ライフサイエンスコーパス: IL-8

1 IL-8 knockdown inhibits tamoxifen-resistant cell growth

2 IL-8 knockdown or ERK inhibition, on the other hand, abo

3 IL-8 production was detected in cultures of CD138(+) pla

4 IL-8 promotes cancer cell growth, survival, angiogenesis

5 IL-8 spiked serum samples were measured with a high repr

6 nd poly(I:C) treatments increased (P < 0.01) IL-8 and chemokine ligand 2.

7 IL-17A, IL-8, IL-6, neutrophils and eosinophils were detected an

8 e expression of its target genes HIF-1alpha, IL-8, BCL-2, and BCL-XL through the accumulation of auto

9 ons of proinflammatory cytokines (IL-1alpha, IL-8, IL-12(p70)) and increased IP-10.

10 kers including: MCP-1 SDF-1a, IL-Ra, MIP-1b, IL-8, and VEGF in comparison to unaffected children.

11 emerin, progranulin, interleukin (IL)-1beta, IL-8, MMP-8, and MMP-13 levels were measured using enzym

12 aracterized by inhibition of IL-6, IL-1beta, IL-8, and TNF-alpha.

13 -1beta (1 ng/mL); 3) IL-6 (10 ng/mL); and 4) IL-8 (10 ng/mL).

14 n molecule (VCAM); 5) interleukin (IL)-6; 6) IL-8; 7) intercellular adhesion molecule; and 8) IL-10.

15 HCAECs showed increased interleukin (IL)-6, IL-8, intercellular adhesion molecule 1, and platelet en

16 ma-inducible protein 10, interleukin (IL)-6, IL-8, vascular endothelial growth factor (VEGF), monocyt

17 Interleukin (IL)-1alpha, IL-6, IL-8 and IL-10 mRNA levels were assessed by real-time PC

18 IL-12p70, IL-13, IL-1beta, IL-2, IL-4, IL-6, IL-8 and tumour necrosis factor-alpha.

19 mokine ligand 18) and tumor-promoting (IL-6, IL-8) cytokines.

20 f pro-tumorigenic molecules, including IL-6, IL-8, and BCL-2.

21 ng of IL-32gamma to IL-32beta and also IL-6, IL-8, and CXCR1 signaling pathways to reverse the proapo

22 ll as the IL-1beta-inducible cytokines IL-6, IL-8, and macrophage inflammatory protein 1alpha/beta.

23 th B. abortus induced the secretion of IL-6, IL-8, and MCP-1, and the upregulation of CD54 (ICAM-1),

24 ecretion of proinflammatory cytokines (IL-6, IL-8, and MIP-1beta) by monocytes and DCs (IC50 < 1 muM)

25 tumor necrosis factor-alpha, IL-1beta, IL-6, IL-8, and monocyte chemoattractant protein-1 by co-cultu

26 d it elevated amniotic fluid IL-1beta, IL-6, IL-8, and PGF2alpha, resulting in PTB and marked neonata

27 kappaB transcriptional targets such as IL-6, IL-8, and the apoptosis inhibitor cIAP2.

28 of the proinflammatory cytokines IL-1, IL-6, IL-8, and TNFalpha.

29 okines/chemokines, including TNFalpha, IL-6, IL-8, CCL4, and CCL5, by human macrophages stimulated wi

30 Up-regulated IL-6, IL-8, CD38, and CD69 and down-regulated macrophage-deriv

31 inal analysis indicated that levels of IL-6, IL-8, CD38, and CD69 were reduced, whereas levels of mac

32 hma and increased BAL fluid IL-1alpha, IL-6, IL-8, granulocyte colony-stimulating factor, and GM-CSF

33 ions of five immune markers (IL-1beta, IL-6, IL-8, IL-10, and TNF-alpha) in maternal serum from 1,494

34 tions of interleukin (IL)-1beta, IL-2, IL-6, IL-8, IL-10, IL-12, interferon gamma, tumor necrosis fac

35 Serum cytokines (IL-4, IL-5, IL-6, IL-8, IL-10, TNF-alpha) were measured in 1157 subjects u

36 the expression and secretion of VEGF, IL-6, IL-8, IL-1beta and MCP-1, leading to neovascularization

37 r (TNF)-alpha, interleukin (IL)-1beta, IL-6, IL-8, IL10, reduced glutathione (GSH), superoxide dismut

38 ar translocation and the production of IL-6, IL-8, MMP-1, and MMP-13 in human RA SFs.

39 ons of angiopoietin-1, angiopoietin-2, IL-6, IL-8, soluble tumor necrosis factor receptor-1, soluble

40 CH suppressed IL-1beta, IL-6, IL-8, TNF-alpha and COX-2, while PPH reduced LPS-induced

41 iators, including IL-1alpha, IL-1beta, IL-6, IL-8, tumor necrosis factor (TNF)-alpha, the proangiogen

42 xpression of proinflammatory genes for IL-6, IL-8, tumor necrosis factor, and IL-1B, whereas keratino

43 ted mRNA expression of AT1R, IL-1beta, IL-6, IL-8, tumor necrosis factor-alpha, and osteoprotegerin (

44 a, interleukin (IL)-1beta, IL-2, IL-4, IL-6, IL-8, tumor necrosis factor-alpha, epidermal growth fact

45 owth factor [TGF]-beta1, interleukin [IL]-6, IL-8 and IL-1beta) and BDNF levels were also measured.

46 ulating factor [MCSF], interleukin-6 [IL-6], IL-8, IL-1alpha, CXCL1, CXCL2, CXCL3, intercellular adhe

47 necrosis factor alpha, interleukin 6 [IL-6], IL-8, interferon gamma-induced protein 10, IL-4, IL-9, I

48 nflammatory cytokines (interleukin-6 [IL-6], IL-8, monocyte chemoattractant protein 1 [MCP-1], and IL

49 ry stimulation showed reduced interleukin 8 (IL-8) and CXCL1 secretion (P < .001).

50 ls showed lower expression of interleukin 8 (IL-8) and CXCL1, both on the mRNA and protein levels, th

51 factor alpha (TNF-alpha), and interleukin 8 (IL-8) were compared between dichotomous groups with low

52 A1 binding to the promoter of interleukin 8 (IL-8), a chemokine previously shown elevated in NEPC, to

53 with increased expression of interleukin 8 (IL-8), CXCL2, IL-1beta, tumor necrosis factor alpha (TNF

54 Interleukin-8 (IL-8) gene polymorphisms have been considered as suscept

55 induced significant levels of interleukin-8 (IL-8) in HT-29 cell culture supernatants by 4 h, which i

56 te dehydrogenase release, and interleukin-8 (IL-8) secretion and decreased apical cilia, cystic fibro

57 ractant protein-1 (MCP-1) and interleukin-8 (IL-8) secretion from 3T3-L1 adipocytes.

58 e detection in serum of human interleukin-8 (IL-8), a pro-angiogenic chemokine implicated in a wide r

59 WF levels of angiopoietin-2, interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-alpha), and vasc

60 age pathway and the chemokine interleukin-8 (IL-8).

61 fibrinogen, and the cytokine interleukin-8 (IL-8).

62 The human chemokine interleukin-8 (IL-8; CXCL8) is a key mediator of innate immune and infl

63 549 cells and found that StmPr1 induces A549 IL-8 secretion via activation of protease-activated rece

64 ction of IL-1beta and IL-18, which activated IL-8 transcription and hepatic NK cell activity, respect

65 magnetic beads, specific antibodies against IL-8 protein, a specific hairpin DNA sequence for IL-8 m

66 uring RSV bronchiolitis reduced upper airway IL-8 levels, prolonged the time to the third wheezing ep

67 lasma levels of tumor necrosis factor alpha, IL-8, IL-10, fibroblast growth factor 2, and IL-7 remain

68 pression with expression of IL-6, TNF-alpha, IL-8, and cyclooxygenase-2 was also investigated.

69 induced significant up-regulation of AMCFII, IL-8, IL-15, VEGFA, LIF, FASL, CXCL11, CCL4, CCL25 and d

70 atients had higher sputum IL-6 (P < .01) and IL-8 (P = .01) levels.

71 d exacerbated TNF-alpha-stimulated MCP-1 and IL-8 secretion.

72 nd a significant increase in serum IL-10 and IL-8 levels after a positive OFC result.

73 c) increased secretion of CCL2, CXCL-12, and IL-8.

74 IL-1beta and IL-8 protein levels were significantly increased in sput

75 f the proinflammatory cytokines IL-1beta and IL-8; abolished chemotaxis to several chemoattractants l

76 les, including TNF, IL-1alpha, IL-1beta, and IL-8.

77 ased tissue produce high levels of CCL-2 and IL-8 and contribute to the inflammatory process promotin

78 reduced P4-PRWT transrepression of COX-2 and IL-8 Notably, GATAD2B expression was significantly decre

79 ion of the NF-kappaB target genes, COX-2 and IL-8 P4-PRWT transrepression occurred at the level of tr

80 recruitment of PRWT and PRmDBD to COX-2 and IL-8 promoters, suggesting that PR inhibitory effects we

81 cruitment of endogenous GATAD2B to COX-2 and IL-8 promoters.

82 appaB p65 and RNA polymerase II to COX-2 and IL-8 promoters.

83 corticoid efficacy by Interleukin (IL)-6 and IL-8 analysis was limited due to the trauma induced by t

84 Expression of IL-17A, IL-6 and IL-8 and neutrophil numbers was significantly elevated i

85 ith Neu5Ac stimulated expression of IL-6 and IL-8 and rescued the tumor growth and migratory phenotyp

86 aureus-infected cells, induction of IL-6 and IL-8 expression was less pronounced than in E. coli-infe

87 and IL-17A increased expression of IL-6 and IL-8 in a concentration-dependent and synergistic manner

88 tan modulated mRNA transcription of IL-6 and IL-8 in HPLF but not in HGF.

89 As expected, IL-6 and IL-8 increased, while CRP decreased, in the tocilizumab

90 Interestingly, reduced IL-6 and IL-8 levels were observed in HCAECs stimulated with Aa i

91 At baseline, IL-1alpha, IL-6 and IL-8 mRNA levels as well as TLR-4 protein expression wer

92 ng intrinsic protease activity, and IL-6 and IL-8 production measured in vitro.

93 and aeroallergens further increased IL-6 and IL-8 production synergistically.

94 Aa-induced IL-6 and IL-8 production was inhibited by rosuvastatin, particula

95 P significantly repress S1P-induced IL-6 and IL-8 production.

96 knockdown impaired IL-1beta-induced IL-6 and IL-8 secretion in cultured HGF and HPLF.

97 ECs and GFs exposed to IL-6 and IL-8 significantly increased synthesis of TNF-alpha and

98 block the induction of interleukins IL-6 and IL-8 triggered by pathologic stimuli relevant to AMD, su

99 rast, IL-1beta-induced secretion of IL-6 and IL-8 was not influenced by losartan in HGF or HPLF.

100 Risk associations with IL-6 and IL-8 were observed for blood samples taken close to diag

101 enic cytokines interleukin-6 and 8 (IL-6 and IL-8) as unexpected outcomes of SHMT1 loss.

102 of inflammatory cytokines, such as IL-6 and IL-8, in primary human periodontal fibroblasts.

103 nts with elevated concentrations of IL-6 and IL-8.

104 on of the proinflammatory cytokines IL-6 and IL-8.

105 presses TNF-induced interleukin 6 (IL-6) and IL-8 mRNA expression and protein secretion from A549 lun

106 butors to these effects, as IL-32, IL-6, and IL-8 expression by epithelial cells exposed to psm mutan

107 L-6, and IL-8, increased IL-1beta, IL-6, and IL-8 in fetal lung, intestine, and brain, and morphologi

108 We determined expression of IL-32, IL-6, and IL-8 in S. aureus- and Escherichia coli-infected bovine

109 -alpha and interleukin (IL)-1beta, IL-6, and IL-8 on epithelial cells (ECs) and human gingival fibrob

110 ressed promoters such as IL-1beta, IL-6, and IL-8 Taken together, our data establish ACTN4 as a trans

111 d IFN-gamma, but not of TNF-alpha, IL-6, and IL-8 upon subsequent infection with Burkholderia pseudom

112 17A, IL-17F, IFN-gamma, TNF-alpha, IL-6, and IL-8 were determined.

113 ines (GM-CSF, IFN-gamma, IL-1beta, IL-6, and IL-8) across stimuli, a higher gene expression level of

114 (e.g., IL-1alpha, MIP-1alpha, TNF, IL-6, and IL-8) as well as regulated a range of CC-induced genes i

115 ines (IL-12, TNF-alpha, IFN-gamma, IL-6, and IL-8), and preferential production of immunomodulatory m

116 reduced MPO, TNF-alpha, IL-1beta, IL-6, and IL-8, and increased IL-10, GSH, SOD, and CAT levels.

117 levated plasma levels of IL-1beta, IL-6, and IL-8, increased IL-1beta, IL-6, and IL-8 in fetal lung,

118 pha, interleukin (IL)-1beta, IL-2, IL-6, and IL-8-were determined using a multiplex bead immunoassay.

119 roinflammatory cytokines IL-1beta, IL-6, and IL-8.

120 phage inflammatory protein 1alpha, IL-6, and IL-8.

121 centration of TNF-alpha, IL-1beta, IL-6, and IL-8.

122 in expression of ZO-1, whereas TNF-alpha and IL-8 mucosal transcript expression concentrations were i

123 d MMP-13 (r = 0.781, P = 0.01); chemerin and IL-8 (r = 0.913, P <0.01), MMP-8 (r = 0.770, P <0.01), a

124 Our findings support a role for CXCL1 and IL-8 in CF lung disease severity and identify STAT3 as a

125 Neutralization of CXCL1 and IL-8 reduced neutrophil chemotaxis >50% to supernatants

126 FeNO, ECP and IL-8 were all low in the paucigranulocytic, whereas as e

127 igh or low expression of MCP-1, eotaxin, and IL-8 discriminates between eosinophilic asthma severity

128 igh or low expression of MCP-1, eotaxin, and IL-8 identified two separate blood eosinophilia patient

129 ffects on eosinophils as assessed by EPO and IL-8 release and eosinophil chemotaxis toward SEB.

130 ), Helios(Low/-), IL-2(+), IFN-gamma(+), and IL-8(+)) compared with typical FOXP3(+) cells.

131 es LPS-induced NF-kappaB phosphorylation and IL-8 production in human neutrophils.

132 signal-regulated kinase phosphorylation and IL-8 release in MCs activated by mvT*s.

133 ratio outperformed plasma procalcitonin and IL-8 and IL-6 in discriminating between CAP and no-CAP p

134 13 (r = 0.788, P <0.01); and progranulin and IL-8 (r = 0.762, P <0.01), MMP-8 (r = 0.845, P <0.01), a

135 ine signature (IL-1beta, IL-6, TNFalpha, and IL-8), neutrophil accumulation, and greater lung patholo

136 rs express more CYP2J2, sFlt1, TNFalpha, and IL-8.

137 e correlations were found among visfatin and IL-8 (r = 0.909, P <0.01), MMP-8 (r = 0.702, P = 0.02),

138 nd point to the potential utility of an anti-IL-8 therapy to prevent unwanted effects of IL-8 up-regu

139 treatment of colonic rho(0) cells augmented IL-8 expression by 9-fold (P < 0.01) via NF-kappaB compa

140 Basal IL-8 and MCP-1 synthesis by monocytes alone did not diff

141 e osteoclastogenesis was markedly reduced by IL-8-specific neutralizing antibodies.

142 In normal human bronchial epithelial cells, IL-8 secretion in response to coal fly ash treatment was

143 erexpression of the pro-angiogenic chemokine IL-8 (CXCL8) is associated with a poor prognosis in seve

144 production of the proinflammatory chemokine IL-8 but not IL-1beta.

145 nflammatory cytokine (IL-10), and chemokine (IL-8) was evaluated at specific hours poststimulation (r

146 the expression of the neutrophil chemokines IL-8 and CXCL1, as well as the Th17 chemokine CCL20.

147 significantly lower levels of the chemokines IL-8 and monocyte chemotactic protein-1 compared with mo

148 ts with NAFLD, whereas liver and circulating IL-8 levels were increased.

149 was associated with decrease of circulating IL-8 and of stimulated production of IL-8 by whole blood

150 nd a single EPIYA-C motif induced comparable IL-8 secretion as isolates carrying multiple EPIYA-C all

151 crophage colony stimulating factor (GM-CSF), IL-8, IL-18, monocyte chemotactic protein-1 (CCL2) (MCP-

152 nding domain for the related chemokine CXCL8/IL-8.

153 ilencing validated its requirement for CXCL8/IL-8 induction.

154 the functional involvement of ZO-1 in CXCL8/IL-8 chemokine expression in lung and breast tumor cells

155 displayed a potent ability to inhibit CXCL8/IL-8-induced neutrophil migration as determined using a

156 n experiments emphasized regulation of CXCL8/IL-8 expression via a cytonuclear pool of ZO-1.

157 assays highlighted a 173-bp region of CXCL8/IL-8 promoter that responded to ZO-1.

158 ion was associated with suppression of CXCL8/IL-8-mediated Ras-related C3 botulinum toxin substrate 1

159 esults demonstrate that ZO-1 regulates CXCL8/IL-8 expression via the NF-kappaB signaling pathway and

160 , compared with the proinflammatory cytokine IL-8.

161 ssion and a reduction in AD-related cytokine IL-8, thymic stromal lymphopoietin, and IL-10 secretion

162 s to produce four proinflammatory cytokines (IL-8, IL-6, IL-1beta, and TNF-alpha) that are necessary

163 through the (49)GITR(52) motif and decreased IL-8 transcription through modification of TAB3.

164 overexpression or supplementation decreased IL-8 secretion by inhibiting Smad 3 phosphorylation.

165 ), which was involved in NF-kappaB-dependent IL-8 expression.

166 secretion by THP-1 macrophages and enhanced IL-8 expression.

167 e that the P2Y6/store-operated calcium entry/IL-8 axis is involved in MSU crystal-induced aggregated

168 lls with miR-629-3p mimic induced epithelial IL-8 mRNA and protein expression.

169 sinophil activation (CD11b expression or EPO/IL-8 release), mCD48 (flow cytometry), sCD48 (ELISA), SE

170 Inhibiting GrmA reduced excessive IL-8 and MCP-1 synthesis in aging to levels similar to y

171 Addition of exogenous IL-8 did not affect growth of HMCLs, although it protect

172 cal established cut-off of 600 pgmL(-1)) for IL-8 protein in undiluted saliva samples.

173 smokers (OR = 1.30, 95% CI: 0.69, 2.44) for IL-8.

174 nt manner from 0.5 to 5.0 micromol/L and for IL-8 up to 1.0 micromol/L.

175 es providing detection limits of 0.21 nM for IL-8 mRNA and 72.4 pgmL(-1) (far below the clinical esta

176 protein, a specific hairpin DNA sequence for IL-8 mRNA and amperometric detection at disposable dual

177 transporter 1); (ii) secretion of pre-formed IL-8, and Charcot Leyden crystal (CLC) formation, which

178 Further, IL-8 upregulation activates the MAPK/ERK pathway, leadin

179 Furthermore, IL-8 induced by stromal-MM cell interactions strongly co

180 ntly, the expression of HBx-regulated genes (IL-8, MMP9, and YAP) and HBV transcription (the activity

181 ocytes from older adults synthesized greater IL-8 (41 +/- 5 versus 9 +/- 2 ng/ml, p < 0.0001) and MCP

182 of cytokines that demonstrated either high (IL-8, IFN-gamma, IL-2, IL-6, and IL-1beta) or low (IL-15

183 s with the same organisms resulted in higher IL-8 and CXCL1 mRNA and protein expression.

184 affold that displays high affinity for human IL-8 with a KD of 35 +/- 10 nM and excellent ligand spec

185 decreased NF-kappaB activation, and impaired IL-8 expression upon exposure to M. smegmatis Collective

186 In conclusion, our results implicate IL-8 in myeloma bone disease and point to the potential

187 IL-1alpha was directly involved in IL-8 production and likely contributed to neutrophilic a

188 of other key inflammatory factors including IL-8, granulocyte-colony stimulating factor (G-CSF), IL-

189 further shown that soluble factors including IL-8, secreted by endothelial cells (ECs) were responsib

190 L-36 induced chemokine production, including IL-8 and CCL20, and reduce further inflammatory cell inf

191 ite increases in KL, TGF-beta also increased IL-8 secretion via activation of FGFR1 and Smad 3 signal

192 ther solid tumors characterized by increased IL-8/CXCL8 expression.

193 tions between MM and stromal cells increased IL-8 secretion by stromal cells through cell-cell adhesi

194 nger adults, p < 0.05) and governs increased IL-8 and MCP-1 synthesis through TLR4 and caspase-1.

195 with lower levels of 15-epi LXA4, increased IL-8 concentrations, and impaired lung function.

196 were unable to interact with TLR4 or induce IL-8 release.

197 se dependent reduction of IL-36gamma induced IL-8 and chemokine ligand 20 (CCL20) levels were detecte

198 nd FGF23 signaling modulate TGF beta-induced IL-8 secretion in CF bronchial epithelia.

199 ly prevented cigarette smoke extract-induced IL-8 release parallel with inhibition of nuclear translo

200 D36 and SR-BI equally, inhibited LPS-induced IL-8 secretion and barrier dysfunction in cultured endot

201 nO NPs, both formulations of CuO NPs induced IL-8 release in the lung epithelial cells already at sub

202 d to a 20-fold increase in palmitate-induced IL-8 expression by hepatocytes.

203 paB activation and blocked palmitate-induced IL-8 expression in hepatocytes.

204 paB activity and increased palmitate-induced IL-8 secretion.

205 ng the brake and enhancing palmitate-induced IL-8 synthesis and secretion.

206 reduced respiratory syncytial virus-induced IL-8 responses and increased 5'-cytosine-phosphate-guani

207 sion or neutralization of vorinostat-induced IL-8/CXCL8 potentiates the vorinostat inhibitory effect

208 te that HDAC inhibition specifically induces IL-8/CXCL8 expression in EOC cells and that the mechanis

209 Apoptosis, oxidative stress, inflammation (IL-8), real-time polymerase chain reaction for epithelia

210 red the ability of an nleE mutant to inhibit IL-8 production during infection.

211 higher secretion of IL-1beta, IL-6, and KC (IL-8) by peritoneal macrophages as compared with WT cont

212 allenged with allergen plus Bet-APE < 3 kDa, IL-8 and IgE was significantly increased as compared to

213 related with elevated bronchoalveolar lavage IL-8 levels (r(2) = 0.6095, p < 0.0001) and neutrophil p

214 Mice in the combination group had the lowest IL-8/CXCL8 tumor levels and the lowest tumor expression

215 lafin), TH9/IL-9, IL-33, and innate markers (IL-8) than adults (P < .02).

216 in part by fetal exposure to lower maternal IL-8, which also predicted higher risks of neurologic ab

217 d PD98059 results in decreased Stx1-mediated IL-8 mRNA.

218 pinning solid-state NMR studies of monomeric IL-8 (1-66) bound to full-length and truncated construct

219 rain carrying the EPIYA-D motif induced more IL-8 secretion than any other EPIYA type, and a single E

220 ent, cells with AG/GG (vs. AA) produced more IL-8 and expressed less antiviral genes, which was coupl

221 y correlated with BAL fluid myeloperoxidase, IL-8, IL-1alpha, IL-6, granulocyte colony-stimulating fa

222 patients with MM secreted higher amounts of IL-8 than healthy donors.

223 agnetic relaxation enhancement broadening of IL-8 (1-66) signals results from interactions of the che

224 Median concentrations of IL-8 were lower in the most disadvantaged pregnancies [-

225 s and to determine the endogenous content of IL-8 protein in saliva samples from 7 healthy individual

226 ethod, and the clinical trajectory course of IL-8 could be sufficiently followed.

227 -IL-8 therapy to prevent unwanted effects of IL-8 up-regulation on survival, angiogenesis, and osteol

228 l numbers also correlated with expression of IL-8 and IL-17A.

229 expression, without affecting expression of IL-8.

230 nhibition specifically induces expression of IL-8/CXCL8 in SKOV3, CAOV3, and OVCAR3 cells.

231 ppaB signaling pathways and the induction of IL-8 and IL-6 cytokine gene expression.

232 on, intracellular survival, and induction of IL-8 production in INT407 cells in vitro The importance

233 on of ALS patients produced higher levels of IL-8 and CCL-2 upon lipopolysaccharide (LPS)-stimulation

234 The mean levels of IL-8 and IL-6 were slightly higher in the DED group at b

235 In addition, a2Neu secrete high levels of IL-8 via NF-kappaB pathway activation.

236 s showed that significantly higher levels of IL-8, hBD-1, and TIMP-2 were secreted from controls than

237 The levels of IL-8, IL-13 and eosinophilic cationic protein (ECP) were

238 ad increased neutrophils and serum levels of IL-8, IL-6, and MCP-1 which varied with cause of death.

239 ells secreted significantly higher levels of IL-8.

240 ibited a linear response versus logarithm of IL-8 concentration from 900 fg/ml to 900 ng/ml.

241 implified mechanistic computational model of IL-8 mediated activation of CXCR-1/2 receptors was devel

242 A three-variable model of IL-8, bicarbonate, and tumor necrosis factor receptor-1

243 In addition, neutralization of IL-8 diminished viral genome amplification in differenti

244 ss, loss of tight junctions or production of IL-8 after 24 hours, but possibly induces epithelial-to-

245 ociated lipid(s) triggered the production of IL-8 and GM-CSF in respiratory epithelial cells through

246 rization and modulation of the production of IL-8 and hBD-2 are suggested mechanisms of action.

247 ulating IL-8 and of stimulated production of IL-8 by whole blood.

248 pression of IL-17RA and increased release of IL-8, even in the presence of budesonide.

249 However, the functional roles of IL-8 gene haplotypes have not been investigated.

250 or, resulting in the high-level secretion of IL-8 by activation of p38 MAPK signaling pathway.

251 was dependent on the autocrine secretion of IL-8 from a2Neu.

252 K5 degraded DSG1 and stimulated secretion of IL-8, IL-10, and thymic stromal lymphopoietin independen

253 emonstrate that most backbone amide sites of IL-8 (1-66) are immobilized and that their chemical shif

254 Herein, we investigated the sources of IL-8 production in multiple myeloma (MM) and its potenti

255 Comparisons of spectra of IL-8 (1-66) bound to full-length CXCR1 (1-350) and to N-

256 tion of wild type NleE in the suppression of IL-8 secretion during enteropathogenic E. coli infection

257 Expression of IL-17A correlated with that of IL-8 and neutrophil numbers.

258 subsequently modulates the transcription of IL-8.

259 In fact, the effect of bortezomib on IL-8 production was higher than that exerted by stromal-

260 of TNF-alpha, but showed a lesser effect on IL-8 secretion and no effect on TGF-beta.

261 n the effects of amino acid substitutions on IL-8 protein structure, function and disease association

262 Only IL-8 and TNF-alpha exhibited increased gene expression.

263 Overexpression of either IL-6 or IL-8 partially rescued SHMT1 loss-induced tumor growth i

264 mation of K63-Ub chains, TAK1 activation, or IL-8 production in human cells, because Pellino1 and Pel

265 llowing TLR stimulation, CD1(+) cDC produced IL-8 and IL-10 while CD1(-) cDC secreted IFN-alpha, IL-1

266 At 3 months, visfatin, progranulin, IL-8, and MMP-8 levels were significantly decreased comp

267 arget for anti-SpyCEP Abs that could protect IL-8 from SpyCEP-mediated proteolysis.

268 cine that induces Abs (anti-S2) that protect IL-8 from proteolysis and other Abs (anti-J8) that cause

269 ssociated with salivary oral cancer, protein IL-8 and its messenger RNA (IL-8 mRNA) associated, in un

270 which can eliminate extracellular protozoa (IL-8) or bridge innate to adaptive immunity (MIP-3alpha

271 Hz, was used as the measure for quantifying IL-8 concentration in the fluid.

272 In contrast, silencing galectin-3 reduced IL-8 response to LPG.

273 as well as proinflammatory cytokine release (IL-8) in the presence and absence of bacterial LPS was s

274 cancer, protein IL-8 and its messenger RNA (IL-8 mRNA) associated, in undiluted human saliva samples

275 Decreases in serum IL-8, IL-6, secretory leukocyte protease inhibitor, and

276 Increased serum IL-8 levels in patients with active FPIES suggest neutro

277 proresolving signal that potently suppresses IL-8-driven neutrophil transepithelial migration in vitr

278 cate that FOXA1 transcriptionally suppresses IL-8, the expression of which would otherwise stimulate

279 t cells; however, it was recently shown that IL-8 production is a signatory effector function of naiv

280 The IL-8/CXCL8 expression induced by vorinostat in EOC cells

281 d antiapoptotic enzyme cyclooxygenase-2, the IL-8 receptor C-X-C chemokine receptor (CXCR) 1, and the

282 inally, in a separate analysis (step 3), the IL-8 deregulation has also appeared to be an important p

283 he third SNP - rs2227306 (alias +781) at the IL-8 locus.

284 se of the CRISPR/Cas9 system to engineer the IL-8 gene, and tested the functionality of different hap

285 coverage and shortlisting of targets in the IL-8 signalling pathway are discussed.

286 pression of virulence factors, including the IL-8 proteaseStreptococcus pyogenescell envelope protein

287 lotype, cells significantly up-regulated the IL-8 at both transcriptional and translational levels.

288 Two sgRNAs vectors targeting the IL-8 gene and the naked homologous repair DNA carrying d

289 dependent recruitment of p65 NFkappaB to the IL-8/CXCL8 promoter.

290 acetylation of p65 and histone H3 and their IL-8/CXCL8 promoter occupancy.

291 hils confirming the functional role for this IL-8 haplotype.

292 Furthermore, this IL-8 response could not be pharmacologically downregulat

293 e cytokines and chemokines (HMGB1, TNFalpha, IL-8, monocyte chemotactic protein-1), and formation of

294 ein 2, and PAI-1, the secretion of TNFalpha, IL-8, and monocyte chemotactic protein-1 and the formati

295 fy a novel signaling pathway contributing to IL-8 secretion in the CF bronchial epithelium with KL fu

296 Unexpectedly, IL-8 was potentiated by TRIM28 knockdown in ECs in an NF

297 t not the pentameric form (pCRP) upregulates IL-8 and CCL2 levels in retinal pigment epithelial cells

298 Our study highlights a role of FOXA1 via IL-8 signaling as a potential therapeutic target in FOXA

299 prostate cancer progression to NEPC, whereas IL-8 and MAPK/ERK pathways may be promising targets for

300 gher in eosinophilic and mixed asthma, while IL-8 was higher in patients with neutrophilic and mixed