HCSGD entry for IL1B


1. General information

Official gene symbolIL1B
Entrez ID3553
Gene full nameinterleukin 1, beta
Other gene symbolsIL-1 IL1-BETA IL1F2
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

color bar
This gene isn't in PPI subnetwork.

3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000165MAPK cascadeIMPbiological_process
GO:0000187Activation of MAPK activityIDAbiological_process
GO:0001660Fever generationIEAbiological_process
GO:0001934Positive regulation of protein phosphorylationIDA NASbiological_process
GO:0002711Positive regulation of T cell mediated immunityICbiological_process
GO:0005125Cytokine activityIDA IEA IMPmolecular_function
GO:0005149Interleukin-1 receptor bindingIEA NASmolecular_function
GO:0005576Extracellular regionIDA NAS TAScellular_component
GO:0005615Extracellular spaceIDA IEA IMPcellular_component
GO:0005829CytosolTAScellular_component
GO:0006915Apoptotic processTASbiological_process
GO:0006954Inflammatory responseIDA IEA NASbiological_process
GO:0006955Immune responseIEAbiological_process
GO:0007165Signal transductionTASbiological_process
GO:0007267Cell-cell signalingTASbiological_process
GO:0007566Embryo implantationTASbiological_process
GO:0008285Negative regulation of cell proliferationIDAbiological_process
GO:0009743Response to carbohydrateIEAbiological_process
GO:0010575Positive regulation vascular endothelial growth factor productionIDA IEA ISSbiological_process
GO:0010829Negative regulation of glucose transportIEA ISSbiological_process
GO:0014805Smooth muscle adaptationNASbiological_process
GO:0019221Cytokine-mediated signaling pathwayIDAbiological_process
GO:0019904Protein domain specific bindingIPImolecular_function
GO:0030141Secretory granuleIEAcellular_component
GO:0030213Hyaluronan biosynthetic processIDAbiological_process
GO:0030593Neutrophil chemotaxisIEAbiological_process
GO:0030730Sequestering of triglycerideIDAbiological_process
GO:0030949Positive regulation of vascular endothelial growth factor receptor signaling pathwayICbiological_process
GO:0031622Positive regulation of fever generationIEA ISSbiological_process
GO:0031663Lipopolysaccharide-mediated signaling pathwayIDAbiological_process
GO:0032308Positive regulation of prostaglandin secretionIEA ISSbiological_process
GO:0032496Response to lipopolysaccharideIEAbiological_process
GO:0032611Interleukin-1 beta productionIEAbiological_process
GO:0032725Positive regulation of granulocyte macrophage colony-stimulating factor productionIDAbiological_process
GO:0032729Positive regulation of interferon-gamma productionIDAbiological_process
GO:0032755Positive regulation of interleukin-6 productionIEA TASbiological_process
GO:0032757Positive regulation of interleukin-8 productionIDAbiological_process
GO:0033129Positive regulation of histone phosphorylationNASbiological_process
GO:0033198Response to ATPIEAbiological_process
GO:0034116Positive regulation of heterotypic cell-cell adhesionIDA NASbiological_process
GO:0035066Positive regulation of histone acetylationNASbiological_process
GO:0035234Ectopic germ cell programmed cell deathIEAbiological_process
GO:0035505Positive regulation of myosin light chain kinase activityIDAbiological_process
GO:0035690Cellular response to drugIDAbiological_process
GO:0042102Positive regulation of T cell proliferationIDAbiological_process
GO:0042346Positive regulation of NF-kappaB import into nucleusIDAbiological_process
GO:0043122Regulation of I-kappaB kinase/NF-kappaB signalingIDAbiological_process
GO:0043123Positive regulation of I-kappaB kinase/NF-kappaB signalingIEAbiological_process
GO:0043407Negative regulation of MAP kinase activityIEA ISSbiological_process
GO:0043491Protein kinase B signalingIMPbiological_process
GO:0045080Positive regulation of chemokine biosynthetic processIEAbiological_process
GO:0045086Positive regulation of interleukin-2 biosynthetic processIMPbiological_process
GO:0045410Positive regulation of interleukin-6 biosynthetic processIEAbiological_process
GO:0045429Positive regulation of nitric oxide biosynthetic processIDAbiological_process
GO:0045766Positive regulation of angiogenesisIEA ISSbiological_process
GO:0045833Negative regulation of lipid metabolic processIEA ISSbiological_process
GO:0045840Positive regulation of mitosisIMPbiological_process
GO:0045893Positive regulation of transcription, DNA-templatedIDAbiological_process
GO:0045944Positive regulation of transcription from RNA polymerase II promoterIEAbiological_process
GO:0046330Positive regulation of JNK cascadeIEAbiological_process
GO:0046627Negative regulation of insulin receptor signaling pathwayIEA ISSbiological_process
GO:0046827Positive regulation of protein export from nucleusNASbiological_process
GO:0050796Regulation of insulin secretionIDAbiological_process
GO:0050995Negative regulation of lipid catabolic processIDAbiological_process
GO:0050996Positive regulation of lipid catabolic processIEA ISSbiological_process
GO:0051044Positive regulation of membrane protein ectodomain proteolysisIDAbiological_process
GO:0051091Positive regulation of sequence-specific DNA binding transcription factor activityIDAbiological_process
GO:0051092Positive regulation of NF-kappaB transcription factor activityIDAbiological_process
GO:0051781Positive regulation of cell divisionIEAbiological_process
GO:0060355Positive regulation of cell adhesion molecule productionNASbiological_process
GO:0060559Positive regulation of calcidiol 1-monooxygenase activityIDAbiological_process
GO:0070164Negative regulation of adiponectin secretionIEA ISSbiological_process
GO:0070487Monocyte aggregationIDAbiological_process
GO:0071260Cellular response to mechanical stimulusIEPbiological_process
GO:0071310Cellular response to organic substanceIDAbiological_process
GO:0071407Cellular response to organic cyclic compoundIDAbiological_process
GO:0071639Positive regulation of monocyte chemotactic protein-1 productionIDAbiological_process
GO:0097192Extrinsic apoptotic signaling pathway in absence of ligandIEAbiological_process
GO:2001240Negative regulation of extrinsic apoptotic signaling pathway in absence of ligandIDAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00000940310.84699261430.01157777781.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up1.8663763797
GSE13712_SHEARUp0.1400389346
GSE13712_STATICUp0.4223620626
GSE19018Down-0.1356256964
GSE19899_A1Up6.4541809153
GSE19899_A2Up9.0583316481
PubMed_21979375_A1Up11.0681300435
PubMed_21979375_A2Up9.9573666984
GSE35957Up0.5757918367
GSE36640Down-2.3422107856
GSE54402Up1.7592415105
GSE9593Up0.0629825847
GSE43922Up7.2993760452
GSE24585Down-0.0852487549
GSE37065Up1.3907005974
GSE28863_A1Up0.1430259582
GSE28863_A2Down-0.0436907661
GSE28863_A3Down-0.0403704663
GSE28863_A4Down-0.0605334261
GSE48662Down-0.1113093867

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Name

Drug

Accession number

MinocyclineDB01017 APRD00547
AV411DB05066 -
VP025DB05133 -
681323DB05250 -
Gallium nitrateDB05260 -
SCIO-469DB05412 -
Etiprednol dicloacetateDB05442 -
VX-702DB05470 -
VX-765DB05507 -
HMPL-004DB05767 -
XOMA 052DB06062 -
CanakinumabDB06168 -
RilonaceptDB06372 -

  • MicroRNAs

    • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-204-5pMIMAT0000265MIRT005830MicroarrayFunctional MTI (Weak)21282569
hsa-miR-21-5pMIMAT0000076MIRT005951Luciferase reporter assay//Microarray//qRT-PCRFunctional MTI21131358
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    • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 47 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27899899Moreover, in the first passages, MSCs were capable to release IL1beta, IL6, and IL8, as well as to produce active MMPs allowing them to migrate
27812125Genes-toll-interacting protein (TOLLIP), mitogen-activated protein kinase 9 (MAPK9), interleukin-1beta (IL-1beta), interleukin-8 (IL-8), and chemokine (C-X-C motif) ligand 1 (CXCL1)-related to these two pathways were validated using western blotting
27547293Compared to their normobilirubinemic siblings, aged hyperbilirubinemic Gunn rats showed significantly smaller amounts of visceral fat, better glucose tolerance, and decreased serum levels of proinflammatory cytokines TNFalpha, IL-1beta, and IL-18
26477312In addition to the activation of oncogenes c-MYC and STAT3 in tumor cells, a number of cytokines and growth factors, such as IL1beta, IL6 and SPP1 (osteopontin, a key biomarker for PCa), were upregulated in NFATc1-induced PCa, establishing a tumorigenic microenvironment involving both NFATc1 positive and negative cells for prostate tumorigenesis
26388614Disc in flames: Roles of TNF-alpha and IL-1beta in intervertebral disc degeneration
26388614Inflammatory processes exacerbated by cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) are believed to be key mediators of disc degeneration and low back pain
26388614In this review, we describe the contributions of TNF-alpha and IL-1beta to changes seen during disc degeneration at both cellular and tissue level, as well as new evidence suggesting a link between infection of the spine and low back pain, and the emerging therapeutic modalities aimed at combating these processes
26341894Interleukin-1beta in intervertebral disk degeneration
26341894Interleukin-1 (IL-1) beta is the most important member of the IL-1 family, and has a strong pro-inflammatory activity by stimulating the secretion of multiple pro-inflammatory mediators
26341894IL-1beta is highly expressed in degenerative intervertebral disk (IVD) tissues and cells, and it has been shown to be involved in multiple pathological processes during disk degeneration, including inflammatory responses, matrix destruction, angiogenesis and innervation, cellular apoptosis, oxidative stress and cellular senescence
26341894However, inhibition of IL-1beta is found to promote extracellular matrix (ECM) repair and protect against disk regeneration
26105007Upon LPS treatment, SV cells also developed senescence-associated secretory phenotype (SASP), as demonstrated by the increased expression of TNFalpha, IL-1beta, IL-6, MCP-1, and VEGFalpha
26091153In vitro experiments used IL-1beta- or TNF-alpha-treated human annulus cells to test for autophagy-related gene expression
26091153In vitro data suggested a mechanism implicating a role of TNF-alpha and IL-1beta in disc autophagy
25989853However, pathological stabilization of the actin cytoskeleton increased LPS-induced release of IL-1beta and IL-18, which belong to an unconventional secretory pathway
25894557These senescent cells expressed proinflammatory cytokines such as interleukin-1beta (IL-1beta)
25894557The penises injected with the senescent cells expressed human IL-1beta and subsequently endogenous proinflammatory cytokines such as mouse IL-1beta and tumor necrosis factor-alpha
25792544In addition, the expression of cellular senescence features, such as the progressive rise in the enzymatic senescence-associated b-galactosidase (SA-b-gal) activity, IL6, IL1b, and TGFb expression, was observed throughout pituitary tumor development
25196711Molecule activity was assessed on reactive oxygen species (ROS) production, on superoxide dismutase (SOD) and catalase activities and, finally, on inflammatory factor production IL-6, IL-8 and IL-1beta
25186470Gene and protein expression of antioxidant proteins and autophagy-related proteins and changes in inflammatory mediators following treatment with interleukin-1beta were assessed
25087910We sought to explore whether glucosamine can activate autophagy in rat nucleus pulposus (NP) cells and protect cells treated with IL-1beta or hydrogen peroxide (H2 O2 )
25087910Autophagy in IL-1beta or H2 O2 -treated cells was increased by glucosamine
25087910Glucosamine attenuated the decrease of aggrecan and prevented the apoptosis of the NP cells induced by IL-1beta, whereas 3-MA partly reversed these effects
24979747Further investigation showed that ginsenoside Rg1 protected NSCs/NPCs (neural stem cells/progenitor cells) shown by increased level of SOX-2 expression; reduced astrocytes activation shown by decrease level of Aeg-1 expression; increased the hippocampal cell proliferation; enhanced the activity of the antioxidant enzymes GSH-Px (glutathione peroxidase) and SOD (Superoxide Dismutase); decreased the levels of IL-1beta, IL-6 and TNF-alpha, which are the proinflammatory cytokines; increased the telomere lengths and telomerase activity; and down-regulated the mRNA expression of cellular senescence associated genes p53, p21Cip1/Waf1 and p19Arf in the hippocampus of aged rats
24964749Inhibiting ERCC1 in chondrocytes under interleukin-1beta stimulation using small interfering RNA (siRNA) was also evaluated
24964749ERCC1 expression was decreased in OA cartilage and increased within 4 h of exposure to interleukin (IL)-1beta, but decreased after 12 h
24801508Measurement of secreted factors showed that E-CSC release larger amounts of proinflammatory cytokine IL1beta compared with D-CSC
24801508Using blocking antibodies, we verified that IL1beta hampers the paracrine protective action of E-CSC on cardiomyocyte viability
24801508IL1beta acts intracranially inducing IKKbeta signaling, a mechanism that via nuclear factor-kappaB upregulates the expression of IL1beta itself
24481487The levels of circulatory inflammatory markers, including interleukin (IL) IL-1beta, IL-6, tumor necrosis factor-alpha (TNF-alpha) and interferon (INF-gamma), are known to increase associated to aging
24481487The two-way ANOVA of pro-inflammatory cytokine levels demonstrated a significant exercise x caffeine interaction for IL-1beta (F (1, 16) = 9
24269635In cultured chondrocytes, IL-1beta and TNF-alpha suppressed FOXO1, while TGF-beta and PDGF increased FOXO1 and FOXO3 expression
24269635FOXO1 and FOXO3 phosphorylation was increased by IL-1beta, PDGF, bFGF, IGF-1, and the oxidant t-BHP
24198727In addition, both treatments induced the expression of a variety of cytokines, including interleukin-1beta (IL-1beta) and nerve growth factor (NGF)
24198727AdRas12V infection induced IL-1beta expression more significantly than H(2)O(2) treatment, whereas both treatments induced comparable mRNA and protein expression levels of NGF
24086293Human fibroblasts from four donors were cultured for 90 days in: 1) medium lacking ascorbic acid only, 2) 10 mM buthionine sulphoximine (BSO) (pro-oxidant), 3) 25 mM D-glucose, 4) 1 ng/ml IL1B and 5) 25 mM D-glucose+1 ng/ml IL1B
24086293Cultures treated with high glucose and BSO displayed a significantly lower growth rate, and cultures treated with IL1B showed a trend towards a higher growth rate, compared to the control [Glucose:0
24086293Telomere shortening with time was significantly accelerated in cultures treated with IL1B compared to the control [IL1B:-0
24086293The hastening of telomere shortening by IL1B was only in part attenuated after adjustment for the number of cell divisions [IL1B:-4
23952478Morin significantly decreased the production of tumor necrosis factor-alpha, interleukin-1beta, and interleukin-6 in the UVB-irradiated KSC
23864729Activation of the AIM2 inflammasome cleaves pro-interleukin (IL)-1beta and pro-IL-18 and promotes the secretion of IL-1beta and IL-18 proinflammatory cytokines
23611899For the next 9 days, the cells were cultured in chondrogenic medium containing 50% conditioned medium derived from C2C12 muscle cells or fibroblast control cells, and were subject to treatments of pro-inflammatory cytokines IL-1beta or TNFalpha
23611899RESULTS: Both IL-1beta and TNFalpha-induced strong expression of multiple MMPs and hypertrophic markers Runx2 and type X collagen
23272236To confirm selectivity of the SASP-RAP response, cells were treated with senescence-related and -unrelated stimuli (IL-1beta, LPS, TNF-alpha and TGF-beta), and induction of senescence markers and activity of SASP-RAP were evaluated in parallel
22454193METHODS: Isolated chondrocytes were cultured in medium containing interleukin-1 beta (IL-1beta) with or without Rg3
22454193RESULTS: Chondrocytes stimulated by IL-1beta showed increased MMP-1, MMP-3, and MMP-13 levels, whereas the expression of COL2A1 and ACAN decreased
22454193However, in cells co-treated with IL-1beta and Rg3, the levels of MMP-1 and MMP-13 were lower than in cells treated with IL-1beta alone, and COL2A1 and ACAN expression levels recovered from the low values seen when cultured only in the presence of IL-1beta
22454193Also, compared to vehicle-treated controls, IL-1beta stimulation alone resulted in an increased number of SA-beta-Gal-positive cells, while co-incubation with IL-1beta and Rg3 significantly suppressed the expression of this senescence marker
21680897Telomere disruption increased monocyte secretion of monocyte chemoattractant protein-1, IL-6, and IL-1beta and oxidative burst, similar to that seen in coronary artery disease patients, and lymphocyte secretion of IL-2 and reduced lymphocyte IL-10
21471287On sensing dsDNA, the IFI16 protein induces the expression of IFN-beta whereas the AIM2 protein forms an inflammasome, which promotes the secretion of IL-1beta
21471287Accordingly, increased constitutive levels of IFI16 and AIM2 proteins in ataxia telangiectasia mutated (ATM) HDFs were associated with the activation of the IFN signaling and increased levels of IL-1beta
21471287The IFN-beta treatment of the young HDFs, which induced the expression of IFI16 and AIM2 proteins, activated a DNA damage response and also increased basal levels of IL-1beta
21224216The changes of SIRT6, p21, and interleukin (IL)-1beta expression levels in HBEC, as well as type I collagen expression levels in fibroblasts, were evaluated
21224216TGF-beta-induced senescent HBEC secreted increased amounts of IL-1beta, which was sufficient to induce myofibroblast differentiation in fibroblasts
21098883The OA-related catabolic factor, IL-1beta induced marked downregulation of cellular activity, expression of a senescent biomarker, specific senescence-associated beta-galactosidase activity and shortening of the cellular lifespan in chondrocytes
20374325Chondrocytes were stimulated with or without IL-1beta (10 ng/mL) in the presence or absence of vascular endothelial growth factor, basic fibroblast growth factor or hepatocyte growth factor (20 ng/mL)
20374325IL-1beta significantly decreased the cellular replicative lifespan in chondrocytes
24281089Proinflammatory cytokines, such as tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma, as well as chemokines and prostaglandins, are synthesized by resident brain cells and lymphocytes invading the affected brain tissue
19584087We have identified a significantly altered cellular phenotype in response to chronic hypoxia as characterized by increased receptor-mediated apoptotic resistance, the induction of cellular senescence, increased invasion and the increased secretion of IL-1 beta, IL6, IL8 and TNFalpha cytokines
16508959This study was undertaken to investigate whether the catabolic factors oxidative stress and interleukin-1beta (IL-1beta) induce features of premature senescence of articular chondrocytes through up-regulation of caveolin 1 expression
16508959We studied whether IL-1beta and H2O2 induce caveolin 1 expression in OA chondrocytes and analyzed the relationship between cellular senescent phenotypes and caveolin 1 expression in human chondrocytes
16508959Both IL-1beta and H2O2 up-regulated caveolin 1 messenger RNA and protein levels, and both treatments induced marked expression of senescent phenotypes: altered cellular morphology, cell growth arrest, telomere erosion, and specific senescence-associated beta-galactosidase activity
16508959CONCLUSION: Our findings suggest that IL-1beta and oxidative stress induce features of premature senescence in OA chondrocytes, mediated, at least in part, by stress-induced caveolin 1 expression
16419088In the current study we examined long-term effects of antioxidants vitamin E and alpha-lipoic acid on cultured rat microglia with respect to proliferative ability, telomere length, telomerase activity, and interleukin-1beta (IL-1beta) production
16419088Production of IL-1beta was significantly decreased in vitamin E-treated microglia in vitro
15876845After culture in vitro, these cells shown increase susceptibility to undergoing spontaneous apoptosis, that is enhanced by IL-4 and prevented by IL-1beta or LPS
15685514Expression of p53, CD14/CD16, and intracellular cytokine production (interleukin-1beta [IL-1beta], IL-6, and IL-4) was evaluated by means of flow cytometry using specific antibodies
15685514RESULTS: Features of senescence were found in a subpopulation of mononuclear cells: (1) accelerated telomere shortening, (2) increased p53 expression, (3) CD14dim/CD16bright expression, and (4) cytokine overproduction (IL-1beta, IL-6, and IL-4)
15685514Finally, mononuclear cells from hemodialysis patients, but not controls, spontaneously produced the proinflammatory cytokines IL-1beta and IL-6
15621568In conclusion, the functional data identifying a difference in mortalin expression in IL-1beta stimulated islets between two rat strains and over-expression of mortalin in NIH3T3 cells associated with decreased viability suggests a functional role for mortalin in cytokine mediated beta cell destruction; however, the identified polymorphisms did not reveal any association in the presence of linkage disequilibrium of mortalin to T1DM in the Danish population
15388329Here, we show that in mouse embryonic fibroblasts (MEFs) culture in vitro, expression of an inflammatory cytokine, interleukin-1beta (IL-1beta) and its antagonist, IL-1 receptor antagonist (IL-1Ra) are induced by senescence
15388329Our results suggest that IL-1beta signaling pathway is involved in activation of p38 linked cellular senescence
10433392Enhancement of lipopolysaccharide-stimulated PGE2 and IL-1beta production in gingival fibroblast cells from old rats
10433392The levels of prostaglandin E2 (PGE2) and interleukin 1beta (IL-1beta) released into the cultured medium were measured by a specific radioimmunoassay
10433392LPS stimulated PGE2 and IL-1beta production in a dose-and time-dependent manner in rGF cells from both young and old rats was seen
10433392Production of PGE2 and IL-1beta by rGF cells from the old rats was higher than those from the young in response to LPS
10433392This greater ability from the older rGF cells to produce PGE2 and IL-1beta was due to higher mRNA levels of cyclooxygenase 2 and IL-1beta, respectively
10433392In contrast, cyclooxygenase-1 and IL-1beta converting enzyme gene mRNA levels remained unchanged
10433392Because LPS-stimulated PGE2 and IL-1beta production was enhanced by in vivo cellular aging, aging of GF may affect the severity of inflammation and bone resorption by producing a large amount of PGE2 and IL-1beta in response to bacterial infection
9722719Amounts of PGE2, interleukin (IL)-1 beta, IL-6, and plasminogen activator (PA) in conditioned media were measured
9722719LPS-stimulated PGE2, IL-1 beta, IL-6, and PA production was increased in "old" HGF compared to younger cells
9722719According to RT-PCR analysis, gene expression of COX-2, IL-1 beta, IL-6, and tissue type (t) PA was higher in old cells than in young cells
9722719Cyclic tension force to HPLF also stimulated phenotypic and gene expression of IL-1 beta, PGE2 (COX-2 gene) and tPA
9423715In further experimentation, media was supplemented with additional calf serum (20%, 30%, 40%, 50%) and growth factors (epidermal growth factor, basic fibroblast growth factor, interleukin-1 beta) in an attempt to stimulate growth
9423715This decreased growth can be stimulated by growth factors basic fibroblast growth factor, epidermal growth factor, and interleukin-1 beta
9255759Contribution of IL-1 beta to the enhancement of Campylobacter rectus lipopolysaccharide-stimulated PGE2 production in old gingival fibroblasts in vitro
9255759The LPS-stimulated IL-1 beta production in each old cell (corresponding to 57-67% of complete life-span) was increased (1
9255759The IL-1 beta mRNA synthesis in the presence of LPS in the old cells was higher than that in the young cells
9207769In vitro cellular aging stimulates interleukin-1 beta production in stretched human periodontal-ligament-derived cells
9207769Interleukin (IL)-1 beta is a key mediator involved in periodontal diseases, a potent stimulator of bone resorption
9207769To investigate the age-related changes in the biosynthetic capacity of IL-1 beta in PDL cells, we examined the effects of in vitro cellular aging with mechanical stress on IL-1 beta protein and gene expression by human PDL cells
9207769We found a two-fold increase in IL-1 beta production by old PDL cells subjected to mechanical tension compared with that by young PDL cells, although the constitutive levels of IL-1 beta were similar in both the young and old PDL cells
9042398We also treated early and late passage cells with agents that may modulate the process of cellular senescence: UV light, retinoic acid, and interleukin-1 beta
7561522Interleukin-1 beta (IL-1 beta) was found to be the strongest single activator in all types of fibroblasts examined
7561522In addition, lipopolysaccharide (LPS) was synergistic with IL-1 beta or tumor necrosis factor-alpha (TNF-alpha) in induction of nitric oxide synthesis
3264123Interleukin-1-beta gene expression in human monocytes and alveolar macrophages from normal subjects and patients with sarcoidosis
3264123To assess the ability of human alveolar macrophages to produce interleukin-1-beta (IL1-beta), we examined IL1-beta mRNA accumulation in autologous monocytes and alveolar macrophages from normal volunteers
3264123Escherichia coli lipopolysaccharide stimulation of monocytes induced rapid IL1-beta mRNA accumulation, reaching a maximum at 2 to 4 h and declining thereafter
3264123This difference could not be explained by differences in kinetics of IL1-beta gene expression between the 2 cell types, isolation techniques, or alveolar macrophage lidocaine exposure
3264123This suggests that differences in transcription of the IL1-beta gene exist between these 2 cell types
3264123To determine if this difference in the capacity to express the IL1-beta gene might be a function of cell maturity, monocytes were aged in vitro for 7 days
3264123After this culture period, monocytes had a marked decrease in the ability to accumulate IL1-beta mRNA, suggesting that cell aging may be one mechanism involved in producing these transcriptional differences
3264123Because IL1-beta has also been implicated in the inflammatory and fibrotic responses in pulmonary sarcoidosis, 4 patients with newly diagnosed sarcoidosis underwent bronchoalveolar lavage, and IL1-beta mRNA accumulation was compared in their alveolar macrophages and blood monocytes
3264123Comparing normal alveolar macrophages to those from patients with sarcoidosis showed no differences in the kinetics of IL1-beta mRNA expression or in the LPS-induced levels of IL1-beta mRNA accumulation
3264123In addition, augmented levels of IL1-beta transcript were not noted in unstimulated sarcoid alveolar macrophages
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