ライフサイエンスコーパス: IL-8

1 IL-8 and IL-1beta levels were lower in women who deliver

2 IL-8 concentrations were found to be strongly associated

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

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

5 IL-8, MMP9, and GM-CSF were measured by ELISA in HBEC an

6 .7] vs 243.3 pg/ml [30.7, 344.4]; p = .001), IL-8 (32.0 pg/ml [5.6, 53.1] vs 59.1 pg/ml [39.2, 119.4]

7 cluding C-reactive protein, MX1, IL-6, IL-1, IL-8, TNFalpha, and NF-kappaB.

8 ry response (elevated IL-1beta, IL-6, IL-10, IL-8, RANTES, and TNFalpha) while the response to the pa

9 s linked to an inflammatory response (IP-10, IL-8, IL-6, and OPG), endothelial dysfunction (sVCAM-1 a

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

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

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

13 se 3, macrophage inflammatory protein 1beta, IL-8, and IL-1beta.

14 31/CCL11/CCL17), and T(H)17/T(H)22 (IL-23p19/IL-8/S100A12) mRNA expression in lesional skin.

15 helial growth factor]), and cluster 4 (n=37; IL-8, IL-4, PDGF-beta [platelet-derived growth factor be

16 ess); and (3) elevated interleukin-6 (IL-6), IL-8, and myeloperoxidase levels in the airway are indic

17 in-1 (MCP-1), IFN-gamma, interleukin (IL)-6, IL-8 and IL-1ra (P < 0.05).

18 els of interferon-gamma, interleukin (IL)-6, IL-8, and IL-13, and lower monocyte chemokine, CCL2 (P <

19 on and protein levels of interleukin (IL)-6, IL-8, monocyte chemoattractant protein (MCP)-1, and oste

20 e assay to measure serum interleukin (IL)-6, IL-8, tumor necrosis factor (TNF)-alpha and IL-1beta in

21 endothelin-1 along with interleukin (IL)-6, IL-8, tumor necrosis factor alpha, and interferon gamma-

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

23 We found that high serum IL-6, IL-8 and TNF-alpha levels at the time of hospitalization

24 ficantly elevated at presentation, and IL-6, IL-8 and TNF-alpha levels were higher in complicated app

25 inflammatory cytokines IL-1beta, IL-2, IL-6, IL-8 and TNF-alpha, prior to starting with the administr

26 flammatory cytokines, including IL-1B, IL-6, IL-8 and TNFalpha; these findings are consistent with ob

27 on of inflammatory cytokines TNFalpha, IL-6, IL-8 or IFNbeta.

28 pression of proinflammatory cytokines (IL-6, IL-8) in NiV-infected PBEpC was not decreased.

29 related to phagocytosis and signaling (IL-6, IL-8, acute phase response) are upregulated in 5xFAD;CD3

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

31 sis factor-alpha, interleukin [IL]-1B, IL-6, IL-8, and IL-10) increased in a time-dependent manner an

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

33 -3 activation synergistically triggers IL-6, IL-8, and MCP-1 production, which was not observed for O

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

35 assign class, inflammatory biomarkers (IL-6, IL-8, and sTNFR-1; P < 0.0001) and 90-day mortality (38%

36 asurements and Main Results: IL-1beta, IL-6, IL-8, and sTNFR1 were all increased in patients with COV

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

38 Candida counts and salivary IL-6, IL-8, and TNF-a levels were higher in the test group tha

39 ompared to control joints, while IL-2, IL-6, IL-8, and TNF-alpha concentrations did not differ betwee

40 ad increased mucus levels of IL-1beta, IL-6, IL-8, and TNF-alpha when compared with their younger cou

41 Five cytokines (IFN-gamma, IL-10, IL-6, IL-8, and TNF-alpha) contributed to the analysis.

42 ificantly increased protein release of IL-6, IL-8, CCL2, CCL20 and CXCL10; however, no alterations in

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

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

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

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

47 e illness.Methods: Levels of IL-1beta, IL-6, IL-8, IL-10, and sTNFR1 (soluble tumor necrosis factor r

48 M, IgA and IgG), and cytokine content (IL-6, IL-8, IL-10, and TNF-alpha), and antioxidant activity of

49 was significantly increased (IL-1beta, IL-6, IL-8, IL-10, and TNF-alpha).

50 levels of IL-1beta, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12, CRP, TNF-alpha, IFN-gamma, GM-CSF, M

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

52 Median values for interleukin (IL)-4, IL-6, IL-8, IL-10, IL-15, granulocyte colony-stimulating facto

53 evels of interleukin-1beta (IL-1beta), IL-6, IL-8, IL-10, IL-17, interferon-gamma and differential T

54 g a panel of five cytokine biomarkers (IL-6, IL-8, IL-10, TRAIL & IP-10), that is attributed as a sig

55 pression levels of eotaxin, IFN-gamma, IL-6, IL-8, IL-16, MCP-1, MIF and MIP-1 beta were significantl

56 om women with optimal microbiota, with IL-6, IL-8, IL-1alpha, IL-1beta and MIP-1alpha/beta production

57 nd in the lungs, most notably, IL-1RA, IL-6, IL-8, IP-10, and monocyte chemoattactant protein-1, cons

58 leukin-1 receptor antagonist [IL-1Ra], IL-6, IL-8, macrophage inflammatory protein-1 beta [MIP-1beta]

59 Production of IL-6, IL-8, MCP-1, and OPG was significantly increased by Poly

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

61 y eculizumab attenuated the release of IL-6, IL-8, TNF, MCP-1, MIP-1alpha, IFN-gamma, LTB-4, MMP-8 an

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

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

64 s), salivary cytokines (interleukin, [IL]-6, IL-8, and tumoral necrosis factor-alpha [TNF-alpha]), an

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

66 ammatory cytokines (Eotaxin, IL-1beta, IL-7, IL-8, IL-12/IL-23p40, IL-12p70, IL-13, IL-16, IP-10, MCP

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

68 ppaB target genes such as the interleukin 8 (IL-8) and TNF genes.

69 bitory effect of metformin in interleukin 8 (IL-8) upregulation by lithocholic acid (LCA) in HCT116 c

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

71 blastemal progenitors through interleukin 8 (IL-8), a highly expressed cytokine in subpopulations of

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

73 macrophages mounted a robust interleukin 8 (IL-8), neutrophil-attracting response to C. burnetii and

74 f cognition, but elevated CSF interleukin 8 (IL-8/CXCL8) only in HIV-NC but not HAND.

75 atform is tested by screening interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) secr

76 Using interleukin-8 (IL-8) as an example analyte, we demonstrated the concept

77 Serum interleukin-8 (IL-8) levels and tumor neutrophil infiltration are assoc

78 ls (NF-kappaB) activation and interleukin-8 (IL-8) secretion are attributed to T4SS-dependent deliver

79 tion, defined as a normalized interleukin-8 (IL-8) value of <0.3 relative to the input H. pylori stra

80 al palsy, the level of plasma interleukin-8 (IL-8) was increased, correlated with motor improvement,

81 production of MIG (CXCL9) and interleukin-8 (IL-8), and decreased production of IL-10, macrophage inf

82 al cellular factors including interleukin-8 (IL-8), in both, normal and tumorigenic cells.

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

84 vasiveness and growth through interleukin-8 (IL-8)-mediated enrichment of CSCs.

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

86 acterized by the secretion of interleukin-8 (IL-8; also called CXCL8) and the expression of CXCL8, tu

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

88 549 cells and found that StmPr1 induces A549 IL-8 secretion via activation of protease-activated rece

89 RID also abolished IL-8 secretion induced by heat-killed bacteria, TNF, or

90 for H. pylori-induced NF-kappaB activation, IL-8 secretion, and TLR9 activation, but Cagbeta was dis

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

92 lli suppressed IL-6 (adjusted p < 0.001) and IL-8 (adjusted p = 0.0170) responses to G. vaginalis.

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

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

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

96 lated longitudinal changes in p-Tau(181) and IL-8 levels (R = 0.841).

97 of bronchoalveolar lavage fluid IL-1beta and IL-8 could effectively and safely improve antibiotic ste

98 Low concentrations of IL-1beta and IL-8 in bronchoalveolar lavage fluid have been validated

99 evels, IL-1beta expression, pro-IL-1beta and IL-8 production in MSU stimulated THP-1 macrophages (p <

100 atients, with concentrations of IL-1beta and IL-8 rapidly determined in bronchoalveolar lavage fluid

101 anine, as well as interleukin (IL)-1beta and IL-8, increased significantly in samples from grade IV g

102 otein, MMP9, and the cytokines, IL-1beta and IL-8.

103 flammatory cytokines TNFalpha, IL-1beta, and IL-8, and reduce capacity to phagocytose bacteria.

104 flammatory cytokines TNFalpha, IL-1beta, and IL-8.

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

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

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

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

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

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

111 inflammatory cytokine expression (IL-33 and IL-8) compared with other dominant nasal bacterial isola

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

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

114 compound that showed activity in an IL-6 and IL-8 cytokine release assay.

115 ere were higher levels of IL-1beta, IL-6 and IL-8 cytokines were quantified in keratitis caused by Gr

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

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

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

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

120 800-IL-Ra reduced IL-1alpha-induced IL-6 and IL-8 levels with comparable potency.

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

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

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

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

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

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

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

128 IL-6 and IL-8 were elevated at 1 and 4 hours in group 1 (P = 0.00

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

130 ecrosis factor (TNF), interleukin (IL)-6 and IL-8 were produced before IFNs in all patients and persi

131 diator mRNA and protein expression (IL-6 and IL-8) and increased anti-inflammatory cytokine mRNA expr

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

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

134 cytokines and chemokines, including IL-6 and IL-8, in response to starvation stress.

135 ormin, also promoted the release of IL-6 and IL-8.

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

137 pro-inflammatory cytokine, such as IL-6 and IL-8.

138 neonatal levels of interleukin-6 (IL-6) and IL-8 compared with GP controls.

139 se in oral Candida counts, GI, PD, IL-6, and IL-8 as well as gain in CAL at 30 and 90 days after NSPT

140 ory cytokines IL-1beta, TNF-alpha, IL-6, and IL-8 at a similar efficacy to dexamethasone.

141 ls of tumor necrosis factor alpha, IL-6, and IL-8 in critically ill patients with coronavirus disease

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

143 ell as increase in VCAM-1, ICAM-1, IL-6, and IL-8 levels.

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

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

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

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

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

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

150 ion of CD69 and secretion of IL-4, IL-6, and IL-8.

151 t protein 1 (MCP-1), interleukin (IL) 6, and IL-8.

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

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

154 ase of eosinophil peroxidase, TNF-alpha, and IL-8 (n = 7-8) but did not promote eosinophil apoptosis

155 te, which was blocked by depleting CXCL1 and IL-8 from the conditioned medium.

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

157 ecause of the greater induction of CXCL1 and IL-8 in human hepatocytes.

158 genic transcripts including VEGF, CXCL1, and IL-8 in hCAECs.

159 Experiments in mice confirmed that ECs and IL-8 stimulate intracranial tumor growth and invasion in

160 a key neuroimmune transcription factor, and IL-8, a chemokine, were significantly increased.

161 nd invasion by increasing CSC frequency, and IL-8 may be explored clinically to inhibit these interac

162 TRADD, and TRADD with active caspase+IR and IL-8+IR, consistent with coordinated activation of neuro

163 pathways such as integrin-linked kinase and IL-8 signaling and previously implicated pathways in sar

164 ls and overall production of IL-6, MCP1, and IL-8.

165 rs, Calprotectin, Myeloperoxidase (MPO), and IL-8 are significantly increased at time of disease comp

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

167 to produce reactive oxygen species (ROS) and IL-8.

168 s of factors such as TGF-b, S100B, sRAGE and IL-8 as well as with myeloid DC counts.

169 lammatory pathways associated with TNFR1 and IL-8 appear to be upregulated.

170 ngiogenic factors including CXCL1, VEGF, and IL-8 are decreased when ILF3 is knocked down by siRNA.

171 ma levels of innate immune cytokines such as IL-8 and IL-18 along with more robust induction of non-c

172 in increased inflammatory mediators, such as IL-8 or PGE(2).

173 PD airway epithelial cells showed attenuated IL-8 responses to TLR2 agonist despite expressing TLR2 s

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

175 e mean difference = -0.07; P = 0.04) and BAL IL-8 were reduced.

176 antidepressant treatment had lower baseline IL-8 levels than the nonresponders (Hedge's g = -0.28; 9

177 Q0(bolton)-AAT bound IL-8 and leukotriene B(4), comparable to healthy control

178 togen-activated protein kinase activation by IL-8 has been identified as a major pathway of NET forma

179 rrangements in MCs triggered to migration by IL-8 or prostaglandin E(2) or to FcepsilonRI-stimulated

180 e production of neutrophilic chemoattractant IL-8 in the absence or presence of M. pneumoniae or HRV1

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

182 FN-gamma, IP-10, IL-1RA, IL-10), chemotaxis (IL-8), systemic and vascular inflammation (CRP, ICAM-1,

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

184 sulted in the polarized secretion of CXCL10, IL-8 and CCL-20 by IEC and could efficiently be prevente

185 CXCL8 (IL-8), IL-6, TNF-alpha (tumor necrosis factor-alpha), an

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

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

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

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

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

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

192 e secretion of the pro-inflammatory cytokine IL-8 by endocervical cells infected with N. gonorrhoeae.

193 10 cytokines, the pro-inflammatory cytokine IL-8 exhibited a strong correlation with delirium severi

194 ory effect on the inhibition of the cytokine IL-8, which is a pro-inflammatory biomarker, was increas

195 e secretion of the proinflammatory cytokines IL-8 and CXCL1, which are associated with CRC progressio

196 he production of pro-inflammatory cytokines (IL-8, IL-1beta, and IL-6).

197 Similarly, all three PGAs elicited IL-8 from iDCs, but B. subtilis PGA also elicited IL-6,

198 All three elicited IL-8 and IL-6 from monocytes, but B. subtilis PGA also e

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

200 Cervical fluid IL-8 and IL-1beta and microflora have the potential to b

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

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

203 ng NF-kappaB signaling that was critical for IL-8 upregulation.

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

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

206 ukin-6 receptor beta (sIL-6Rbeta, or gp130), IL-8, IL-20, IL-26, IL-34, soluble tumor necrosis factor

207 Here we report the detection of hCGbeta, IL-8 and TNFalpha from conditioned culture media of sing

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

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

210 A 30% increase in IL-8 suppression by FLU (P = .04) and a trend for increa

211 An increase in IL-8 was especially significant in the ASD group with ea

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

213 In contrast, no changes between V0 and V6 in IL-8 and TNF-alpha suppression by FLU were observed in p

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

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

216 Because increased IL-8 and CXCL1 production in tumors is associated with i

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

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

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

220 inhibited superantigen and bacterial-induced IL-8 production by model human epithelial cells.

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

222 n species (ROS) were involved in LCA-induced IL-8 upregulation through activation of the transcriptio

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

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

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

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

227 ssociated with NET formation, and inhibiting IL-8 significantly attenuated NETosis.

228 ived 4-hydroxy-2-nonenal induced interleukin IL-8 release from monocytes.

229 A trend towards lower IL-8 responses was shown following gangrenous appendicit

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

231 ding protein 5) and transrepression markers (IL-8 and TNF-alpha) were measured by using RT-PCR in fre

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

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

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

235 ated the gene expression of Cxcl2, the mouse IL-8 homologue and increased the expression of its recep

236 ow) CD206(hi) phenotype downregulating mTOR, IL-8 signaling and oxidative phosphorylation.

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

238 ar anti-oxidation and anti-inflammation (NO, IL-8 secretion).

239 extending the relevance of the activation of IL-8 pathway to the class of platinum chemotherapeutics.

240 Blockade of IL-8 inhibited these effects in GBM-EC co-cultures, whil

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

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

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

244 d the tumor bearing as well as expression of IL-8 and matrix metalloproteinase 9, ankle loading decre

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

246 Therapies that can reverse the impacts of IL-8-mediated myeloid inflammation will be essential for

247 tributed to delirium severity independent of IL-8.

248 ctivator in reporter cells and an inducer of IL-8 production by HT29-MTX cells.

249 investigated a novel selective inhibitor of IL-8 receptors, DF2726A, and showed its effects in count

250 nd MCP-1 (0.779, p<0.05) and lower levels of IL-8 (-1.293, p<0.05) in the periphery, as well as eleva

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

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

253 non-viable embryos produce higher levels of IL-8 and TNFalpha, associated with abnormal cell divisio

254 High levels of IL-8 in plasma, peripheral blood mononuclear cells and t

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

256 rman correlations identified nasal levels of IL-8, IL-33, and Betula verrucosa 1-specific IgG(4) (sIg

257 Nasal levels of IL-8, IL-33, sIgG(4) and sIgE could be predictive biomar

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

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

260 ciated lipid(s), triggered the production of IL-8 in respiratory epithelial cells through a TLR2-, NF

261 ling significantly reduced the production of IL-8, IL-6, and CXCL1, suggesting a hierarchy of mechani

262 We unveil an ERK3-mediated regulation of IL-8 and epithelial secretome for chemotaxis.

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

264 This study aimed to elucidate the role of IL-8 in the therapeutic effects of hUCBCs in a mouse mod

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

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

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

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

269 Therefore, we have co-opted IL-8 release from tumors to enhance intratumoral T-cell

270 ) or CD4(+) cells secreted IFNgamma/IL-10 or IL-8, respectively, in cells from PD/T2D samples as comp

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

272 Hepatic overexpression of Cxcl1 and/or IL-8 promoted steatosis-to-NASH progression in HFD-fed m

273 a therapeutic effect (ps < 0.01) of hUCBC or IL-8 administration, which was correlated with decreases

274 s of inflammatory stress response in plasma (IL-8, MCP-1 and CRP collected two hours after temporary

275 oduction and NF-kappaB activation to prevent IL-8 upregulation stimulated by LCA; this prevention thu

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

277 eta1-mim downregulated TNF-alpha production, IL-8 gene expression, and cytokine secretion, upregulate

278 GAS virulence factors Streptolysin S, PrtS (IL-8 degrading proteinase), and SpeB (cysteine protease)

279 rferon (IFN)-gamma, IFN-alpha, IL-2, IL-2 R, IL-8, macrophage inflammatory protein (MIP)-1alpha, MIP-

280 These data suggest reduced IL-8 relative to IP-10 and reduced p-Tau(181) to charact

281 revealing the importance of assessing serum IL-8 levels in identifying unfavorable tumor immunobiolo

282 alysis, we show that elevated baseline serum IL-8 levels are associated with poor outcome in patients

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

284 ithelial cells and an inability to stimulate IL-8.

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

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

287 erm compared to those who delivered at term (IL-8 P = 0.02; IL-1beta P = 0.04).

288 Here, we demonstrate that IL-8 receptor, CXCR1 or CXCR2, modified CARs markedly en

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

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

291 ed Cxcl2, which led to the activation of the IL-8-mediated p-p38 signalling pathway.

292 s response ATF4, which bound directly to the IL-8 promoter.

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

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

295 al neuropathic pathways previously linked to IL-8 pathway.

296 antly decreased neutrophil transmigration to IL-8, but did not affect respiratory burst.

297 ls were higher in subjects with SAR, whereas IL-8 levels were higher in subjects without allergy.

298 ected by any of the treatments applied while IL-8 and TNF-alpha were reduced at treatments which comb

299 d these effects in GBM-EC co-cultures, while IL-8 supplementation increased CSC-mediated growth and i

300 imbs induced myeloid cell recruitment, while IL-8 knockdown resulted in defective myeloid cell retent