OBJECTIVE: To investigate the characteristic changes of the plasma cytokine profile in Chinese patients with idiopathic multicentric Castleman diseases (iMCD). METHODS: The plasma samples from 22 patients with confirmed diagnosis of iMCD were collected before treatments; Specimens from 17 patients with newly diagnosed multiple myeloma, 10 non Hodgkin's lymphoma, and 15 healthy donors were used as control. Seventeen kinds of cytokines were measured by cytokine beads array (CBA) and ELISA respectively. RESULTS: Six cytokines were measured by ELISA. The concentrations of IL-2, IL-6, IL-21 and VEGF were significantly higher in the plasma of iMCD patients than those of the healthy donors (P＜0.01) and the level of IL-21 was highest in the iMCD group. There was no significant difference in the levels of IL-1β and IL-4 between the iMCD and healthy donor groups. Thirteen cytokines were measured by CBA assay, besides IL-6 level was confirmed to be higher in iMCD group than that in healthy controls (P＜0.01）, IL-12-p70 and IL-33 levels were also higher in iMCD group than those in control group (P＜0.05）, no significant difference of the rest cytokines was found between iMCD and the control group. CONCLUSION IL-6 and VEGF has shown to involved in the pathogenesis of iMCD, the results of preliminary study imply the role of IL-2 、IL-21、IL-12-p70 and IL-33 in this rare lymphoproliferative disease. Further studies are needed to elucidate the mechanism of these cytokines, which may shed some light on the identification of novel therapeutic targets against iMCD.
Castleman Disease ; Cytokines ; Humans ; Interleukin-12 ; Interleukin-1beta ; Plasma

No abstract available.
Animals ; Interleukin-1 ; Interleukin-1beta ; Islets of Langerhans ; Rats

OBJECTIVETo observe the production of interleukin (IL)-1beta, IL-6 and tumor necrosis factor alpha (TNFalpha) from stimulated human fibroblast with abstract from cell wall of Actinomyces naeslundii ATCC19246.

METHODSThe abstract from the cell wall from Actinomyces naeslundii were extracted and purified with the method of purifying lipoteichoic acid(LTA) and stimulated the THP-1 with three different concentrations (1, 10, 100 mg/mL). The level of IL-1beta, IL-6 and TNFalpha in the supernatant was quantitatively analyzed by ELISA. Results Abstracts at the concentrations of 10, 100 mg/mL significantly produced IL-1beta, IL-6 and TNFalpha, especially 10 mg/mL.

CONCLUSIONThe abstract from cell wall of Actinomyces naeslundii may significantly increase IL-1beta, IL-6 and TNFalpha level in the supernatant of THP-1, and the increasing level is different with the concentrations.

No abstract available.
Fetal Blood* ; Interleukin-1beta* ; Tumor Necrosis Factor-alpha*

The purpose of this study was to evaluate the effects of caffeine and calcium on the activities of the osteoblastic cell from mouse calvaria. The author cultured osteoblastic cells obtained from the mouse calvaria and were divided into three groups: the caffeine-treated, the calcium-treated and the combine-treated group. In caffeine-treated group, the cell toxicity was measured by MTT assay at 1, 2 and 4 days after treatment of caffeine. In all groups, the densities of the mineralized bone nodules were measured by imaging analyzer after Von Kossa staining. The alkaline phosphotase (ALP) activities were measured at 2, 7, 14, 21 and 28 days and the interleukin-1beta activities at 48 hours after treatment of caffeine and calcium. The measurements were statistically executed with ANOVA test and the results were as follows. 1. The cellular toxicity of the caffeine increased with the concentration of caffeine during the incubation period. 2. The maximum densities of mineralization were observed at 0.2 mM caffeine-treated group, 1.2 mM calcium-treated group, 0.1 mM caffeine and 1.8 mM calcium-treated group. 3. The activities of ALP were peaked at 14 days at calcium-treated group as no-treated. But, the activities of ALP increased with concentrations of caffeine at caffeine-treated group. At combine-treated group, the act of ALP were peaked at 24 days at 1.2 mM, 1.8 mM calcium-treated group, But decreased at 2.5 mM calcium-treated group. 4. The activites of the IL-1beta were increased significantly at 0.2 mM caffeine-treated group, 1.8 mM calcium-treated group and 0.1 mM caffeine and 1.8 mM calcium-treated group. But, they were decreased at all groups of high concentration.
Animals ; Caffeine* ; Calcium* ; Interleukin-1beta ; Mice* ; Osteoblasts* ; Skull

This study was designed to investigate the expression and production of interleukin-1beta (IL-1beta) in human peripheral blood of trained runners and untrained controls after temporary moderate intensity exercise. Male long-distance trained runners (TR) and untrained sedentary control subjects (SED) ran for 1 h at 70% of heart rate reserve (HRR). IL-1beta gene and protein expressions were significantly higher in TR than those with SED at all 3 intervals examined independently. Significant increases in total sweat volume and oral temperature were observed after exercise in both groups, however, there were some differences between the groups. We conclude, therefore, that sweating due to exercise is associated with increase of IL-1beta and it is correlated with decrease of oral temperature.
Body Temperature* ; Heart Rate ; Humans ; Interleukin-1beta* ; Male ; Sweat* ; Sweating*

To explore the effects of miR-101-3p on IL-1β-induced chondrocyte injury and its underlying mechanisms.
 Methods: Chondrocytes were divided into 4 groups: a control group (NC group), a IL-1β group, a negative control group (IL-1β+miR-NC group), and a miR-101-3p group (IL-1β+miR-101-3p group), which were treated with IL-1β after transfecting with miR-101-3p mimic or negative mimic. The expressions of miR-101-3p-5p and stanniocalcin 1 (STC1) at different concentrations of IL-1β (1, 5, 10 ng/mL)-induced chondrocytes were detected by Western blotting and real-time PCR. MTT assay was used to detect cell proliferation rate, while caspases assay kits and flow cytometry were used to measure the cell caspase and apoptosis level. Western blotting assay was used to detect the expression levels of pro-inflammatory and ECM-related protein, such as matrix metalloproteinase 9 (MMP9) and collagen Type II. In addition, 3'-untranslated regions (UTR) of wild-type STC1 (STC1-3'-UTR-WT) or 3'-UTR of mutant STC1 (STC1-3'-UTR-MUT) were co-transfected with miR-101-3p mimic or miR-NC, respectively, while luciferase reporter assay was used to examine the regulative role of miR-101-3p in STC1. In order to detect whether STC1 was involved in the effect of miR-101-3p on chondrocytes, miR-NC (miR-NC group), miR-101-3p (miR-101-3p group), anti-NC (anti-NC group) and anti-miR-101-3p (anti-miR-101-3p group) were respectively transfected into the cells, and the expression of STC1 protein was detected by Western blotting. Subsequently, the cells were randomly divided into a miR-101-3P group (IL-1β+miR-101-3p group), an over-expression control group (IL-1β+miR-101-3p+ad-GFP group), and an over-expression STC1 group (IL-1β+miR-101-3p+ad-STC1 group) to investigate whether STC1 was involved in the role of miR-101-3p in chondrocyte. Similarly, MTT assay was used to detect cell proliferation rate, caspases assay kits and flow cytometry were used to measure the cell caspase and apoptosis level. Western blotting assay was used to detect the expression levels of pro-inflammatory and ECM-related protein MMP9 and collagen Type II.
 Results: Compared with the 0 ng/mL IL-1β, the expression of miR-101-3p was decreased in chondrocyte at different concentration of IL-1β (1, 5, 10 ng/mL) (all P<0.05), while the level of STC1 was increased (P<0.05). Compared with the NC group, the chondrocyte proliferation rate was down-regulated (P<0.05), while the apoptosis rate, the levels of caspases, IL-6 and TNF-α were increased in the IL-1β group (P<0.05). Moreover, the MMP9 levels were increased obviously, and the protein levels of collagen Type II were decreased in the IL-1β group compared with the NC group (both P<0.05). Compared with the IL-1β+miR-NC group, the proliferation rate was increased (P<0.05), whereas the apoptosis rates, the caspase-3/9 levels, the IL-6 and TNF-α levels were increased in the IL-1β+miR-101-3p group (all P<0.05). Then MMP9 levels were decreased obviously (P<0.05), and the protein levels of collagen Type II were increased in IL-1β+miR-101-3p group compared with the IL-1β+miR-NC group (both P<0.05). In addition, the double luciferase assay showed that the STC1 levels could be inhibited in the miR-101-3p group compared with the miR-NC group (P<0.05). STC1 levels were decreased in the miR-101-3p group compared with the miR-NC group (P<0.05), and the STC1 levels were increased in the anti-miR-101-3p group compared with those in the anti-NC group (P<0.05). The results of miR-101-3p+ad-STC1 group showed that compared with the miR-101-3p+ad-GFP group, the STC1 could reverse the effects of miR-101-3p on IL-1β-induced proliferation, apoptosis, inflammatory responses and ECM protein of chondrocytes.
 Conclusion: The regulation of miR-101-3p/STC1 signal pathway may have a role in reducing the IL-1β-induced chondrocyte injury.
Cell Proliferation ; Chondrocytes ; Glycoproteins ; metabolism ; Interleukin-1beta ; metabolism ; MicroRNAs

OBJECTIVE: To study whether pyroptosis is involved in the bilirubin-induced injury of primary cultured rat cortical microglial cells. METHODS: Primary cultured rat cortical microglial cells were randomly administered with 30 μmol/L bilirubin (bilirubin group), 30 μmol/L bilirubin following 30 μmol/L VX-765 pretreatment (VX-765+bilirubin group), or an equal volume of dimethyl sulfoxide (control group). Modified MTT assay was used to measure the viability of microglial cells. Western blot was used to measure the expression of the pyroptosis-related proteins Caspase-1 and gasdermin D (GSDMD). Lactate dehydrogenase (LDH)-release assay was used to evaluate the cytotoxicity of microglial cells. EtBr/EthD2 with different molecular weights (394 Da/1 293 Da) was used to measure the size of plasma membrane pores. ELISA was used to measure the level of the inflammatory factor interleukin-1β (IL-1β) in culture supernatant. RESULTS: After bilirubin stimulation, the viability of microglial cells decreased and LDH release increased, both in a time-dependent manner. Compared with the control group, the bilirubin group had a significantly higher positive rate of small-molecule EtBr passing through the cell membrane (P<0.001), while there was no significant difference in the pass rate of large-molecule EthD2 between groups (P>0.05). The expression of activated Caspase-1 significantly increased at 0.5 hour after bilirubin stimulation (P<0.05), and that of activated GSDMD significantly increased at 6 hours after bilirubin stimulation (P<0.05). The release of IL-1β significantly increased at 6 hours after bilirubin stimulation and reached the peak at 24 hours (P<0.001). Compared with the bilirubin group, the VX-765+bilirubin group had a significant increase in cell viability (P<0.05) and significant reductions in the expression of activated GSDMD, the pass rate of EtBr, and the release of LDH and IL-1β (P<0.05). CONCLUSIONS Pyroptosis is involved in bilirubin-induced injury of primary cultured microglial cells.
Animals ; Bilirubin ; Caspase 1 ; Cell Survival ; Interleukin-1beta ; Pyroptosis ; Rats

The present study was carried out in order to investigate the relationship between immune function and the activity of hypothalamic-pituitary-adrenal(HPA) axis in patients with major depression. The subjects were 16 female major depressives and 16 female healthy controls. We measured mitogen-induced production of IL-1 beta, IL-2, IL-6 and serum level of IL-1 beta, IL-2, IL-6 and basal plasma cortisol levels at 8 00 a.m. We measured post-DST(dexamethasone suppression test) cortisol levels in 16 major depressives. The result were as follows : 1) Basal cortisol level was significantly higher in the patients with major depression than in the healthy controls(14.4+/-4.6 microgram/dl, 10.1+/-5.2microgram /dl, respectively, p<0.05). 2) IL-2 production was significantly lower in the patients with major depression than in the healthy controls(1747.3+/-387.9 pg/ml, 2520.2+/-884.1 pg/ml, respectively, p<0.05). There were no significant differences in IL-1 beta and IL-6 production between the patients with major depression and the healthy controls. 3) Serum level of IL-2 was detectable in 12 of 16 patients with major depression and in 10 of 16 healthy controls. There was no significant difference in serum level of IL-2 between two groups. Serum level of IL-1 beta was detectable in 3 of 16 patients with major depression and of 16 healthy controls. We could not detect serum level of IL-6 in both groups. 4) There was significant negative correlation between IL-2 production and post-DST cortisol level(r= -0.89) in the 16 patients with major depression. There was significant negative correlation between serum level of IL-2 and post-DST cortisol level(r= -0.97) in the 12 patients with major depression. There was significant negative correlation between serum level of IL-2 and basal cortisol level(r= -0.65) in the 12 patients with major depression. But there was no significant correlation between IL-2 production and basal cortisol level in the 16 patients with major depression. These findings suggest that immune function is decreased in major depression and the decreased immune function is highly related to the hyperactivity of the HPA axis.
Axis, Cervical Vertebra* ; Depression* ; Female ; Humans ; Hydrocortisone ; Interleukin-1* ; Interleukin-1beta* ; Interleukin-2 ; Interleukin-6 ; Interleukins ; Plasma

OBJECTIVETo study the effect of carboxyamidotriazole (CAI) on adjuvant arthritis (AA) in rats.

METHODSThe rats were randomly divided into normal group,two vehicle groups (polyethylene glycol 400 control and normal sodium control group), CAI-treated groups (10, 20, and 40 mg/kg) and positive control dexamethasone group. Freund's completed adjuvant was used to induce AA in rats. The arthritis index (AI) was scored, and X-ray check of the hind limbs and histopathological examination were performed. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in the inflamed paw tissues were measured.

RESULTSThe administration of CAI significantly decreased the AI, restored the body weights, and ameliorated the radiological and histopathological features of joint destruction in AA rats (P<0.05, P<0.01). In addition, CAI reduced the TNF-α, IL-1β, and IL-6 levels in the inflamed paw tissues (P<0.05, P<0.01).

CONCLUSIONCAI has therapeutic effect on AA rats, which may be achieved by decreasing the pro-inflammatory cytokines at the site of inflammation.