Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Interleukins”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed2000

Correlation of metalloproteinase-2 and -9 with proinflammatory cytokines interleukin-1b, interleukin-12 and the interleukin-1 receptor antagonist in patients with chronic uveitis.

PURPOSE: Matrix metalloproteinases have been shown to play a role in active uveitis. Transcription of MMPs is induced by a number of growth factors and cytokines. This study investigates the role of MMPs in chronic uveitis and correlates the amounts of MMP-2 and -9 in intraocular samples to the intraocular levels of proinflammatory cytokines (Interleukin-1 [IL-1], Interleukin-12 [IL-12] and Interleukin-1 receptor antagonist [IL-1ra]). METHODS: Aqueous humor of 16 patients was collected during surgical or diagnostic procedures (control group: cataract patients). MMP-2 and -9 were measured using zymography. IL-1beta, IL-12 and IL-1ra were evaluated by ELISA. RESULTS: We found MMP-2 and -9 in all of our uveitis patients. In the control group only MMP-2 was seen. Higher levels of MMP-2 and -9 were found in patients with higher activity of uveitis (p < 0.014 for MMP-2, p < 0.0054 for MMP-9). The amounts of IL-1beta, IL-12 and IL-1ra detected in our uveitis patients correlated with levels of MMP-2 (p < 0.07, p < 0.0004, p < 0.03) and MMP-9 (p < 0. 003, p < 0.0001, p < 0.002), and IL-12 (p < 0.004, p < 0.0001). Patients with moderately active uveitis presented with twice the level of MMP-2 as the control group; MMP-9 levels reached up to 92% of the amounts found in patients with active uveitis. Two patients in remission for almost one year still had detectable intraocular MMP-9 levels. CONCLUSION: Our data suggests that the high levels of MMPs found in patients with chronic uveitis might contribute to the damage often seen in these eyes. Since MMPs are capable of releasing proinflammatory cytokines bound to components of the extracellular matrix, and facilitate the secretion of active TNF-alpha by cleavage of the membrane bound form, it is conceivable that MMPs contribute to the chronicity of some uveitis cases.

Aqueous Humor↗
PubMedDate not supplied

The interleukin-1, interleukin-2, interleukin-6 and tumour necrosis factor alpha serological levels in localised and systemic sclerosis.

Serological level of interleukin-1 (IL-1), Interleukin-2 (IL-2), Interleukin-6 (IL-6) and tumour necrosis factor (TNF) alpha was investigated in 26 patients with scleroderma, divided into three lots, by the extension and the progress of the disease. Determinations were performed by ELISA in attack and in remission (after treatment with prednison). Normal values: IL-1 (0-5 pg/ml), IL-2 (0-5 pg/ml), IL-6 (5-15 pg/ml), TNF (0-16 pg/ml). Lot A. Results obtained at the first determination showed that IL-1 is elevated in 4 cases (10-15 pg/ml), IL-2 in 5 cases (10-32 pg/ml), IL-6 in 5 cases (15-42 pg/ml) and TNF in 4 cases (18-34 pg/ml). In the second determination IL-1 was increased in 1 case (8 pg/ml), IL-2 in 1 case (9 pg/ml), IL-6 in 2 cases (12 pg/ml) and TNF was normal. Lot B. In the first determination IL-1 was elevated in 5 cases (8-12 pg/ml), IL-2 in 5 cases (10-15 pg/ml), IL-6 in 7 cases (16-20 pg/ml) and TNF was raised in 3 cases (18-25 pg/ml). At the second determination IL-1 showed normal values in all the cases, IL-2 was raised in 2 cases (10 pg/ml), IL-6 in 2 cases (12.15 pg/ml), TNF in 1 case (20 pg/ml). Lot C. In the first determination there were raised values in 4 cases for IL-1 (6-8 pg/ml), 3 cases for IL-2 (10-18 pg/ml), 5 cases for IL-6 (18-20 pg/ml), 2 cases for TNF (20 pg/ml). At the second determination IL-2 was elevated in 1 case (10 pg/ml), IL-6 in 1 case (15 pg/ml). We consider that in scleroderma there is a disturbance of the investigated cytokines due to the activation and involvement of the secretory cells into the pathogenesis of the disease. The increase of the serological levels of IL-1, IL-2, IL-6 and TNF depends on the extension of the lesions and the clinical and biological activity periods of the disease. The absence of the increase of the serological levels does not exclude their activity at the lesional site.

Adolescent↗
PubMedDate not supplied

Plasma levels of interleukin-6, interleukin-10, and interleukin-1 receptor antagonist in depression: comparison between the acute state and after remission.

There is now some evidence that major depression is accompanied by an immune response with an increased production of pro-inflammatory cytokines. The aim of the present study was to examine serum level of cytokines: interleukin-6 (IL-6), which is considered pro-inflammatory one and anti-inflammatory cytokines: interleukin 10 (IL-10), and interleukin-1 receptor antagonist (IL-1Ra) in acute clinical state of depression and after 6-week antidepressant treatment. Serum IL-6, IL-10, IL-1Ra levels were higher in the subjects with major depression than in normal controls although these results were not statistically significant. The mean score according to the Hamilton Depression Rating Scale (HDRS) in the patients significantly decreased during the 6 weeks of the study, demonstrating an overall improvement. Successful antidepressant treatment had no significant effect on serum level of this cytokines.

Analysis of Variance↗
PubMed2002

[Changes of plasma interleukin-4, interleukin-10 and interleukin-13 in patients with acute respiratory distress syndrome].

OBJECTIVE: To explore the anti-inflammatory mechanisms of interleukin-4 (IL-4), interleukin-10 (IL-10) and interleukin-13 (IL-13) in acute respiratory distress syndrome (ARDS). METHODS: Enzyme-linked immunosorbent assay (ELISA) was employed to determine the plasma levels of IL-4, IL-10 and IL-13 in patients with ARDS (n = 22) and systemic inflammatory response syndrome (SIRS, n = 8). Ten normal subjects were enrolled as controls. RESULTS: The plasma levels of IL-4, IL-10 and IL-13 were (261 +/- 55) microg/L, (458 +/- 112) microg/L and (5.21 +/- 2.02) microg/L, respectively in patients with ARDS; (155 +/- 26) micro g/L, (260 +/- 54) microg/L and (1.69 +/- 0.39) microg/L respectively in patients with SIRS; and (43 +/- 13) microg/L, (135 +/- 15) microg/L and (0.33 +/- 0.10) microg/L, respectively in normal controls. They were significantly increased in patients with ARDS and SIRS as compared to normal controls, and the levels were higher in patients with ARDS than in patients with SIRS. CONCLUSIONS: Increased release of anti-inflammatory cytokines, such as IL-4, IL-10 and IL-13, may be one of the underlining mechanisms for the development of ARDS and SIRS.

Adult↗
PubMed2003

[Predictive value of plasma interleukin 1, interleukin 6, interleukin 8 and C-reactive protein (CRP) in patients with myocardial infarction].

Long-term risk of mortality in patients with myocardial infarction is thought to be linked with plasma concentrations of proinflammatory cytokines and CRP (markers of inflammation). The aim of our study was to analyze plasma levels of interleukin (IL) 1, interleukin 6, interleukin 8 and C-reactive protein (CRP) in patients with myocardial infarction. One hundred and seven (107) patients with myocardial infarction hospitalized at the Cardiac Care Unit of St. Elizabeth's Sisters' Hospital in Warsaw and a control group of 10 subjects were enrolled in our study. The samples of peripheral venous blood were withdrawn from the patients on 2nd and 7th of infarction and plasma levels of IL-1, IL-6, IL-8 and CRP were determined. The patients were followed-up for a year. The analysis of survivals and deaths caused by acute coronary syndrome allowed to determine the predictive value of IL-1, IL-6, IL-8 and CRP in myocardial infarction. Twenty-two (22) of the total 107 patients died of acute coronary syndrome during one-year follow-up. Plasma IL-6 and CRP levels were higher in non-survivors as compared to the levels of IL-6 and CRP in living subjects, whereas plasma levels of IL-1 and IL-8 were comparable in both groups. IL-6 and CRP proved to be of predictive value in patients with myocardial infarction during one-year follow-up. It has also been found that plasma IL-6 level correlates with plasma CRP concentration and that there is a positive correlation between the former and CK-MB levels. IL-6 and CRP levels were higher in patients with Q wave infarction in comparison with non-Q wave infarction. Plasma levels of IL-1 and IL-8 have not been found to be good predictors of death during 12-month follow-up.

Aged↗
PubMed1989

T-lymphocyte activation in IgA nephropathy: serum-soluble interleukin 2 receptor level, interleukin 2 production, and interleukin 2 receptor expression by cultured lymphocytes.

The present study was undertaken to examine the T-lymphocyte activation in IgA nephropathy. Serum-soluble interleukin 2 receptor (sIL2R) levels were studied in 29 IgA nephritic patients, 17 patients with chronic glomerulonephritis (non-IgA nephropathy), and 30 healthy controls during an infection-free period. No difference in serum sIL2R level was demonstrated among these three groups of subjects. However, the serum sIL2R levels of IgA nephritic patient rose significantly during clinical exacerbation with synpharyngitic macroscopic hematuria and the serum sIL2R levels fell when hematuria subsided. Mitogen-stimulated cellular interleukin 2 receptor (IL2R) expression, sIL2R release, and interleukin 2 (IL2) production were also examined in peripheral blood mononuclear cells (PBMC) cultured for 24-48 hr in 21 patients with IgA nephropathy, 17 patients with chronic glomerulonephritides, and 17 healthy controls. The total cellular IL2R expression and sIL2R release did not differ among these three groups of subjects. However, the individual T-cell subsets bearing IL2R were distinctly different between IgA nephritic patients and the other two groups of controls. IgA nephritic patients had increased activated CD4+ lymphocytes and reduced activated CD8+ lymphocytes. Furthermore, IL2 production in response to phytohemagglutinin and pokeweed mitogen stimulation was increased in lymphocytes from patients with IgA nephropathy. The IL2 production did not correlate with the quantities of cellular and sIL2R yet the cellular IL2R expression paralleled the sIL2R released by cultured lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Decreased interleukin generation in patients with cancer of the digestive system. A correlation between interleukin 1 and interleukin 2 production.

The generating capacity of interleukin 1 (IL-1) and interleukin 2 (IL-2) by peripheral blood mononuclear cells (PBMNC) was measured in 40 patients with digestive cancer (20 localized and 20 disseminated) and 20 age- and sex-matched control subjects. The localized carcinoma patients showed normal IL-1 production and a significantly depressed IL-2 production (p less than 0.05) when compared to the healthy individuals. The disseminated carcinoma patients exhibited a significant impairment of both IL-1 and IL-2 production in comparison with the healthy controls (IL-1: p less than 0.001, IL-2: p less than 0.001) and the localized carcinoma patients (IL-1: p less than 0.001, IL-2: p less than 0.001). A significant correlation was observed between IL-1 and IL-2 generation in all the cancer patients (r = 0.458, p less than 0.01). These results suggest that progressive tumor growth may result in decreased interleukin production by the host PBMNC, and that related mechanisms, which are more susceptible to lymphocytes than monocytes, may be involved in the impairment of both IL-1 and IL-2 production.

Gastrointestinal Neoplasms↗
PubMed1993

Human macrophage responses to vaccine strains of influenza virus: synthesis of viral proteins, interleukin-1 beta, interleukin-6, tumour necrosis factor-alpha and interleukin-1 inhibitor.

Interactions between influenza viruses and human macrophages were examined to detect potential mechanisms for enhanced febrile reactions previously associated with administration of an avian-human H1N1 reassortant vaccine. Cells exposed to that strain were compared with cells exposed to wild-type and cold-adapted H1H1 and H3H2 strains and an avian-human H3N2 strain. Cells exposed to the avian-human H1N1 virus showed increased synthesis of viral neuraminidase, previously reported to induce fever-producing cytokines, but no detectable increase in production of interleukin-1 beta, interleukin-6 and tumour necrosis factor-alpha measured by immunoassay, or decrease in interleukin-1 inhibitor activity by bioassay.

Fever↗
PubMed1997

Plasma interleukin-1alpha, interleukin-1beta and interleukin-1 receptor antagonist levels in pre-eclampsia.

The values of plasma interleukin-1alpha (IL-1alpha), interleukin-1beta (IL-1beta) and interleukin-1 receptor antagonist (IL-1ra) levels were evaluated as the markers of pre-eclampsia in 35 serial plasma samples from ten pregnant women who subsequently developed pre-eclampsia and in 74 plasma samples from 20 uncomplicated pregnancies, retrospectively. No correlation was found between plasma IL-1alpha, IL-1beta and IL-1ra levels, liver and renal function tests, thrombocyte and white blood cell counts, proteinuria, systolic and diastolic blood pressures and gestational weeks. Almost equal levels of IL-1alpha and IL-1beta were measured in all corresponding groups, but these were too few in number to statistically analyze. IL-1ra values were higher in the pre-eclampsia group than in the uncomplicated pregnancy group, at 20-25 and 31-35 gestational weeks significantly and 26-30 gestational weeks insignificantly and showed an increase during labor in both groups. It was found to have 58% positive predictivity, 100% negative predictivity, 50% specificity and 100% sensitivity at gestational weeks 20-25. According to these results, IL-1ra seems to be considered for its high negative predictivity in the exclusion of the probability of pre-eclampsia development during antenatal visits, but its plasma level is not correlated with the severity of the disease.

Acute-Phase Reaction↗
PubMed2000

Regulation of CD31 expression and interleukin-4 production by human cord blood CD4+ T cells with interleukin-4 and interleukin-7.

BACKGROUND: T helper 2 cell type cytokines, such as interleukin (IL)-4 and IL-5, play pivotal roles in the development of allergic diseases. However, the mechanism by which naive CD4+ T cells acquire the ability to produce these cytokines remains unclear. Recently, it was reported that IL-7 induces the ability to produce IL-4 as well as interferon (IFN)-gamma and IL-5 in naive CD4+ T cells without TCR stimulation. To further analyze the mechanism of acquiring IL-4-producing ability by naive CD4+ T cells, the effects of IL-7 on human cord blood CD4+ T cells were compared with those of IL-4, which induced the ability to produce IFN-gamma but not IL-4. RESULTS: Interleukin-7 preserved the population of CD4+CD31- T cells in cord blood and induced their IL-4-producing ability without T cell receptor (TCR) stimulation, while IL-4 induced CD31 on CD31- T cells and could not induce their IL-4-producing ability. Both the CD31-inducing effect and the inhibitory priming effect for IL-4-production by IL-4 were also observed after cord blood CD4+ T cells had been primed with IL-7 and acquired the IL-4-producing ability. CONCLUSIONS: Interleukin-7 induced the IL-4-producing ability in naive CD4+CD31- T cells without TCR stimulation, suggesting that the signal transduction via CD31 may have an inhibitory effect on the acquisition of the IL-4-producing ability by cord blood CD4+ T cells in the absence of TCR stimulation.

CD4-Positive T-Lymphocytes↗
PubMed1994

Neonatal tumor necrosis factor, interleukin-1 alpha, interleukin-1 beta, and interleukin-6 response to infection.

Various studies have shown that in vitro production of cytokines by leukocytes from the newborn are normal, decreased, or increased. We investigated the blood levels of tumor necrosis factor-alpha (TNF-alpha) interleukin-1 alpha, interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) simultaneously to assess the cytokine response to systemic infection during the neonatal period. One or more cytokine levels were elevated in all of the newborns with sepsis. Serum TNF levels in the newborns with sepsis were significantly higher than the two control groups (P < 0.002). Serum IL-6 levels in the study group were also found to be significantly higher than the control groups (P < 0.0004 for sepsis vs adult controls and P < 0.03 for sepsis vs newborn controls). We could not find statistically significant correlation between any of the cytokine levels, C-reactive protein, white blood cells, and platelet counts and the outcome. Gram-negative bacteria were the main causative agents in these patients, although one of them was infected with gram-positive bacteria, besides one premature infant (29 weeks) with Candida sepsis also had significantly elevated TNF, IL-1 beta, and IL-6 levels. Our data show that both mature and premature neonates were able to produce and significantly increase the blood levels of the cytokines in response to sepsis. Because the biologic relevance of cytokine levels is not known, further prospective and sequential studies on cytokine levels simultaneously and correlation with clinical parameters are needed to clarify the biological role of this important component of the host defense system.

Adult↗
PubMed1994

Serum levels of interleukin-1 alpha, interleukin-1 beta, interleukin-6, and tumor necrosis factor in patients with acute viral hepatitis.

Serum levels of interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) in patients with acute viral hepatitis were investigated. Twelve patients suffering from acute viral hepatitis were studied; 8 patients presented with acute hepatitis B, 2 patients with acute hepatitis A, and 2 patients with acute hepatitis C. Serum levels of IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha were significantly increased in all patients with acute viral hepatitis. Decreased serum levels of all cytokines were noted in four patients with acute hepatitis B during the recovery phase of infection. In addition, IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha were undetectable at the end of a follow-up period of 6 months. Our study shows that increased levels of IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha are probably related to hepatitis activity and thus may have some role in hepatocytic injury.

Acute Disease↗
PubMed2004

Anaemia of chronic disease in AA amyloidosis is associated with allele 2 of the interleukin-1beta-511 promoter gene and raised levels of interleukin-1beta and interleukin-18.

OBJECTIVE: In amyloid A (AA) amyloidosis the receptor for advanced glycation end products is a target for the circulating amyloid precursor protein (SAA) resulting in upregulation of the proinflammatory cytokine pathway. Besides inducing hepatic SAA synthesis the interleukin-1 cytokine family is involved in the regulation of haematopoiesis. We therefore studied the relationship between the circulating levels of interleukin-1beta (IL-1beta) and interleukin-18 (IL-18), a new member of the IL-1 complex, as well as polymorphisms within the IL-1 cluster with the occurrence of anaemia in patients with AA amyloidosis. DESIGN, SETTING AND SUBJECTS: The study included 54 adult patients with biopsy-proven reactive amyloidosis allocated into three groups on the basis of haemoglobin (Hb) level: group I included all patients with Hb < 110 g L(-1) (n = 16); group II patients (Hb > 110 g L(-1), n = 16) were selected to match group I patients with respect to sex, age, underlying disease (seropositive, erosive rheumatoid arthritis) and renal function; and group III patients (n = 38) represented all patients (unselected) with Hb > or = 110 g L(-1). Gene polymorphisms were studied by polymerase chain reaction restriction length assay and included the base exchange at position-889 of the IL-1alpha gene, the polymorphic region at position-511 and the polymorphic locus at exon 5, position +3954 of the IL-1beta gene, as well as the IL-1 receptor antagonist (IL-1Ra) exon 2 polymorphism caused by the 86-bp tandem repeats. Plasma IL-1beta, IL-1alpha, IL-18, IL-1 Ra, SAA, ferritin, soluble transferrin receptor and erythropoietin levels were studied by enzyme immunoassays. RESULTS: Circulating IL-beta and IL-18 were significantly raised in the anaemic patients with AA amyloidosis when compared with group II patients (matched, Hb > 110 g L(-1)) as well as group III patients (nonmatched, Hb > or = 110 g L(-1)). A significant inverse relationship was found between IL-1beta and haemoglobin levels, as well as between IL-18 and haemoglobin levels. The frequency of allele 2 (T) of the IL-1beta-511 promoter gene was significantly increased and that of allele 1 (C) decreased in anaemic amyloid patients (group I) when compared with group II and III patients. Circulating IL-1beta levels tended to be higher amongst the IL-1beta-511 allele 2 carriers than amongst the noncarriers, as well as amongst the anaemic amyloid patients filling all criteria of anaemia of chronic disease. CONCLUSION: The occurrence of anaemia in patients with AA amyloidosis is associated with allele 2 (T) of the IL-1beta-511 promoter gene and elevated levels of circulating IL-1beta and IL-18. In AA amyloidosis the raised cytokine levels may generate a vicious cycle leading to accelerated amyloidogenesis, suppression of erythropoiesis and aggravation of the underlying inflammatory disorder.

Adult↗
PubMed1989

T lymphocyte activation in euthyroid Graves' ophthalmopathy: soluble interleukin 2 receptor release, cellular interleukin 2 receptor expression and interleukin 2 production.

The present study was undertaken to examine the cellular control arm of the immune response with regard to T lymphocyte proliferation in euthyroid Graves' ophthalmopathy. Twenty patients with euthyroid Graves' ophthalmopathy (7 on antithyroid drugs and 13 on no treatment) and 18 healthy controls were studied in an infection-free period. Mitogen-stimulated cellular interleukin 2 (IL2) receptor expression, soluble interleukin 2 receptor release, and interleukin 2 production, were studied in peripheral blood mononuclear cells cultured for 24 h. The cellular IL2 receptor expression and soluble IL2 receptor release did not differ between the patients and healthy controls. In contrast, IL2 production in response to pokeweed mitogen stimulation was increased in lymphocytes from patients with Graves' ophthalmopathy. The IL2 release did not correlate with the quantities of cellular and soluble IL2 receptor. The mitogen-stimulated cellular IL2 receptor expression, IL2 receptor release, and IL2 production did not differ between patients with or without carbimazole therapy. Despite a suggested role of autoreactive T cells in mediating the development and propagation of autoimmune thyroid disease, this study fails to demonstrate a defective T lymphocyte activation state in patients with Graves' ophthalmopathy during an euthyroid state.

Adolescent↗
PubMed2002

Interleukin-4, interleukin-10, and interleukin-1-receptor antagonist but not transforming growth factor-beta induce ramification and reduce adhesion molecule expression of rat microglial cells.

The activity of microglial cells is strictly controlled in order to maintain central nervous system (CNS) immune privilege. We hypothesized that several immunomodulatory factors present in the CNS parenchyma, i.e., the Th2-derived cytokines interleukin (IL)-4 and IL-10, interleukin-1-receptor-antagonist (IL-1-ra), or transforming growth factor (TGF)-beta can modulate microglial morphology and functions. Microglial cells were incubated with IL-4, IL-10, IL-1-ra, TGF-beta, or with astrocyte conditioned media (ACM) and were analyzed for morphological changes, expression of intercellular adhesion molecule (ICAM)-1, and secretion of IL-1beta or tumor necrosis factor (TNF)-alpha. Whereas untreated controls showed an amoeboid morphology both Th2-derived cytokines, IL-1-ra, and ACM induced a morphological transformation to the ramified phenotype. In contrast, TGF-beta-treated microglial cells showed an amoeboid morphology. Even combined with the neutralizing antibodies against IL-4, IL-10, or TGF-beta ACM induced microglial ramification. Furthermore, ACM did not contain relevant amounts of IL-4 and IL-10, as measured by enzyme-linked immunosorbent assay (ELISA). Flow cytometry showed that lipopolysaccharide (LPS)-induced ICAM-1-expression on microglial cells was strongly suppressed by ACM, significantly modulated by IL-4, IL-10, or IL-1-ra, but not influenced by TGF-beta. The LPS-induced secretion of IL-1beta and TNF-alpha was only reduced after application of ACM, whereas IL-4 or IL-10 did not inhibit IL-1beta- or TNF-alpha secretion. TGF-beta enhanced IL-1beta- but not TNF-alpha secretion. In summary, we demonstrate that IL-4, IL-10, and IL-1-ra induce microglial ramification and reduce ICAM-1-expression, whereas the secretion of proinflammatory cytokines is not prevented. TGF-beta has no modulating effects. Importantly, unidentified astrocytic factors that are not identical with IL-4, IL-10, or TGF-beta possess strong immunomodulatory properties.

Animals↗
PubMed1996

The combination of endotoxin and dexamethasone induces type II interleukin 1 receptor (IL-1r II) in monocytes: a comparison to interleukin 1 beta (IL-1 beta) and interleukin 1 receptor antagonist (IL-1ra).

Soluble type II interleukin 1 receptor (IL-1r II) and interleukin 1 receptor antagonist (IL-1ra) regulate inflammation by competitively inhibiting the binding of IL-1 beta to the signalling IL-1 receptor. In addition, glucocorticoids also regulate IL-1 beta by suppressing gene transcription. More recently, glucocorticoids have been shown to increase soluble IL-1r II concentrations, which may contribute to their anti-inflammatory properties. Interestingly, increased serum levels of soluble IL-1r II and IL-1ra have been measured in septic patients, although the mechanism is unclear. In this respect, the authors characterize new pathways in which IL-1r II and IL-1ra may be regulated in sepsis through combined stimulation with lipopolysaccharide (LPS) and dexamethasone of peripheral blood mononuclear cells (PBMC). This paper confirms that while dexamethasone induces release of IL-1r II, LPS augments dexamethasone-induced IL-1r II release 45-fold. Furthermore, LPS plus dexamethasone induces IL-1r II protein and mRNA, whereas LPS alone does not. Additionally, it was shown by flow cytometric analysis that the monocyte is the primary IL-1r II producer in response to LPS and dexamethasone administration. Therefore, LPS and dexamethasone synergism in IL-1r II induction may be important in controlling IL-1 beta effects. In contrast, LPS alone induces IL-1ra, while dexamethasone attenuates this LPS-induced response. Although IL-1r II and IL-1ra may work together to suppress IL-1 beta effects in sepsis, inflammatory cells differentially regulate these cytokines.

Blotting, Western↗
PubMed1996

Interleukin-1 beta differentially affects interleukin-6 and soluble interleukin-6 receptor in the blood and central nervous system of the monkey.

Two studies were conducted to investigate whether behavioral and physiological responses induced by administration of interleukin-1 beta (IL-1 beta) were also associated with changes in interleukin-6 (IL-6) and soluble IL-6 receptor levels (sIL-6R). Following intravenous injection of rhIL-1 beta, blood and cerebrospinal fluid (CSF) samples were collected from juvenile rhesus monkeys. Marked increases in IL-6 levels were evident at 1 h in both blood and intrathecal compartments. IL-1 beta also induced significant elevations in the release of ACTH and cortisol into the blood stream, and following high doses, the monkeys evinced signs of sickness behavior. The second study characterized the IL-beta dose-response relationship showing that these physiological changes were most evident at doses between 0.5 microgram and 1.0 microgram IL-1/kg body weight. Soluble IL-6 receptor concentration was also increased, but only in plasma. There was no detectable sIL-6R in CSF. The large release of IL-6 into CSF suggests that some behavioral symptoms may be due to intrinsic changes in central nervous system activity concomitant with the alterations in peripheral physiology.

Adrenocorticotropic Hormone↗
PubMed1994

Synthesis of interleukin-1 alpha, interleukin-6, and interleukin-8 by cultured human nasal epithelial cells.

Nasal epithelium forms the initial barrier between the environment and the respiratory system and may be a potential source of proinflammatory interleukins, which contribute to the pathophysiology of allergic and nonallergic rhinitis. To explore this possibility, epithelium and cultured human nasal epithelial cells from nasal turbinates of patients undergoing surgery for treatment of upper airway obstruction were examined for the spontaneous expression of interleukin (IL)-1 alpha, IL-1 beta, IL-6, and IL-8. Human nasal epithelial cell lysates and culture supernatants were assayed by two-site ELISAs specific for IL-1 alpha, IL-1 beta, IL-6, or IL-8. Maximum concentrations of these cytokines in supernatants ranged from approximately 0.2 to 2 ng/ml for IL-1 alpha, 1.5 to 7 ng/ml for IL-6, and 100 to 3000 ng/ml for IL-8. IL-1 alpha was predominantly cell-associated, whereas most of the IL-8 and all of the IL-6 were detected in the supernatant. Little or no IL-1 beta was detected by ELISA in the supernatants or cell lysates. Whole tissue turbinates and isolated epithelium were also examined for IL-1 beta, IL-6, and IL-8 mRNA expression by Northern blot analysis. IL-6 and IL-8 mRNAs were detected, whereas IL-1 beta mRNA was not. Furthermore, IL-6 and IL-8 release from human nasal epithelial cell cultures was enhanced by addition to the cultures of lipopolysaccharide, and IL-6 release was inhibited by polymyxin B. Thus human nasal epithelium may be a major source of IL-1 alpha, IL-6, and IL-8 in allergic and nonallergic rhinitis. Production of those proinflammatory cytokines by epithelial cells of the nasal and sinus mucosa may contribute to the pathologic and clinical events that occur in these diseases.

Adolescent↗