear cells (PBMC) in patients with rheumatic diseases that correlated with the systemic inflammatory activity. However, the main factor(s) modulating the beta 2R on lymphocytes in inflammatory diseases are still unidentified. The present study aimed at evaluating the influence of interleukin 1 beta (IL-1 beta) and interleukin 2 (IL-2) on the number and on the dissociation constant (KD) of beta 2R on PBMC in vitro. PBMC from healthy volunteers were incubated with different concentrations of IL-1 beta (10-100 U/ml) or IL-2 (10-50 U/ml) for 1,6,12,24 and 72 hours (h), respectively. Cultures with medium alone served as controls. beta 2R were determined using a radioligand binding assay with 125Iodo-cyanopindolol. The results showed a significant spontaneous decline of beta 2R after 72 h (mean +/- SEM = 2674 +/- 392 binding sites/cell (bs/c) vs. 1131 +/- 149 bs/c P < 0.02). IL-2 at a concentration of 50 U/ml diminished this spontaneous reduction of beta 2R numbers significantly (control: 1439 +/- 139 bs/c vs. IL-2: 1724 +/- 107 bs/c, P < 0.05). However, beta 2R densities did not hold baseline levels and were still significantly lower as compared to preculture values. Incubation with 100 U/ml IL-1 beta for 6 h induced a significant increase of beta 2R densities (control: 1760 +/- 214 bs/c vs. IL-1: 2233 +/- 424 bs/c, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of cytokines on the density of beta 2-adrenergic receptors on peripheral blood mononuclear cells in vitro. 764 Mar 46

To investigate the effect of surgical trauma and other factors on the postoperative elevation of serum interleukin 6 (IL-6), we examined changes in IL-6 concentration after major thoracoabdominal surgery. Serum IL-6 levels reached the maximum concentration on the first postoperative day in all 38 patients, with peak ranging from 1400.8 +/- 383.4 pg/ml (mean +/- SEM) to 29.8 +/- 3.8 among six groups who underwent surgery at different sites. The IL-6 peak was significantly correlated with surgical trauma as defined by the operation length and the volume of blood loss during surgery (r = 0.554, P < 0.01 and r = 0.427, P < 0.01, respectively). The peak concentration of serum IL-6 in patients undergoing esophagectomy was significantly higher than in those undergoing pancreaticoduodenectomy (P < 0.05), despite a similar degree of surgical trauma defined by the operation length and volume of blood loss during surgery. Peak IL-6 concentration observed in a patient who underwent esophagectomy was about 100-fold greater in fluid drained from the thorax than in the peripheral blood. IL-6 mRNA was demonstrated in leukocytes from thoracic and abdominal exudate at 6, 24 and 48 h after surgery. In contrast, IL-6 mRNA could not be detected in leukocytes from the peripheral blood. Similar findings were also observed for interleukin 8 (IL-8). However, interleukin 1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) were detected only once after surgery in the drainage fluid.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevation of circulating interleukin 6 after surgery: factors influencing the serum level. 803 1

In vitro islet exposure to interleukin 1 beta inhibits the beta-cell response to glucose. We have studied whether a similar inhibition also occurs in response to the sulphonylurea glyburide. Rat pancreatic islets were cultured for 24 h in the presence or absence of 50 U/ml interleukin 1 beta and then stimulated with either glucose or glyburide for 1 h at 37 degrees C. In control islets basal insulin secretion was 117 +/- 32 pg.islet-1.h-1 (mean +/- SEM, n = 7) and greatly increased in response to 16.7 mmol/l glucose (2140 +/- 293) or 10 mumol/l glyburide (1464 +/- 234). When islets were pre-exposed to interleukin 1 beta, insulin release was significantly reduced in response to glucose (323 +/- 80, p < 0.001) but not in response to glyburide (1316 +/- 185). Since both glucose and glyburide influence beta-cell K+ and Ca2+ efflux, to further investigate this different response in islets exposed to interleukin 1 beta we measured both Rb+ efflux (as index of the ATP-sensitive K+ channel activity) and Ca2+ uptake. In control islets, the increased insulin secretion in response to 16.7 mmol/l glucose or 10 mumol/l glyburide was associated with a reduction of 86Rb efflux (decrement of -50 +/- 1.2% and -49 +/- 2.3%, respectively, mean +/- SEM, n = 5). In contrast, in interleukin 1 beta pre-exposed islets both glucose and glyburide stimulation only slightly modified 86Rb efflux (decrement of -19 +/- 1.9% and -5.3 +/- 3.1%, respectively, n = 5, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Different effects of glucose and glyburide on insulin secretion in rat pancreatic islets pre-exposed to interleukin-1 beta. Possible involvement of K+ and Ca2+ channels. 840 48

During adult cardiac surgery the plasma pro-inflammatory cytokine response is balanced by a phased anti-inflammatory cytokine response. Whether a similar balanced plasma pro- and anti-inflammatory cytokine response occurred in paediatric cardiac surgery was investigated. Changes in intra-pulmonary cytokine balance by measuring bronchoalveolar lavage (BAL) cytokine content were also estimated. Plasma and BAL samples were obtained from 10 children (aged 15 months to 10 years) 10 min after induction of anaesthesia (sample 0), 5 min after the onset of cardiopulmonary bypass (CPB) (sample 1), 10 min after release of the aortic cross clamp (sample 2), and 2 and 24 h after the end of CPB (samples 3 and 4). BAL and plasma was assayed for interleukin 1 beta (IL-1 beta), tumour necrosis factor alpha (TNF-alpha), IL-8, IL-10, interleukin 1 receptor antagonist (IL-1ra) and the TNF soluble receptors (TNFsrs). There was a phased plasma anti-inflammatory response commencing with IL-10 (sample 2), and followed by significant increases in IL-1ra (samples 3, 4 and 5) and TNF soluble receptors (sample 5). Plasma TNF-alpha and IL-1 beta concentrations were not significantly elevated from baseline. Mean baseline plasma IL-8 was 30 (SEM 9) pg/ml. This was significantly elevated at sample 4 (112 (SEM 68) pg/ml). In BAL, only IL-8 and IL-10 were significantly elevated after CPB as compared with baseline. During paediatric cardiac surgery there is a significant increase in plasma and BAL IL-8. This is balanced within the plasma by a phased anti-inflammatory cytokine response, and within the lung by IL-10.
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PMID:The balance of pro and anti-inflammatory cytokines in plasma and bronchoalveolar lavage (BAL) at paediatric cardiac surgery. 893 84

Our objective was to investigate the initial levels of circulating proinflammatory cytokines, such as interleukin 1 beta (IL-1 beta), interleukin 6 (IL-6), and tumour necrosis factor alpha (TNF-alpha), of certain acute-phase proteins, such as C-reactive protein (CRP), fibrinogen (FBN) and albumin, and of the glycoprotein fibronectin at presentation and their daily variation during the clinical course of community-acquired pneumonia (CAP) in relation to clinical and laboratory indices of infection. Thirty otherwise healthy hospitalized patients aged 48 +/- 3 years (mean +/- SEM) and with bacteriologically confirmed CAP were studied prospectively. IL-1 beta and IL-6 were found to be 15-fold higher on admission (122 +/- 9 pg mL-1 and 60 +/- 4 pg mL-1 respectively), whereas TNF-alpha was three-fold higher (102 +/- 5 pg mL-1) than those of controls, all of them showing a decline towards normal. Initial CRP levels were increased 90-fold (416 +/- 1 mg L-1), whereas fibronectin levels were reduced (242 +/- 9 mg dL-1). The presence of parapneumonic effusion was associated with a higher TNF-alpha serum level (127 +/- 7 vs. 86 +/- 4 pg mL-1, P = 0.0002), a more rapid daily decline in TNF-alpha (-7.2 +/- 0.7 vs. -3.8 +/- 0.5 pg mL-1 day-1, P = 0.0005), a slower rate of decline in CRP (-42.8 +/- 3.0 vs. -54.6 +/- 3.0 mg L-1 day-1, P = 0.02) and a slower rate of increase in FBN (5.9 +/- 1.0 vs. 11.7 +/- 1.0 mg dL-1 day-1), P = 0.001]. Furthermore, daily progression of serum levels of cytokines and acute-phase proteins correlated strongly with pyrexia, erythrocyte sedimentation rate (ESR), neutrophil count, alveolar-arterial oxygen difference and radiographic resolution, clinically manifested by improvement in the patients' condition.
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PMID:Daily variation in circulating cytokines and acute-phase proteins correlates with clinical and laboratory indices in community-acquired pneumonia. 913 79


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