ライフサイエンスコーパス: IL-1 alpha

1 IL-1 alpha and IL-1 beta appear to have critical and non

2 IL-1 alpha and IL-1 beta are important inhibitors of hai

3 IL-1 alpha and IL-1 beta bind to receptors termed the ty

4 IL-1 alpha and IL-1 beta proteins were elevated (P < 0.0

5 IL-1 alpha production by PBMC from dialyzers reprocessed

6 crease in the proinflammatory forms of IL-1 (IL-1 alpha and mature IL-1 beta) and a decrease in the b

7 e MMPs processed the second isoform of IL-1, IL-1 alpha.

8 monoclonal antibodies or recombinant IL-1RA, IL-1 alpha, or IL-1 beta.

9 rine cytokines such as interleukin-6 (IL-6), IL-1 alpha or beta, TGF-alpha, lymphotoxin, and TNF alph

10 Additionally IL-1 alpha did not compensate for neutralized IL-1 beta,

11 samples with neutralizing antibodies against IL-1 alpha but not against IL-1 beta.

12 CO2 for 24 h, and total interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-alpha (TNF alpha)

13 with recombinant human interleukin-1 alpha (IL-1 alpha) for up to 4 weeks.

14 d in murine models that interleukin 1 alpha (IL-1 alpha) induces acute hemorrhagic necrosis, microvas

15 Interleukin 1 alpha (IL-1 alpha) is a pleiotropic cytokine involved in the im

16 ctor alpha (TNF-alpha), interleukin-1 alpha (IL-1 alpha) or IL-1 beta (13-23 micrograms/kg) into endo

17 or by stimulation with interleukin-1 alpha (IL-1 alpha) or phorbol 12-tetradecanoate 13-acetate (TPA

18 oncentrations of either interleukin-1 alpha (IL-1 alpha) or tumor-necrosis factor-alpha (TNF-alpha).

19 ro and in vivo and that interleukin-1 alpha (IL-1 alpha) potentiates the cytotoxicity of certain clin

20 antagonist (IL-1Ra) or interleukin-1 alpha (IL-1 alpha) production was measured by a specific non-cr

21 S-induced TNF-alpha and interleukin-1 alpha (IL-1 alpha) release, thereby preventing endotoxic death.

22 edium was identified as interleukin-1 alpha (IL-1 alpha), and a secondary stimulator was characterize

23 lation of the cytokines interleukin-1 alpha (IL-1 alpha), IL-1 beta, and IL-6 or of the microglial ma

24 necrosis factor alpha, interleukin-1 alpha (IL-1 alpha), IL-1 beta, CCL5, IL-6, and KC.

25 at day 4 and levels of interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-2, IL-6, G-CSF, and tumor nec

26 These include interleukin-1 alpha (IL-1 alpha), IL-1 beta, IL-6, IL-8, and tumor necrosis f

27 on, the upregulation of interleukin-1 alpha (IL-1 alpha), IL-3, and tumor necrosis factor alpha cytok

28 r alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha), whereas on human dermal microvascular EC (H

29 pidermal mRNA levels of interleukin-1 alpha (IL-1 alpha).

30 a one (TGF-beta 1) or interleukin-one alpha (IL-1 alpha) enhanced the secretion of MCP-1 by the cells

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

32 e NF-kappa B sites appears to function as an IL-1 alpha-mediated transcriptional repressor within HDM

33 e inhibitory than either antibody alone, and IL-1 alpha and IL-1 beta in combination appeared to work

34 Both TNF-alpha and IL-1 alpha were present in CCCM and MCM but not EC-condi

35 ing the cytokines TGF-beta 1, TNF-alpha, and IL-1 alpha.

36 n IRF-1 activation but did inhibit basal and IL-1 alpha-stimulated NF-kappa B activation.

37 l factor (SCF), granulocyte CSF (G-CSF), and IL-1 alpha).

38 oting the survival of FL-, SCF-, G-CSF-, and IL-1 alpha-stimulated Lin-Sca-1+ progenitors, FL was mor

39 metry to confirm that IL-8R beta (CXCR2) and IL-1 alpha were significantly down-regulated during PMN

40 12/23p40), gamma interferon (IFN-gamma), and IL-1 alpha; increased neutrophil respiratory burst; and,

41 d with 75 and 13% in the presence of SCF and IL-1 alpha, respectively.

42 Both anti-IL-1 alpha and the IL-1 receptor antagonist resulted in

43 Addition of neutralizing anti-IL-1 alpha Abs to fibroblast cultures did not diminish b

44 Furthermore, combinations of anti-IL-1 alpha and anti-IL-1 beta were more inhibitory than

45 due increased intracellular camptothecin as IL-1 alpha failed to effect cellular uptake of camptothe

46 that cancer cell-derived cytokines, such as IL-1 alpha, induce cachexia by affecting leptin-dependen

47 of the interleukin-1 (IL-1) family, such as IL-1 alpha/beta and IL-18, have important functions in h

48 The presence of functional, cell-associated IL-1 alpha activity in infected cells was confirmed, fol

49 ide evidence that activation of an autocrine IL-1 alpha feedback loop is an important mechanism by wh

50 imicked SDF-1 alpha induction of NF-kappa B, IL-1 alpha/beta, and RANTES, as well as cell death; neut

51 mmatory cytokines (interleukin-1 alpha/beta [IL-1 alpha/beta], IL-18, gamma interferon, IL-6, and mac

52 e was a less than twofold difference between IL-1 alpha and TNF-alpha in their capacity to induce GRO

53 e activity in response to cross-talk between IL-1 alpha-expressing cancer cells and fibroblasts.

54 Blocking IL-1 alpha activity prevented both constitutive and stim

55 Both IL-1 alpha and IL-1 beta lack an N terminus secretory se

56 Both IL-1 alpha and TNF-alpha induced significant levels of G

57 that ATP stimulates externalization of both IL-1 alpha and IL-1 beta.

58 Induction of ICAM-1 expression by IL-1 alpha and VCAM-1 expression by IFN-gamma was attenu

59 hways of keratinocyte activation mediated by IL-1 alpha in vivo, and suggest that level of expression

60 hesion molecule-1 (CD31), P-selectin (CD62), IL-1 alpha, IL-16, and granulocyte chemoattractant prote

61 1:1000 dilution of the bacterial challenge, IL-1 alpha production by PBMC harvested from the blood c

62 We conclude that constitutive IL-1 alpha expression rendered FVB mice completely resis

63 ratum corneum attached to the tape contained IL-1 alpha.

64 This repressor region conveys IL-1 alpha-dependent, but not TNF alpha-dependent, inhib

65 expression of IFN-gamma, TNF-alpha, GM-CSF, IL-1 alpha, IL-2, IL-6, IL-10, and IL-12 p40.

66 The proinflammatory cytokines IL-1 alpha, IL-1 beta, IL-6, and TNF-alpha are produced

67 expression of the bone-resorptive cytokines IL-1 alpha and TNF-alpha was also investigated.

68 we report that other inflammatory cytokines (IL-1 alpha, IL-1 beta, and IL-6) are also neuroprotectiv

69 ins of 33% released 66 +/- 9% of cytoplasmic IL-1 alpha over 1 h (p < 0.001).

70 In response to Ad, macrophage-derived IL-1 alpha triggered IL-1RI-dependent production of a de

71 allenging the dialysate with 1:100 dilution, IL-1 alpha production by PBMC harvested from the blood c

72 Exposure to keratocytes to either IL-1 alpha or TNF-alpha resulted in > 100-fold increases

73 We used immunohistochemistry to examine IL-1 alpha expression in hairless mouse skin under basal

74 ed from the uninjured cornea did not express IL-1 alpha.

75 growth factor (TGF)-beta, and Steel factor, IL-1 alpha-induced release of IL-6 and G-CSF is signific

76 Within the IL-1 family, IL-1 alpha/beta, IL-1Ra, and IL-18 have been matched to

77 neal fluorescein staining and the tear fluid IL-1 alpha concentration (r(2) = 0.17, P < 0.02) and the

78 than in those from normal eyes (P < 0.01 for IL-1 alpha, P < 0.009 for mature IL-1 beta, and P < 0.05

79 -1 alpha, decreased basal immunostaining for IL-1 alpha and blunted the increase in IL-1 alpha usuall

80 mice were observed in circulating levels for IL-1 alpha, IL-6, or TNF-alpha after the systemic admini

81 s (100-500 U/ml for IL-6 and 50-200 U/ml for IL-1 alpha+beta) were also carried out to investigate th

82 nstrate a distinct and unrecognized role for IL-1 alpha in inducing intestinal inflammation that cann

83 ogen, we have identified a specific role for IL-1 alpha in inducing pathologic inflammation during ba

84 th mechanisms are consistent with a role for IL-1 alpha in the regulation of proinflammatory and home

85 ination and immunohistochemical staining for IL-1 alpha dna TNF-alpha.

86 Positive immunofluorescent staining for IL-1 alpha, mature IL-1 beta, and IL-1Ra was observed in

87 Nitrite production from IL-1 alpha/IFN-gamma was sensitive to the nitric oxide s

88 nificantly inhibited nitrite production from IL-1 alpha/IFN-gamma-treated, tumor-derived endothelial

89 Upregulation of IFN-gamma, IL-1 alpha, IL-1 beta, and IL-8 and increased severity o

90 Upregulation of IFN-gamma, IL-1 alpha, IL-1 beta, and IL-8 and marked hyperplasia o

91 However, IL-1 alpha-stimulated cells produced > 10 times more GRO

92 Thus, these data identify IL-1 alpha-IL-1RI as a key pathway allowing for the acti

93 f tissue factor expression, thus implicating IL-1 alpha in autocrine cell stimulation.

94 Since the increase in IL-1 alpha immunostaining after acute barrier abrogation

95 g for IL-1 alpha and blunted the increase in IL-1 alpha usually seen following barrier disruption.

96 f the cells had previously been incubated in IL-1 alpha, although there appears to be a threshold con

97 lf-life of the GRO alpha mRNA synthesized in IL-1 alpha-stimulated cells was > or = 9 hours.

98 The cytokines assessed included IL-1 alpha, IL-1 beta, IL-1ra, IL-6, IL-8, IL-12, IL-13,

99 r a wider range of cytokines, also including IL-1 alpha and IL-1 beta.

100 uirement for additional cofactors, including IL-1 alpha and TNF-alpha, which were provided by spleen

101 Furthermore, EGF has been shown to increase IL-1 alpha, IL-1 beta, IL-6 mRNA and protein levels in h

102 formed, epidermal pool, as well as increased IL-1 alpha synthesis; both mechanisms are consistent wit

103 x vivo at 4 degrees C, resulted in increased IL-1 alpha immunostaining within the upper nucleated epi

104 ore, a bacterial mutant that does not induce IL-1 alpha expression but induces normal levels of IL-1

105 Interestingly, IL-1 alpha expression alone was not sufficient for metas

106 s (interleukin-12 [IL-12], gamma interferon, IL-1 alpha, IL-1 beta), CC chemokines (CC chemokine liga

107 ients express higher levels of intracellular IL-1 alpha than fibroblasts from healthy controls.

108 K14/IL-1 alpha mice crossed with the highly sensitive TG.AC

109 Strikingly, the K14/IL-1 alpha mice were completely resistant to papilloma a

110 When the K14/IL-1 alpha transgene was bred onto a recombinase-activat

111 levels of cytokines regulated by NF-kappaB (IL-1 alpha, IL-1 beta, IL-10, and IFN-gamma).

112 FVB/N transgenic mice overexpressing 17-kDa IL-1 alpha in the epidermis under the keratin 14 (K14) p

113 ast, ATP-treated cells do not contain 17-kDa IL-1 alpha.

114 stitutive, aberrant expression of the 31-kDa IL-1 alpha precursor (pre-IL-1 alpha) in the nuclei of f

115 8, fourfold lower IL-1 beta, and 20-30% less IL-1 alpha than macrophages from wild-type Casp1(+/+) or

116 mulated with LPS produced significantly less IL-1 alpha than macrophages from IL-1 beta +/+ mice (p <

117 binding, 17-kDa C-terminal component (mature IL-1 alpha) that results from proteolytic processing of

118 idermal layers, as well as release of mature IL-1 alpha into the medium, as measured by Western blott

119 In essential fatty acid deficient mice IL-1 alpha was present in all epidermal layers and the d

120 In untreated mice, IL-1 alpha was present in the dermis and nucleated epide

121 no effect on the activity of human or mouse IL-1 alpha.

122 Injection of murine IL-1 alpha does not induce detectable serum IL-6 levels

123 fter 6 h of TNF-alpha treatment, but neither IL-1 alpha nor IL-1 beta was detectable.

124 IL-1 beta did not compensate for neutralized IL-1 alpha, suggesting the 2 monokines have separate rol

125 he IL-1 receptor with IL-1RA or neutralizing IL-1 alpha or IL-1 beta with specific antibody dramatica

126 NF-IL-1 alpha contains a 5'-GGAA-3' sequence that is essent

127 -82 (nuclear factor-interleukin-1 alpha [NF-IL-1 alpha]) was the most important for transcription of

128 otein complex disappeared with the use of NF-IL-1 alpha probes that had mutations of the Ets binding

129 xtracts from affected fibroblasts and the NF-IL-1 alpha probe, whereas no specific band was detected

130 udies suggest that the antitumor activity of IL-1 alpha may be mediated through the production of NO

131 ivascular myofibroblast cell type capable of IL-1 alpha synthesis and processing, results in malignan

132 The capacity of IL-1 alpha to stimulate the synthesis of significantly h

133 inducing nitrite but that the combination of IL-1 alpha/IFN-gamma induced dose-dependent nitrite, wit

134 gainst solid tumors in vivo, combinations of IL-1 alpha with these active drugs may lead to more effe

135 d with normal subjects, the concentration of IL-1 alpha and mature IL-1 beta in the tear fluid was in

136 o significant change in the concentration of IL-1 alpha, precursor IL-1 beta, and IL-1Ra in reflex te

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

138 However, the relative contribution of IL-1 alpha and IL-1 beta to the inflammatory response ha

139 Depletion of IL-1 alpha in mice infected with wild-type Y. enterocoli

140 both the immediate release and dispersion of IL-1 alpha from a pre-formed, epidermal pool, as well as

141 not required for the promotional effects of IL-1 alpha on neutrophil recovery and alloengraftment.

142 Changes in expression of IL-1 alpha, IL-8, collagenase, and ENA-78 were determine

143 ncer cells overexpressing a secreted form of IL-1 alpha (MCF-7IL-1 alpha) in nude mice.

144 A fivefold increase in levels of IL-1 alpha antigen was measured in cell lysate samples b

145 A dramatic increase in the levels of IL-1 alpha mRNA occurred following infection, as measure

146 pecifically reduces epidermal mRNA levels of IL-1 alpha, decreased basal immunostaining for IL-1 alph

147 were found to express substantial levels of IL-1 alpha, regulated through an autocrine feedback loop

148 sed icIL-1Ra did not have elevated levels of IL-1 alpha.

149 The majority of IL-1 alpha remained cell associated, as no significant i

150 Direct measurement of IL-1 alpha protein levels revealed that this cytokine wa

151 med as a result of proteolytic processing of IL-1 alpha.

152 Dexamethasone suppressed production of IL-1 alpha, TNF-alpha, and MIP-1 alpha; GM-CSF reduced s

153 The epidermis contains large quantities of IL-1 alpha in keratinocytes, which may play a role in in

154 0 times greater by mass than the quantity of IL-1 alpha released, but only a small fraction of cytopl

155 released a small but significant quantity of IL-1 alpha, while strains of 33% released 66 +/- 9% of c

156 inogenesis has been linked to the release of IL-1 alpha and the induction of chronic inflammation in

157 tern analysis, and ELISA that the release of IL-1 alpha is dependent on the amplitude of the strain.

158 Release of IL-1 alpha was accompanied by rapid release of large sto

159 uman keratinocytes leads to rapid release of IL-1 alpha, possibly through transient disruptions in th

160 To test the role of IL-1 alpha and inflammation in models of cutaneous carci

161 Thus, the role of IL-1 alpha and, by extension that of other proinflammato

162 rneal fibroblasts, demonstrating the role of IL-1 alpha as a necessary intermediate for expression of

163 , little is known to distinguish the role of IL-1 alpha from that of IL-1 beta during this process.

164 To understand the role of IL-1 alpha in breast cancer progression in vivo, we stud

165 mechanical strain promotes the secretion of IL-1 alpha, and deformation of keratinocytes in the epid

166 of functional NF-kappa B and stimulation of IL-1 alpha, indicating that NF-kappa B-dependent and -in

167 ytic maturation of IL-1 beta exceeds that of IL-1 alpha in both formats, but pulsed cells process the

168 critical component in the transformation of IL-1 alpha-producing cells in the bone marrow or the per

169 c transplants demonstrated similar levels of IL-1-alpha, IL-12 (p40), TNF-alpha, IL-2, IFN-gamma, IL-

170 ely increased IL-6, but had little effect on IL-1 alpha and IL-1 beta mRNA levels.

171 increased LIF and IL-6, had little effect on IL-1 alpha, and slightly decreased IL-1 beta mRNA levels

172 m from T cell-EC cocultures, or with IL-2 or IL-1 alpha similarly primes CD4+ T cells for the costimu

173 were cultured with IL-1 alpha, IFN-gamma, or IL-1 alpha/IFN-gamma at various doses with NO production

174 o our knowledge, of a nuclear target for pre-IL-1 alpha.

175 mechanism by which nuclear expression of pre-IL-1 alpha affects fibroblast growth and matrix producti

176 onstitutively up-regulated expression of pre-IL-1 alpha in the nuclei of SSc fibroblasts up-regulates

177 We mapped the region of pre-IL-1 alpha responsible for necdin binding and found it t

178 N terminus, a region that is present on pre-IL-1 alpha, but not the mature 17-kDa cytokine.

179 sion of the 31-kDa IL-1 alpha precursor (pre-IL-1 alpha) in the nuclei of fibroblasts from the lesion

180 Expression studies demonstrated that pre-IL-1 alpha associates with necdin in the nuclei of mamma

181 a yeast two-hybrid method, we found that pre-IL-1 alpha binds necdin, a nuclear protein with growth s

182 We established that pre-IL-1 alpha expression was associated with increased fibr

183 ible relationship between elevated precursor IL-1 alpha (preIL-1 alpha) and elevated icIL-1Ra was inv

184 beta, but it does not prevent release of pro-IL-1 alpha, pro-IL-1 beta, or LDH.

185 of pro-IL-1 beta and prevent release of pro-IL-1 alpha/beta and LDH; they do not inhibit ATP-induced

186 g concentrations of either human recombinant IL-1 alpha or TNF-alpha.

187 ta 3 integrin as the key receptor regulating IL-1 alpha activity.

188 tinuously or only for a 15-min pulse release IL-1 alpha, IL-1 beta, and lactate dehydrogenase (LDH).

189 ar endothelium through mechanically released IL-1 alpha.

190 At 10% STE, secreted IL-1 alpha was decreased (P < 0.05) relative to 2.5% STE

191 a 35 +/- 6% decrease in endotoxin-stimulated IL-1 alpha production by PBMC incubated with plasma draw

192 d 60 +/- 5% decrease in endotoxin-stimulated IL-1 alpha production in the presence of 1 ng/ mL, 10 ng

193 cute barrier disruption with tape-stripping, IL-1 alpha increased in the epidermis and dermis within

194 We conclude that IL-1 alpha can augment post-BM transplantation hematopoi

195 bset of breast cancers and demonstrated that IL-1 alpha is an autocrine and paracrine inducer of prom

196 nas gingivalis, prompted the hypothesis that IL-1 alpha, IL-1 beta, and IL-RA may help regulate human

197 Studies indicated that IL-1 alpha significantly increased topoisomerase I-catal

198 Additionally, these results suggest that IL-1 alpha-induced inflammation is a major contributor t

199 eata [OR 1.48 (0.96, 2.29)], suggesting that IL-1 alpha may have a particular role in the pathogenesi

200 pha cell-derived tumors, which suggests that IL-1 alpha increases leptin expression in stromal cells

201 The IL-1 alpha-mediated response required a selective intera

202 Surprisingly, although the IL-1 alpha mice still did not develop papillomas, they d

203 as mediated only partially by changes at the IL-1 alpha synthesis level.

204 Studies also showed that the potency of the IL-1 alpha effects was related to the degree of donor ce

205 ndings suggest that nuclear transport of the IL-1 alpha N-terminal component may represent a critical

206 The functionally bipartite nature of the IL-1 alpha precursor represents a unique combination of

207 Evidence is also presented that the IL-1 alpha autocrine controls expression of an IL-8 rela

208 ralization experiments demonstrated that the IL-1 alpha autocrine is largely responsible for controll

209 e increase in mRNA, we hypothesized that the IL-1 alpha might derive from a pre-formed pool.

210 We report that the IL-1 alpha N-terminal propiece is concentrated by means

211 electin was completely inhibited by an Ab to IL-1 alpha.

212 Abs to IL-1 alpha, IL-1 beta, IL-2, IL-3, IL-10, IL-15, GM-CSF,

213 as inhibited when neutralizing antibodies to IL-1 alpha and IL-1 beta were used in combination.

214 tes, exposure of corneal epithelial cells to IL-1 alpha and TNF-alpha did not induce significant incr

215 Exposure of corneal epithelial cells to IL-1 alpha and TNF-alpha did not stimulate MCP-1 secreti

216 n nine times more stable in cells exposed to IL-1 alpha than in cells exposed to TNF-alpha.

217 part, to IFN-beta, and to a lesser extent to IL-1 alpha.

218 duction of interleukin (IL)-6 in response to IL-1 alpha or tumor necrosis factor (TNF)-alpha was near

219 of VCAM-1 gene transcription in response to IL-1 alpha, but not TNF alpha.

220 LPH level increased substantially after UVR, IL-1 alpha, or TPA.

221 When IL-1 alpha was delivered subcutaneously using a mini-osm

222 n diseased than in healthy biopsies, whereas IL-1 alpha, IL-1 beta, and IL-1ra mRNA were found in mos

223 In cultures of nasal cartilage with IL-1 alpha, almost all the proteoglycan was released wit

224 Pretreatment of the ovarian cells with IL-1 alpha did not result in increased expressions of mR

225 eeth and implants positively correlated with IL-1 alpha and IL-1 beta and with the proportions of Sel

226 Articular cartilage cultured with IL-1 alpha lost proteoglycan progressively during the 4-

227 normal endothelial cells were cultured with IL-1 alpha, IFN-gamma, or IL-1 alpha/IFN-gamma at variou

228 cells grown as xenografts in nude mice with IL-1 alpha followed by CPT-11 at minimally toxic doses s

229 ollagen from nasal cartilage stimulated with IL-1 alpha was inhibited by BB87, an inhibitor of both c

230 e aortic endothelial cells were treated with IL-1 alpha (100 units/ml)/IFN-gamma (10 units/ml), tumor

231 ivity, which was augmented by treatment with IL-1 alpha.