Plasma Concentrations Of Interleukin-1 Beta Research Articles

The Effect of a Prophylactic Dose of Ibuprofen on Plasma Level of Interleukin 1, Interleukin 6 and Tumor Necrosis Factor-Alpha in a 1500 m Running Practice

Problem statement: there are controversies about the effects of anti-inflammatory drugs on exercised induced changes on plasma cytokines in untrained male athletes, so the primary purpose of this study was to measure the influence of a prophylactic dose of ibuprofen use on plasma cytokines during a 1500 m running race. Approach: Subjects were 10 untrained male Medical University students who consumed 400 mg ibuprofen two hours before the 1500 m running practice and 10 controls that competed in the race but avoided ibuprofen and all other medications. Blood samples were collected before, 1h and 24 h following the 1500 m exercise bout to measure plasma concentrations of interleukin-1 beta (IL-1β ), interleukin-6(IL-6) and tumor necrosis factor alpha (TNF- α ). Results: There were not any significant differences between plasma concentration of IL-1β, IL-6 and TNF- α during the study period. Also the data showed that there were not any significant differences between plasma level of IL-1β, IL-6 and TNF- α in ibuprofen and control group during the study period. Conclusions/Recommendation: Our result showed that a prophylactic dose of ibuprofen did not affect acute inflammatory cytokines levels (IL-1β, IL-6 and TNF- α) in untrained healthy young males. So the etiology of the muscle soreness in athletes actively participating in sport races seems to be independent of inflammatory processes.

Serotoninergic and suprachiasmatic nucleus involvement in the corticotropic response to systemic endotoxin challenge in rats.

We have investigated whether the serotonin system participates in the mechanisms underlying the corticotropic response in experimentally infected rats. Intra-arterial injection of lipopolysaccharide (LPS; 25 microg/kg b.w.) resulted in a slight but significant increase in serotonin (5-HT) metabolism, detectable 60 min after the stimulus and lasting more than 480 min. Adrenocorticotropin (ACTH) and corticosterone (CORT) responses in intact rats conformed to earlier reports, increasing as early as 30 min after LPS injection and reaching maximal concentrations in the circulation 60 min after the bacterial endotoxin injection. Plasma concentrations of interleukin-1beta (IL-1beta) increased only after 60 min, reaching maximal levels 120 min after LPS. Depletion of hypothalamic 5-HT (-93%) by pretreatment of the animals with para-chlorophenylalanine (p-CPA), resulted in a halved ACTH response to LPS, despite an overall unchanged secretory pattern. Neither CORT nor IL-1beta secretory patterns were affected in these rats pretreated with p-CPA. Complete bilateral electrochemical lesions of the suprachiasmatic nucleus (SCN), which is innervated by mesencephalic 5-HT, impaired the early phase of the ACTH (-75% at 30 min) and CORT (-40% at 30 min) responses but did not affect the later increases of the corticotropic and the plasma IL-1beta responses following the LPS injection. These results indicate that serotonin pathways and SCN are involved in the earlier mechanisms of corticotropic axis recruitment following systemic LPS endotoxemia.

Effect of acetate, bicarbonate dialysis, and acetate-free biofiltration on nitric oxide synthesis: Implications for dialysis hypotension

The effect of acetate dialysis (AD), bicarbonate dialysis (BD), and acetate-free biofiltration (AFB) on nitric oxide (NO) synthesis and the implications for dialysis hypotension was studied. The finding that uremic plasma is a potent inducer of NO synthesis by endothelial cells in vitro suggested that the cardiovascular instability of dialysis patients might result from excessive NO formation. Cardiovascular instability is more frequent in patients undergoing AD than BD. To see whether these differences were attributable to NO, we studied the NO synthetic pathway ex vivo in patients undergoing different dialysis procedures. Five patients were treated, in a random order, with AD, BD, and AFB, a technique using a buffer-free dialysate and postdilution of a sterile bicarbonate solution. Each type of dialysis was used for 1 week, comprising three dialysis sessions. A polyacrylonitrile dialyzer was used for all three methods. Before and after the third dialysis, plasma was collected, added to [3H]L-arginine, and incubated with human umbilical vein endothelial cells (HUVECs) for 24 hours. NO synthesis was evaluated as [3H]L-citrulline formation. Plasma concentrations of interleukin-1beta (IL-1beta), a potent inducer of inducible NO synthase (iNOS) in endothelial cells, were also measured. Plasma collected from patients after AD stimulated endothelial NO synthesis more than plasma from the same patients before the dialysis session (pre-AD, 0.173+/- 0.028 nmol/10(5) cells v post-AD, 0.280+/-0.093 nmol/10(5) cells; P < 0.05). A slight, although not significant, increase was also observed when HUVECs were incubated with plasma drawn after BD (pre-BD, 0.151+/- 0.014 nmol/10(5) cells; post-BD, 0.230+/-0.055 nmol/10(5) cells). AFB did not aggravate the stimulatory effect of uremic plasma on endothelial NO synthesis (pre-AFB, 0.184+/-0.038 nmol/10(5) cells; post- AFB, 0.189+/-0.040 nmol/10(5) cells). Plasma IL-1beta was greater (P < 0.01) after AD than after BD and AFB (post-AD, 0.234+/-0.028 pg/mL; post-BD, 0.124+/-0.019 pg/mL; post-AFB, 0.120+/-0.013 pg/mL). With AD, there was a greater intradialytic decrease in systolic blood pressure than with BD or AFB. Weight and blood volume loss and sodium balance were similar in AD, BD, and AFB. These data were consistent with the possibility that NO and cytokines, released in excessive amounts during AD, may contribute to hemodynamic instability. (Am J Kidney Dis 1998 Jul;32(1):115-24)

Blood levels of cytokines in elderly patients with major depressive disorder.

Plasma concentrations of interleukin-1beta (IL-1beta), interleukin-6 (IL-6) and tumour necrosis factor alpha (TNFalpha) were measured in 10 elderly women with major depressive disorder (MDD) and in two groups of controls, one consisting of 10 age-matched healthy female volunteers and one consisting of 10 young healthy female volunteers. The cytokine concentrations were measured in MDD patients before and after 30 days of treatment with phosphatidylserine (BC-PS), 600 mg daily p.o. The plasma IL-Ibeta, IL-6 and TNFalpha concentrations did not differ significantly in young controls, elderly controls and MDD patients. BC-PS therapy, while significantly improving the depressive symptoms, did not alter the cytokine concentrations.

Respuesta inflamatoria en el infarto agudo de miocardio. Valores predictivos

Our purpose was to investigate the significance of inflammatory acute phase response early after myocardial infarction. We also observed how these indices were influenced by trombolytic therapy. We examined the blood samples of 200 non consecutive patients at the first day of acute myocardial infarction (155 [77%] males; mean age 65 +/- 13 years) to characterize the proteins and proinflamatory reactants profile. Results were correlated with hospital mortality. Thrombolytic therapy was administrated to 117 patients on admission and in these patients the samples were taken after the procedure. Overall mortality was 8%. Serum C-reactive protein (69 vs 41 mg/l), haptoglobine (237 vs 190 mg/dl), gammaglobuline (0.93 vs 0.84 g/dl), alpha-1-globuline (0.28 vs 0.23 g/dl) and alpha-2-globuline (0.7 vs 0.6 g/dl) were significantly higher in patients without trombolytic therapy. Conversely, patients who had received lytic therapy, had higher plasma concentrations of interleukin-1 beta (104 vs 40 pg/dl). The only clinical variable which was associated with mortality was a Killip class > or = 2 on admission (mortality = 21%; odds ratio = 5.2; p = 0.02). Other biochemical variables associated with a higher mortality were a white blood cell count > 10/nl (mortality = 12%; odds ratio = 5.4; p = 0.01), increased activated neutrophils > 80% (mortality = 18%; odds ratio = 5.4; p = 0.004) and C-reactive protein > 20 mg/l (mortality = 11%; odds ratio = 6; p = 0.05). Only patients with activated neutrophils > 80% on admission had a higher probability of dying during hospital stay (Exp[B] = 3.6; B = 1.2; r = 0.29; p = 0.001). The acute phase reaction in early myocardial infarction is determined by thrombolytic treatment. A high increase of activated neutrophils on patient admission is the only biochemical predictive value for hospital mortality.

Plasma-soluble interleukin-2 and transferrin receptor in schizophrenia and major depression.

This study was carried out to examine some components of in vivo immune function in major depression and schizophrenia. Toward this end, plasma concentrations of interleukin-1 beta (IL-1 beta) and IL-6, soluble IL-2 receptor (sIL-2R), and transferrin receptor (TfR) were measured in 28 normal controls, 11 schizophrenics and 13 major-depressed patients. Schizophrenic and major-depressed patients showed significantly higher plasma sIL-2R and TfR than normal controls. There was a trend toward higher plasma IL-6 in the psychiatric patients, and particularly in schizophrenic patients, than in normal volunteers. In normal controls and in the total study group, there were highly significant and positive correlations between plasma TfR and sIL-2R concentrations. It is suggested that schizophrenia and major depression are characterized by immune disorders that may indicate activation of cell-mediated immunity such as T-cell activation.

Cytokine plasma levels and lymphocyte subsets in patients with newly diagnosed insulin-dependent (type 1) diabetes mellitus before and following initial insulin treatment.

Changes in the plasma concentrations of interleukin-1 beta (IL-1 beta), tumour necrosis factor alpha (TNF alpha), interleukin 2 (IL-2), and lymphocyte subsets were investigated in 19 persons with newly diagnosed (type 1) insulin-dependent diabetes mellitus (IDDM) from admission to hospital prior to insulin treatment and following 1 week and 1 month of treatment. Furthermore, the cytokines were measured 16-28 months after the presentation of IDDM. The mean TNF alpha values were all within the normal range, but demonstrated a slight increase in all the samples taken (Friedman 0.06). The mean plasma IL-1 beta value was initially at the upper normal limit, but gradually increased significantly from admission to hospital to 1 week, 1 month, and 16-28 months afterwards (Friedman 0.031). No IL-2 activity was detectable in the majority of the samples. No significant changes in total leukocyte and lymphocyte counts were found. The lymphocyte subsets (CD5+, CD8+, CD4+, CD16+, CD20+, HLA-DR+) did not show any significant changes from admission to after the start of insulin treatment. It is concluded that the gradual increase in IL-1 beta and TNF alpha plasma levels may reflect an ongoing autoimmune inflammatory reaction at the onset of IDDM.

Nocturnal plasma levels of cytokines in healthy men.

Nocturnal cytokine levels were measured serially in 12 healthy male volunteers for 12 h, including 8 h of polygraphically monitored nocturnal sleep. Plasma concentrations of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were determined in 30-min intervals by enzyme-linked immunoadsorbent assays. In some subjects cytokines were not detectable at all. In the remaining volunteers (27% for IL-1 beta, 58% for IL-6 and TNF-alpha, respectively) occasional values near to the detection limits (DL) of the assays could be measured. With respect to IL-1 beta and IL-6, plasma levels above the DL were significantly more frequent during sleep than during the preceding time of wakefulness. No temporal association with NREM or REM episodes could be shown. TNF-alpha values above the DL were randomly distributed across the 12-h period investigated. It is concluded that in a considerable percentage of healthy subjects small amounts of cytokines are released at night. Release of IL-1 beta and IL-6 is temporally associated with sleep, whereas the release of TNF-alpha is not. It remains to be established whether nocturnal cytokine release reflects either an interaction between sleep and host defense mechanisms or a sleep-independent circadian rhythmicity.