ライフサイエンスコーパス: IL-1 beta

1 IL-1 beta abundance was determined by enzyme-linked immu

2 IL-1 beta activated phosphatidylinositol (PI) 3-kinase,

3 IL-1 beta also induced cartilage proteoglycan degradatio

4 IL-1 beta and ATRA induced TG transamidation activity an

5 IL-1 beta and CDCA reduced CYP7A1 but induced c-Jun mess

6 IL-1 beta and TNF alpha stimulated the transcript (7-8-f

7 IL-1 beta antagonists or proteasome inhibitors might inc

8 IL-1 beta expression was elevated in lung macrophages ex

9 IL-1 beta expression was examined in lung macrophages ex

10 IL-1 beta greatly increased the levels of FGF-2 mRNA in

11 IL-1 beta has emerged as a prime candidate underlying th

12 IL-1 beta induced robust expression of COX-2 and PGE(2)

13 IL-1 beta initially induced nuclear accumulation of FGF-

14 IL-1 beta mRNA also increased after infection and IL-1 b

15 IL-1 beta release and cell permeability are suppressed b

16 IL-1 beta resulted in a decrease in HNF-4 alpha levels i

17 IL-1 beta significantly decreased glucose-stimulated ins

18 IL-1 beta stimulated the expression of C/EBP beta and -d

19 IL-1 beta treatment of cultured primary rat hepatocytes

20 IL-1 beta treatment of primary hepatocytes reduced Mrp2

21 IL-1 beta up-regulated GCLC expression (10 ng/ml IL-1 be

22 IL-1 beta, the most potent inducer of COX-2, also result

23 IL-1 beta-converting enzyme (ICE; caspase-1) is the intr

24 IL-1 beta-induced production of COX-2 protein and PGE(2)

25 IL-1 beta-mediated degradation of cartilage proteoglycan

26 ytokines transforming growth factor-beta(1), IL-1 beta, and IL-4 in the heart.

27 ytokines transforming growth factor-beta(1), IL-1 beta, and IL-4 in the hearts of IFN-gamma-deficient

28 ease of the proinflammatory cytokines IL-18, IL-1 beta, and IFN-gamma from total colon cultures.

29 , IFN-gamma-inducible protein-10, IL-1alpha, IL-1-beta, IL-1Ralpha, IL-18, IL-6, and IFN-gamma), or h

30 decreased when DCs were incubated with IL-4, IL-1 beta, TNF alpha, and an agonistic CD40 antibody (ma

31 ry cytokines and their mRNAs measured (IL-6, IL-1 beta, IL-8, and tumor necrosis factor alpha), IL-8

32 insulin secretion (control, 123.8 +/- 17.7; IL-1 beta, 40.2 +/- 3.9 microunits/ml insulin/islet).

33 te for neutralized IL-1 beta, and additional IL-1 beta did not compensate for neutralized IL-1 alpha,

34 98059) or p38 MAPK (SB203580) did not affect IL-1 beta-mediated suppression of Ntcp gene expression,

35 ight increase in COX-2 mRNA expression after IL-1 beta treatment.

36 s assessed (i.e., interleukin [IL]-1 alpha , IL-1 beta , IL-2, IL-4, IL-6, IL-10, interferon- gamma ,

37 cytokines interleukin-1 alpha (IL-1 alpha), IL-1 beta, and IL-6 or of the microglial marker F4/80 at

38 tor alpha, interleukin-1 alpha (IL-1 alpha), IL-1 beta, CCL5, IL-6, and KC.

39 se include interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-6, IL-8, and tumor necrosis factor alpha.

40 The concentrations of IL-1 alpha, IL-1 beta (precursor and mature forms), and IL-1 recepto

41 in-12 [IL-12], gamma interferon, IL-1 alpha, IL-1 beta), CC chemokines (CC chemokine ligand 3 [CCL3]/

42 Upregulation of IFN-gamma, IL-1 alpha, IL-1 beta, and IL-8 and increased severity of inflammato

43 Upregulation of IFN-gamma, IL-1 alpha, IL-1 beta, and IL-8 and marked hyperplasia of secondary

44 is, prompted the hypothesis that IL-1 alpha, IL-1 beta, and IL-RA may help regulate human IgG2 respon

45 ytokines regulated by NF-kappaB (IL-1 alpha, IL-1 beta, IL-10, and IFN-gamma).

46 feron (IFN-gamma), interleukin (IL)-1 alpha, IL-1 beta, IL-4, IL-6, IL-8, IL-10, and IL-12 p40 and hi

47 expression levels of TNF-alpha, IL-1 alpha, IL-1 beta, VEGF-A, VEGF-C, and VEGFR2.

48 imulated significant increases in TNF alpha, IL-1 beta, and IL-6 due to the absence of estrogen.

49 KO) mice produced lower levels of TNF-alpha, IL-1 beta, and IFN-gamma than did wild-type (WT) mice.

50 nterleukin-1 beta, and IFN-gamma (TNF-alpha, IL-1 beta, and IFN-gamma) function synergistically for i

51 ensitive bioassays to measure net TNF-alpha, IL-1 beta, and IL-6 activity.

52 of inflammatory mediators such as TNF-alpha, IL-1 beta, and IL-6, vs late stage infections, which are

53 MIP-1 beta, IL-8) and cytokines (TNF-alpha, IL-1 beta, IL-6) from human dendritic cells and macropha

54 to be dependent on the cytokines TNF-alpha, IL-1 beta, IL-6, and IFN-gamma, nor is it dependent on t

55 s inflammatory stimuli, including TNF-alpha, IL-1 beta, IL-6, and LPS.

56 pression of cytokines, IFN-gamma, TNF-alpha, IL-1 beta, IL-6, IL-4, IL-10, and chemokines, MIP-1, MIP

57 on of pro-inflammatory mediators, TNF-alpha, IL-1 beta, IL-6, MMP-2 and MMP-9 in HCECs exposed to hyp

58 that A beta-induced expression of TNF-alpha, IL-1 beta, MCP-1, IL-8, and MIP-1 beta was abrogated in

59 proinflammatory cytokines such as TNF-alpha, IL-1 beta, or other host factors.

60 Although IL-1 beta and RANTES mRNA could be detected in the splee

61 The results revealed an IL-1 beta-responsive element located between -2138 and -

62 s of IL-10 (P=.003), IFN-gamma (P=.007), and IL-1 beta (P=.05) than children with UM.

63 factors, and the inflammasome, caspase-1 and IL-1 beta were critical for the recruitment of microglia

64 s of MCP-1 following stimulation by IL-2 and IL-1 beta; RA FLS produced significantly more MCP-1 than

65 rane permeability, caspase-1 activation, and IL-1 beta release without cell cytotoxicity.

66 ts positively correlated with IL-1 alpha and IL-1 beta and with the proportions of Selenomonas, Prevo

67 IL-1 alpha and IL-1 beta appear to have critical and non-redundant role

68 IL-1 alpha and IL-1 beta are important inhibitors of hair growth in vit

69 eric symptoms, suggesting that TNF-alpha and IL-1 beta are not key mediators of diarrhea in human cry

70 NA viruses, is known to induce TNF-alpha and IL-1 beta in a variety of cells.

71 an either antibody alone, and IL-1 alpha and IL-1 beta in combination appeared to work additively in

72 g that dsRNA treatment induces TNF-alpha and IL-1 beta in human lung epithelial cells via two differe

73 CL-9, CCL-3, CCL-4, IFN-gamma, TNF-alpha and IL-1 beta in sIBM muscle compared to PM, DM and controls

74 eduction in lung and BAL fluid TNF-alpha and IL-1 beta protein and/or mRNA levels.

75 ctin expression in response to TNF-alpha and IL-1 beta was developed to measure the ability of aPDT t

76 um levels of tumor necrosis factor-alpha and IL-1 beta were significantly depressed in M40401-treated

77 duced expression of cytokines (TNF-alpha and IL-1 beta) and chemokines (MCP-1, IL-8, and MIP-1 beta)

78 sibly through an inhibition of TNF-alpha and IL-1 beta, which are potent neutrophil recruiting mediat

79 inflammatory cytokines such as TNF-alpha and IL-1 beta.

80 ecrease in local production of TNF-alpha and IL-1 beta.

81 Increased expression of iNOS, TNF-alpha, and IL-1 beta were observed in the affected white matter, co

82 mRNA expression of cytokines (TNF-alpha, and IL-1 beta) and chemokines (monocyte chemoattractant prot

83 macrophage inflammatory protein 1 beta, and IL-1 beta levels were significantly upregulated in the i

84 Our observations that blebbing and IL-1 beta release are dissociable suggest these events o

85 ammatory cytokines TNF-alpha, IFN-gamma, and IL-1 beta.

86 beta mRNA also increased after infection and IL-1 beta protein was synthesized, but it remained intra

87 mined as release of the CXC chemokine KC and IL-1 beta, was inhibited by the more selective MC3-R ago

88 appa B alpha degradation elicited by LPS and IL-1 beta but not that stimulated by tumor necrosis fact

89 3-kinase is an important mediator of LPS and IL-1 beta signaling leading to NF-kappa B activation in

90 d Akt kinase activity in response to LPS and IL-1 beta.

91 appa B luciferase activity evoked by LPS and IL-1 beta.

92 the exogenous proinflammatory agents LPS and IL-1 beta.

93 g TNF, phorbol ester, okadaic acid, LPS, and IL-1 beta.

94 cate that FADD negatively regulates LPS- and IL-1 beta-induced NF-kappa B activation and that this re

95 Mrp2 down-regulation and IL-1 beta up-regulation were observed in liver after BDL

96 re, combinations of anti-IL-1 alpha and anti-IL-1 beta were more inhibitory than either antibody alon

97 Both inflammatory cytokines such as IL-1 beta and bacterial constituents may be responsible

98 Because IL-1 beta function involves nuclear factor kappa B (NF-k

99 rences, the induction of interleukin-1 beta (IL-1 beta) and intracellular adhesion molecule-1 was mod

100 ed significant levels of interleukin-1 beta (IL-1 beta) but not endothelin-1 or tumor necrosis factor

101 We report that interleukin-1 beta (IL-1 beta) elicits PECAM-1-dependent transmigration that

102 opolysaccharide (LPS) or interleukin-1 beta (IL-1 beta) for 0, 2, 4, 6, or 8 h.

103 ro-inflammatory mediator interleukin-1 beta (IL-1 beta) in their joints, suggesting inefficient activ

104 Interleukin-1 beta (IL-1 beta) is a cytokine and a member of the beta-trefoi

105 Interleukin-1 beta (IL-1 beta) is a cytokine whose levels are increased in v

106 Interleukin 1 beta (IL-1 beta) is a key cytokine in the inflammatory respons

107 proinflammatory cytokine interleukin-1 beta (IL-1 beta) mediates COX-2 expression in HT-29 human colo

108 activity in response to interleukin-1 beta (IL-1 beta) or lipopolysaccharide (LPS) + interferon-gamm

109 bovis BCG vaccination on interleukin-1 beta (IL-1 beta) or regulated-upon-activation, normally T-cell

110 Significant variation in interleukin-1 beta (IL-1 beta) protein secretion between subjects has been o

111 xycholic acid (CDCA) and interleukin-1 beta (IL-1 beta) regulation of human CYP7A1 gene expression vi

112 lpha:RXR alpha, and that interleukin 1 beta (IL-1 beta) repressed promoter activity via this element.

113 in treatment of rats and interleukin-1 beta (IL-1 beta) treatment of liver-derived HepG2 cells leads

114 actor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-6 from human peripheral blood mononuc

115 lpha receptors I and II; interleukin 1 beta (IL-1 beta), IL-1 beta receptor antagonist, and soluble I

116 ndent antigen and normal interleukin-1 beta (IL-1 beta), IL-6, and TNF production after LPS treatment

117 Levels of interleukin-1 beta (IL-1 beta), IL-6, IL-8, and tumor necrosis factor alpha

118 interferon (IFN-alpha), interleukin-1 beta (IL-1 beta), IL-8, IL-12, MIP-1 alpha, and RANTES but not

119 pression is repressed by interleukin 1 beta (IL-1 beta).

120 opolysaccharide (LPS) or interleukin-1 beta (IL-1 beta).

121 er it is up-regulated by interleukin-1 beta (IL-1 beta).

122 e band was identified as interleukin-1 beta (IL-1 beta).

123 actor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta-6, gamma interferon (IFN-gamma), MIP-1 alpha M

124 ristate 13-acetate (PMA), interleukin-1 beta(IL-1 beta), or lipopolysaccharide (LPS).

125 rs I and II; interleukin 1 beta (IL-1 beta), IL-1 beta receptor antagonist, and soluble IL-1 receptor

126 he following: 1) a novel correlation between IL-1 beta secretion and the release of the MHC-II membra

127 ve JNK expression plasmid completely blocked IL-1 beta-mediated suppression.

128 e stability of COX-2 mRNA was not altered by IL-1 beta treatment.

129 ucose-stimulated insulin secretion caused by IL-1 beta.

130 olved in activation of NF-kappa B complex by IL-1 beta stimulation.

131 ctivation and cytokine expression induced by IL-1 beta and lipopolysaccharide.

132 esistant to NF-kappa B activation induced by IL-1 beta.

133 the repression of NF-kappa Bp50 induction by IL-1 beta.

134 s and collagen type II that are inhibited by IL-1 beta.

135 0 protein production in conditioned media by IL-1 beta and TNF-alpha.

136 ProIL-1 beta processing by IL-1 beta-converting enzyme (ICE) and the subsequent rel

137 tion in pathologic calcification promoted by IL-1 beta and ATRA.

138 by which CD-RAP expression is suppressed by IL-1 beta, deletion constructs of the mouse CD-RAP promo

139 and -11 were dose dependently upregulated by IL-1 beta and TNF-alpha, whereas MMP-8 and -14 and tissu

140 nflammatory colonic and plasma IL-6, colonic IL-1 beta and higher levels of colonic IL-17 when compar

141 In conclusion, IL-1 beta and CDCA inhibit HNF4 alpha but induce c-Jun,

142 these cells to the proinflammatory cytokine IL-1 beta increased the expression of the NK-1R gene at

143 inflammatory molecules, such as the cytokine IL-1 beta, may have beneficial and protective effects.

144 ated with the release of all four cytokines (IL-1 beta [R(2) = 0.382; P = 0.006], IL-6 [R(2) = 0.393;

145 red the levels of proinflammatory cytokines (IL-1 beta, TNF-alpha, and S100B), the chemokine CCL2, mi

146 tiate that the observed NF-kappa B-dependent IL-1 beta induction of the human NK-1R gene is regulated

147 vities of IL-1 beta were further determined; IL-1 beta altered the shape of CECs from polygonal to fi

148 scription, perhaps as a result of diminished IL-1 beta, IL-6, and IFN-gamma levels.

149 ha ligands (clofibrate and WY14643) enhanced IL-1 beta-induced COX-2 expression in human astrocytes a

150 bodies that contain exosomes with entrapped IL-1 beta, caspase-1, and other inflammasome components.

151 olunteers expressed TNF-alpha; 14% expressed IL-1 beta.

152 Following IL-1 beta or TGF-beta(1) stimulation, HMMP13 mRNA levels

153 little effect on the kinetics of folding for IL-1 beta.

154 LISA analysis showed that protein levels for IL-1 beta, macrophage-inflammatory protein 2, and macrop

155 tion was essential for TNF-alpha but not for IL-1 beta expression.

156 lts demonstrate a possible adaptive role for IL-1 beta-driven neuroinflammation in AD and may help ex

157 interleukin-6 (IL-6), and IL-8; and weak for IL-1 beta and monocyte chemotactic peptide 1 (MCP-1).

158 The total amount and concentration of GCF IL-1 beta, IL-4, IL-10, and TNF-alpha were similar in RA

159 How IL-1 beta signaling leads to reduced RXR:RAR nuclear bin

160 , including interleukin (IL)-1 alpha (IL1A), IL-1 beta (IL1B), IL8, RANTES, colony stimulating factor

161 PDTC, resulted in dose-dependent decrease in IL-1 beta-induced COX-2 gene expression and PG productio

162 ne contribute to the observed differences in IL-1 beta protein secretion.

163 anscription of NF-kappa B-dependent genes in IL-1 beta-induced rheumatoid arthritis-derived synovial

164 h is atypical for destabilizing mutations in IL-1 beta.

165 tuberculosis showed 75 to 90% reductions in IL-1 beta expression and 25 to 60% reductions in RANTES

166 atment potently and functionally inactivated IL-1 beta and TNF-alpha.

167 sion of proinflammatory cytokines, including IL-1 beta, macrophage-inflammatory protein-2, and TNF-al

168 vealed that inflammatory mediators including IL-1 beta co-localized to beta-amyloid depositions withi

169 several key inflammatory mediators including IL-1 beta, IL-8, and tumor necrosis factor-alpha are up-

170 ibitors Fasudil and Y-27632, but ATP-induced IL-1 beta release was unaffected.

171 ibute to observed differences in LPS-induced IL-1 beta protein secretion.

172 ated with a 2-3-fold increase in LPS-induced IL-1 beta protein secretion.

173 h a panel of melanocortin peptides inhibited IL-1 beta release and PMN accumulation elicited by urate

174 umin, but not PD98059 or SB203580, inhibited IL-1 beta-mediated suppression of nuclear RXR:RAR bindin

175 n astrocytes and microglia, while inhibiting IL-1 beta plus IFN-gamma induction of iNOS in astrocytes

176 EP4(-/-) animals produced significantly less IL-1 beta and IL-6 than control samples.

177 t untreated endothelial cells express little IL-1 beta or TNF-alpha, but incubation with TGF-beta res

178 produced no detectable IL-18, fourfold lower IL-1 beta, and 20-30% less IL-1 alpha than macrophages f

179 In contrast, LPS, IL-1 beta, and PMA each upregulated IL-8.

180 ema, pulmonary neutrophil accumulation, lung IL-1 beta, macrophage-inflammatory protein-2, and TNF-al

181 2 mRNA in a time- and dose-dependent manner; IL-1 beta stimulated expression of all isoforms of FGF-2

182 ofluorescent staining for IL-1 alpha, mature IL-1 beta, and IL-1Ra was observed in a significantly gr

183 , the concentration of IL-1 alpha and mature IL-1 beta in the tear fluid was increased, and the conce

184 mmatory forms of IL-1 (IL-1 alpha and mature IL-1 beta) and a decrease in the biologically inactive p

185 < 0.01 for IL-1 alpha, P < 0.009 for mature IL-1 beta, and P < 0.05 for IL-1Ra).

186 e (ICE) and the subsequent release of mature IL-1 beta are highly regulated events in the monocyte/ma

187 t initiates cleavage and secretion of mature IL-1 beta.

188 hondrocytes with the osteoarthritis mediator IL-1 beta, with the all-trans form of retinoic acid (ATR

189 (CNV) was induced by suture or micropellet (IL-1 beta, VEGF-A) placement.

190 ence of 100 units/ml IFN-gamma plus 10 ng/ml IL-1 beta for 48 h.

191 beta up-regulated GCLC expression (10 ng/ml IL-1 beta, 3.76 +/- 0.86; 100 ng/ml IL-1 beta, 4.22 +/-

192 10 ng/ml IL-1 beta, 3.76 +/- 0.86; 100 ng/ml IL-1 beta, 4.22 +/- 0.68-fold control) via the p38 form

193 sed reactive oxygen species levels (10 ng/ml IL-1 beta, 5.41 +/- 1.8-fold control).

194 H/GSSG ratio (control, 7.1 +/- 0.1; 10 ng/ml IL-1 beta, 8.0 +/- 0.5; 100 ng/ml IL-1 beta, 8.2 +/- 0.5

195 ; 10 ng/ml IL-1 beta, 8.0 +/- 0.5; 100 ng/ml IL-1 beta, 8.2 +/- 0.5-fold control; p < 0.05).

196 L-1 alpha did not compensate for neutralized IL-1 beta, and additional IL-1 beta did not compensate f

197 Dexamethasone, neutralizing IL-1 beta antibody, or the selective COX-2 inhibitor, SC

198 dose-dependent manner, whereas neutralizing IL-1 beta antibody, neutralizing antibody to FGF-2, and

199 nstitute the major pathways for nonclassical IL-1 beta secretion from ATP-stimulated murine macrophag

200 sociated with induction of TNF-alpha but not IL-1 beta expression.

201 sRNA-induced elevations in TNF-alpha but not IL-1 beta mRNA in epithelial cells.

202 B) signaling pathways blocked the ability of IL-1 beta to induce COX-2 mRNA.

203 to FGF-2, and LY294002 blocked the action of IL-1 beta.

204 ivity of MMP-9, a physiological activator of IL-1 beta, was significantly elevated in the tear fluid

205 Biological activities of IL-1 beta were further determined; IL-1 beta altered the

206 LY294002 hampered the induction activity of IL-1 beta.

207 in conjunction with biochemical analyses of IL-1 beta release.

208 V had significantly higher concentrations of IL-1 beta in vaginal wash samples than did women with no

209 d MHC-II; and 3) mechanistic dissociation of IL-1 beta export from either secretory lysosome exocytos

210 The effect of IL-1 beta and TNF alpha on the expression and secretion

211 c inhibitor blocked the inhibitory effect of IL-1 beta on HNF4 alpha expression and CYP7A1 reporter a

212 B was inhibited, the antiapoptotic effect of IL-1 beta was partially reversed, suggesting that NF-kap

213 he islet and prevents the adverse effects of IL-1 beta on glucose-induced insulin secretion, islets w

214 ts the beta cell from the adverse effects of IL-1 beta.

215 (JNK), completely ameliorated the effects of IL-1 beta.

216 ase-1 in triggering the cotemporal export of IL-1 beta and MHC-II; and 3) mechanistic dissociation of

217 optotic cells or FBS, elicited expression of IL-1 beta by NOD macrophages is markedly reduced compare

218 An interesting feature in the folding of IL-1 beta, shared with some other members of the same to

219 t induce TNF-alpha and was a weak inducer of IL-1 beta, IL-6, macrophage inflammatory protein 1 alpha

220 fering RNA did not limit NO-np inhibition of IL-1 beta secretion from monocytes, and neither TNF-alph

221 ells are treated with TGF-beta and levels of IL-1 beta and TNF-alpha determined.

222 lpha expression but induces normal levels of IL-1 beta, TNF-alpha, and IFN-gamma, causes greatly redu

223 compensated for by the endogenous levels of IL-1 beta, TNF-alpha, or IFN-gamma that are produced in

224 with high IgG2 levels had elevated levels of IL-1 beta.

225 Our findings suggest an alternative model of IL-1 beta release that may involve the P2X7R-induced for

226 in which local hippocampal overexpression of IL-1 beta in an Alzheimer disease (AD) transgenic mouse

227 ular protease that cleaves the precursors of IL-1 beta and IL-18 into active cytokines.

228 atory caspase-1, which cleaves precursors of IL-1 beta and IL-18, were protected against ischemic acu

229 The presence of IL-1 beta in vaginal wash samples was associated with >3

230 e findings show that caspase-1 processing of IL-1 beta and IL-18 is not absolutely required for media

231 The release of IL-1 beta is a tightly controlled process that requires

232 monocytes leads to maturation and release of IL-1 beta via the P2X(7) receptor.

233 sma membrane organization and the release of IL-1 beta, we generated time-lapse movies of ATP-stimula

234 ity) and simultaneously initiates release of IL-1 beta.

235 eptor NALP3, which results in the release of IL-1 beta.

236 e administration of LPS may be the result of IL-1 beta-induced degradation, and likely contributes to

237 plasma membrane morphology, and secretion of IL-1 beta from LPS-primed macrophages.

238 or association with LPS-induced secretion of IL-1 beta protein as measured by an ex vivo blood stimul

239 ulation of ICE activation and suppression of IL-1 beta processing and release.

240 tinguish the role of IL-1 alpha from that of IL-1 beta during this process.

241 t is characterized by the underexpression of IL-1 beta and multiple other cytokines.

242 5 seconds), we made ten sequence variants of IL-1 beta (L10A, T9Q, T9G, C8S, C8A, N7G, N7D, L6A, R4P,

243 APPswe/PS1dE9 mouse model of AD, 4 weeks of IL-1 beta overexpression led to a reduction in amyloid p

244 hat BCG vaccination has a positive effect on IL-1 beta and RANTES mRNA expression by host cells in a

245 Similarly, a milder effect of ETA on IL-1 beta and IL-18 was observed for IRF-1 KO than for W

246 udying the effects of isoprenoid shortage on IL-1 beta generation, we identified a new inflammasome a

247 ATP concentrations > or = 3 mM, but optimal IL-1 beta release occurred at 1 mM ATP.

248 or with IL-1RA or neutralizing IL-1 alpha or IL-1 beta with specific antibody dramatically suppressed

249 macrophage inflammatory protein 1 alpha, or IL-1 beta.

250 bodies or recombinant IL-1RA, IL-1 alpha, or IL-1 beta.

251 d significantly suppressed suture-induced or IL-1 beta-induced hemangiogenesis (HA) but not lymphangi

252 tion of NF-kappa B elicited by either LPS or IL-1 beta.

253 inocytes appeared to be unaffected by LPS or IL-1 beta.

254 homology to MyD88, failed to inhibit LPS- or IL-1 beta-induced Akt activity.

255 but did not effect either the spontaneous or IL-1 beta-induced secretion of MCP-1.

256 lysis using probes generated from guinea pig IL-1 beta or RANTES cDNA.

257 mal quantities of the leaderless polypeptide IL-1 beta, but sequential treatment of wild-type, but no

258 ion was upregulated as early as 2 hours post IL-1 beta challenge and was accompanied by a sustained P

259 n the concentration of IL-1 alpha, precursor IL-1 beta, and IL-1Ra in reflex tear fluid, indicating t

260 rease in the biologically inactive precursor IL-1 beta in tear fluid.

261 ncreased, and the concentration of precursor IL-1 beta was decreased in patients with MGD (P < 0.05,

262 0.17, P < 0.02) and the mature-to-precursor IL-1 beta ratio (r(2) = 0.46, P < 0.001).

263 face may be one mechanism by which precursor IL-1 beta is cleaved to the mature, biologically active

264 In response to ATP, however, pro-IL-1 beta produced by the P2X(7)R(-/-) cells is not exte

265 uires induced synthesis of the precursor pro-IL-1 beta and a second stimulus that initiates cleavage

266 lain the rapid export of caspase-1-processed IL-1 beta from monocytes/macrophages in response to acti

267 eficient mice had diminished proinflammatory IL-1 beta , IL-13, and IL-33 chemokines production, whil

268 We conclude that endogenous LL37 may promote IL-1 beta processing and release via direct activation o

269 h ATP as a second stimulus potently promotes IL-1 beta maturation and release via P2X(7) receptor act

270 terleukin (IL)-18, a member of the pyrogenic IL-1 beta family.

271 or longer, limiting the activity of soluble IL-1 beta and TNF-alpha in the lungs at the onset of ARD

272 tion of these mechanisms to P2X7R-stimulated IL-1 beta secretion in primary bone marrow-derived macro

273 scribe a transgenic mouse model of sustained IL-1 beta overexpression that was capable of driving rob

274 These data demonstrate that IL-1 beta induces COX-2 expression in HT-29 cells throug

275 This study demonstrated that IL-1 beta and TNF-alpha upregulate collagenases (MMP-1,

276 assay on nuclear extracts demonstrated that IL-1 beta induced NF-kappa B DNA binding activity in HT-

277 These novel findings indicate that IL-1 beta, which is rapidly induced in response to T. cr

278 oprecipitation and ChIP assays revealed that IL-1 beta and CDCA reduced HNF4 alpha bound to the CYP7A

279 These observations suggest that IL-1 beta takes part in endothelial to mesenchymal trans

280 The IL-1 beta mRNA levels peaked as soon as 1 h after PPD st

281 COX-2 inhibitor, SC-236, attenuated both the IL-1 beta-induced PGE(2) production and cartilage proteo

282 Furthermore, the IL-1 beta pathway was essential for the microglial synth

283 and -delta may play an important role in the IL-1 beta-induced repression of cartilage-specific prote

284 However, when the IL-1 beta-dependent induction of NF-kappa B was inhibite

285 This IL-1 beta-induced decrease was likely caused by degradat

286 Exposure of these cells to IL-1 beta or overexpression of NF-kappa B cDNAs resulted

287 In human myotubes, exposure to IL-1 beta caused upregulation of APP with subsequent int

288 greatly stimulated after a 5-min exposure to IL-1 beta.

289 P motif abolished the inhibitory response to IL-1 beta.

290 NF-kappaB nuclear translocation, IL-1 beta and TNF-alpha gene expression, and protein con

291 hages was determined using recombinant trout IL-1 beta, where a clear induction was apparent by 2 h a

292 a in primary sinus epithelial cells, whereas IL-1 beta, IL-4, IL-13, and IL-17 did not influence IL-3

293 -2-produced PGE(2) is one mechanism by which IL-1 beta modulates cartilage proteoglycan degradation i

294 Treatment of HT-29 cells with IL-1 beta induced expression of COX-2 mRNA and protein i

295 RA- and OA-derived synovial fibroblasts with IL-1 beta and TNF alpha further suggests that the expres

296 l epithelial cell cultures were treated with IL-1 beta or TNF-alpha, with or without their correspond

297 human corneal epithelial cells treated with IL-1 beta, TNF-alpha, and doxycycline, a medication used

298 oplasty and cultured ex vivo with or without IL-1 beta and COX inhibitors.

299 nto rat chondrocytes treated with or without IL-1 beta.

300 ature of this slow step in the folding of WT IL-1 beta (tau(1)=45 seconds), we made ten sequence vari