ライフサイエンスコーパス: interleukin-8

1 the expression of tumor necrosis factor and interleukin 8.

2 neutrophil spreading onto glass coated with interleukin 8.

3 expression or secretion of interleukin 6 and interleukin 8.

4 rkers, intercellular adhesion molecule 1 and interleukin 8.

5 ing to significant increases in secretion of interleukin 8.

6 ivin (BIRC5) and the CSC-associated cytokine interleukin-8.

7 a modulation of the proinflammatory cytokine interleukin-8.

8 o migrate towards HIE supernatant containing interleukin-8.

9 ely correlated with proinflammatory cytokine interleukin-8.

10 n 3 (two transcription factors); and induced interleukin-8.

11 ophils via vascular smooth muscle release of interleukin-8.

12 crosis factor receptor-1, interleukin-6, and interleukin-8.

13 proinflammatory cytokines interleukin-6 and interleukin-8.

14 nd protein production of NF-kappaB-regulated interleukin-8.

15 motif chemokine ligand 2, interleukin-6, and interleukin-8.

16 ligodeoxynucleotides, ammonium chloride, and interleukin-8.

17 elease of pro-inflammatory mediators such as interleukin-8.

18 is factor (44.73 vs 21.68 pg/mL; p < 0.001), interleukin-8 (124.76 vs 47.48 pg/mL; p = 0.028), and in

19 +/- 20.2 vs 111.5 +/- 29.6 pg/mL, P = .02), interleukin-8 (2196.1 +/- 737.9 vs 3753.2 +/- 1106.0 pg/

20 = 0.02), interleukin-6 (+91%; p = 0.03), and interleukin-8 (+42%; p = 0.02) upon the second challenge

21 osis factor: 26.95 vs 18.38 pg/mL, p = 0.02; interleukin-8: 70.75 vs 27.86 pg/mL, p = 0.002; interleu

22 (grades 3 and 4), the greatest of which was interleukin-8 (92,940 pg/mL, grade 4).

23 ne exposure, we observed a 98.9% increase in interleukin-8, a 21.4% decrease in plasminogen activator

24 ine MIP-2 is the functional homolog of human interleukin-8, a known risk factor for human TRALI.

25 BAL parameters, including neutrophil count, interleukin-8, alpha defensins and MMP-9, demonstrate hi

26 eron gamma, tumor necrosis factor alpha, and interleukin 8 and 10) were similar in both groups.

27 The association between interleukin 8 and GBA mutation status was replicated (P

28 levated interleukin-1 receptor antagonist or interleukin-8 and 2) whether bilateral infiltrates are a

29 receptor 9 was induced by costimulation with interleukin-8 and ammonia.

30 direct and indirect mechanisms by targeting interleukin-8 and CXCL1 secreted by the tumour endotheli

31 dysfunction, as demonstrated through reduced interleukin-8 and elevated leptin in VEDS.

32 Increased secretion of interleukin-8 and higher expression levels of the mucin

33 Increased levels of interleukin-8 and interleukin-10 were observed in childr

34 th of proinflammatory response, particularly interleukin-8 and interleukin-6 concentrations, inversel

35 nsfusion-related acute lung injury, systemic interleukin-8 and interleukin-6 levels were higher compa

36 udy identifies an association between plasma interleukin-8 and microvesicle tissue factor activity me

37 o analyze the effects of Klotho signaling on interleukin-8 and monocyte chemoattractant protein-1 pro

38 In contrast, the chemokines interleukin-8 and monocyte chemotactic protein-1 stayed

39 Lavage interleukin-8 and neutrophil levels were elevated.

40 BALF was assessed for pepsin, bile salts, interleukin-8 and neutrophils.

41 receptor 9 expression correlated with plasma interleukin-8 and peak ammonia concentration (r = 0.6; p

42 Interleukin-8 and S-100beta levels in quartile 4 were al

43 The gene expression of interleukin-6, interleukin-8 and tumor necrosis factor alpha was signif

44 d hyperproteinorrachia, and showed increased interleukin-8 and tumor necrosis factor-alpha concentrat

45 Levels of interleukin-8 and tumor necrosis factor-alpha produced b

46 Macrophages produced cytokines, such as interleukin-8 and tumor necrosis factor-alpha, to stimul

47 patients, men had higher admission levels of interleukin-8 and tumor necrosis factor-alpha.

48 ontained relatively higher concentrations of interleukin-8 and VEGF due to GRM1-mediated activation o

49 luding interleukin 1beta, interleukin 6, and interleukin 8, and marked inflammatory cervical infiltra

50 nducible protein 10/CXC chemokine ligand 10, interleukin 8, and monocyte chemotactic protein-1/CC che

51 onic acid and higher d-dimer, interleukin 6, interleukin 8, and soluble CD14 levels were associated w

52 C-reactive protein, temperature, interleukin 8, and soluble tumor necrosis factor recepto

53 20, hBD-2, interleukin 1beta, interleukin 6, interleukin 8, and tumor necrosis factor alpha) that can

54 matrix-degrading enzymes (MMP-2 and MMP-9), interleukin-8, and chemokine receptors (CXCR1, CXCR4, an

55 increase in plasma levels of interleukin-6, interleukin-8, and elastase-alpha1-antitrypsin complexes

56 ition, we measured changes in interleukin-6, interleukin-8, and interleukin-10 blood levels.

57 opoietin-2) and inflammation (interleukin-6, interleukin-8, and interleukin-33 and soluble suppressio

58 rleukin-1beta, interleukin-2, interleukin-6, interleukin-8, and monocyte chemoattractant protein 1),

59 rations of tumor necrosis factor receptor-1, interleukin-8, and regenerating islet-derived protein 3-

60 including interleukin-6, C-reactive peptide, interleukin-8, and soluble tumor necrosis factor recepto

61 r respiratory rate condition, interleukin-6, interleukin-8, and tumor necrosis factor-alpha concentra

62 ssion model incorporating oxygenation index, interleukin-8, and tumor necrosis factor-R2 was superior

63 of sepsis-related biomarkers have identified interleukin-8 as a robust outcome biomarker in pediatric

64 , arterial ammonia concentration, and plasma interleukin-8 associated with neutrophil exhaustion.

65 F6 by RNA interference and neutralization of interleukin-8, basic fibroblast growth factor, and vascu

66 1 (growth-related oncogene alpha) and CXCL8 (interleukin-8), both classes of nanobodies displayed inv

67 rease in concentrations of procalcitonin and interleukin-8, but not of interleukin-6.

68 ing pathway responsible for the induction of interleukin 8 by wood smoke extract in lung epithelial c

69 at of monocyte chemoattractant protein 1 and interleukin-8 by cultured adipocytes.

70 cytokine secretion (interleukin-6 P<0.0001, interleukin-8/C-X-C motif chemokine ligand 8 P=0.04, and

71 ysteine reduced the levels of interleukin-6, interleukin-8/C-X-C motif chemokine ligand 8, and monocy

72 ophage inflammatory protein-1alpha/CCL3, and interleukin-8/CCL8) and cytokines (interleukin-6, interl

73 noassay was evaluated by detecting the human interleukin 8 chemokine.

74 Serum levels of interleukin 8, chemokine (C-C motif) ligand 3, and tumor

75 d on myeloid cells [sTREM-1], interleukin-6, interleukin-8, chitinase-3-like protein-1, soluble tumor

76 ney injury marker 1 (Kim-1) and the cytokine interleukin-8 compared to the 2D cell cultures.

77 n in airway epithelial cells correlated with interleukin-8 concentrations and absolute neutrophil num

78 er interleukin-15 concentrations, and higher interleukin-8 concentrations, than were no acute exacerb

79 l airway abnormality, and interleukin-15 and interleukin-8 concentrations.

80 spholipase A2; at CYP2F1, with higher plasma interleukin-8 concentrations; at TREH, with lower concen

81 cantly increased levels of interleukin-5 and interleukin-8, critical cytokines of the innate immune s

82 findings in pediatric septic shock, a plasma interleukin-8 cutoff <220 pg/mL had a negative predictiv

83 ant 1-month increases in CRP, D-dimer, IL-6, interleukin 8, CXCL10, TNF-alpha, and interferon-gamma l

84 cell effector function in human newborns is interleukin-8 (CXCL8) production, which has the potentia

85 Interleukin-8 (CXCL8) release by neutrophils after IgLC

86 roduction around day +14 was associated with interleukin-8-driven neutrophil recovery.

87 eolar lavage fluid, levels of interleukin-6, interleukin-8, elastase-alpha1-antitrypsin complexes, th

88 E2 production and pro-inflammatory cytokine interleukin 8 expression and secretion.

89 Interleukin 8 expression was evaluated by using wild-typ

90 TFF2 and Muc2 was inversely correlated with interleukin-8 expression in CD (p = 0.027).

91 ection were assessed by measuring release of interleukin 8 from AGS cells (to detect cag pathogenicit

92 n the change in bronchoalveolar lavage fluid interleukin-8 from baseline to day 4 (p = .37) or day 8

93 thelium, and they enhanced the production of interleukin-8 from both types of cells.

94 city-induced release of the pro-inflammatory interleukin-8 from human corneal epithelial cells and re

95 d, including interleukin-1RA, interleukin-6, interleukin-8, G-CSF, and M-CSF (p < 0.001).

96 The interleukin 8 gene single-nucleotide polymorphism rs4073

97 eterious non-synonymous SNPs (nsSNPs) in the interleukin-8 gene using three steps.

98 s of RANKL, OPG, and inflammatory cytokines (interleukin-8, granulocyte colony-stimulating factor) we

99 Interleukin-4, interleukin-8, granulocyte macrophage colony-stimulating

100 protein BMP4 and several cytokines including interleukin-8, growth-related protein (GRO), and CCL2.

101 tor-alpha, interleukin-2, interleukin-6, and interleukin-8) have been associated with AF.

102 merged from initial screening-interleukin 6, interleukin 8, hepatocyte growth factor (HGF), tissue in

103 ion of macrophage inflammatory protein 2 (an interleukin-8 homolog) in lung epithelial cells and lung

104 ring inflammatory stimulation showed reduced interleukin 8 (IL-8) and CXCL1 secretion (P < .001).

105 miR-126 KD cells showed lower expression of interleukin 8 (IL-8) and CXCL1, both on the mRNA and pro

106 We determined fecal interleukin 8 (IL-8) and lactoferrin protein concentrati

107 itochondrial depolarization and secretion of interleukin 8 (IL-8) and leukotriene B4 (LTB4) and was p

108 gation of NF-kappaB target genes such as the interleukin 8 (IL-8) and TNF genes.

109 ation of NF-kappaB p65 and the expression of interleukin 8 (IL-8) following ectopic expression and du

110 SP6 also elicited higher levels of interleukin 8 (IL-8) in the lower genital tract and incr

111 Specifically, CCL3 levels, but not CXCL8/interleukin 8 (IL-8) levels, were higher within discrete

112 Specific inhibition of neutrophil influx by interleukin 8 (IL-8) neutralization resulted in the coor

113 lly, Xps, and predominantly StmPr1, degraded interleukin 8 (IL-8) secreted by A549 cells during cocul

114 ants were tested for their ability to induce interleukin 8 (IL-8) secretion and translocation of Stx2

115 ng N. lactamica PorB induces lower levels of interleukin 8 (IL-8) secretion than wild-type N. meningi

116 by the gastric cell "hummingbird" phenotype, interleukin 8 (IL-8) secretion, and CagA translocation a

117 results also indicate the essential role of interleukin 8 (IL-8) signaling for the acquisition and/o

118 scribe the inhibitory effect of metformin in interleukin 8 (IL-8) upregulation by lithocholic acid (L

119 tumor necrosis factor alpha (TNF-alpha), and interleukin 8 (IL-8) were compared between dichotomous g

120 mediated by FOXA1 binding to the promoter of interleukin 8 (IL-8), a chemokine previously shown eleva

121 atory role for blastemal progenitors through interleukin 8 (IL-8), a highly expressed cytokine in sub

122 tor alpha (TNF-alpha), interleukin 6 (IL-6), interleukin 8 (IL-8), and interleukin 10 (IL-10) concent

123 n 1, growth-related oncogene, interleukin 6, interleukin 8 (IL-8), and tumor necrosis factor were det

124 were associated with increased expression of interleukin 8 (IL-8), CXCL2, IL-1beta, tumor necrosis fa

125 che showed that macrophages mounted a robust interleukin 8 (IL-8), neutrophil-attracting response to

126 ell adhesion molecule 1 (PECAM-1), CD99, and interleukin 8 (IL-8).

127 ty and with certain cytokines, in particular interleukin 8 (IL-8)/CXCL8.

128 IV regardless of cognition, but elevated CSF interleukin 8 (IL-8/CXCL8) only in HIV-NC but not HAND.

129 for their anti-inflammatory activity against interleukin-8 (IL-8) and for the inhibition of matrix me

130 Both interleukin-8 (IL-8) and human beta-defensin 2 (HbetaD2)

131 associations between dupA cluster status and interleukin-8 (IL-8) and IL-12 production were also exam

132 es), we show the induction of TLR2-dependent interleukin-8 (IL-8) and IL-6 secretion in vitro, the in

133 atory activity response relationship against interleukin-8 (IL-8) and inhibition of matrix metallopro

134 kinase (MAPK) and proinflammatory cytokines interleukin-8 (IL-8) and KC (from human and mouse cells,

135 other cell types secreted various levels of interleukin-8 (IL-8) and monocyte chemoattractant protei

136 induces greater expression of the chemokine interleukin-8 (IL-8) and the cytokine tumor necrosis fac

137 This platform is tested by screening interleukin-8 (IL-8) and vascular endothelial growth fac

138 Using interleukin-8 (IL-8) as an example analyte, we demonstra

139 ant release of the immunomodulatory cytokine interleukin-8 (IL-8) as well as the antimicrobial peptid

140 n2 (Ent+Lcn2) leads to enhanced secretion of interleukin-8 (IL-8) compared to that induced by either

141 ropean strains promoted significantly higher interleukin-8 (IL-8) expression than did African strains

142 and the contribution of ERK1/2 activation to interleukin-8 (IL-8) expression.

143 escape coincided with increased secretion of interleukin-8 (IL-8) from tumors into the plasma, and co

144 Interleukin-8 (IL-8) gene polymorphisms have been consid

145 MIT 97-6194-5 induced significant levels of interleukin-8 (IL-8) in HT-29 cell culture supernatants

146 Serum interleukin-8 (IL-8) levels and tumor neutrophil infiltr

147 cancer cells, and that adipokines including interleukin-8 (IL-8) mediate these activities.

148 n of TREM-1 on the GEC led to an increase in interleukin-8 (IL-8) mRNA levels.

149 their inhibitory activity against chemokine interleukin-8 (IL-8) production before and after cigaret

150 lation of nuclear factor-kappaB, and reduced interleukin-8 (IL-8) production in human neutrophils.

151 ing sites abolished or decreased IKK-induced interleukin-8 (IL-8) promoter activity.

152 SF from these patients did not stimulate interleukin-8 (IL-8) release from TLR transfectants.

153 culture cells and mouse ilium, resulting in interleukin-8 (IL-8) release.

154 -induced NF-kappaB and inflammatory cytokine interleukin-8 (IL-8) reporter activation depended on Rel

155 ) cells and neutrophils as well as a reduced interleukin-8 (IL-8) response.

156 ad cells, lactate dehydrogenase release, and interleukin-8 (IL-8) secretion and decreased apical cili

157 activated B cells (NF-kappaB) activation and interleukin-8 (IL-8) secretion are attributed to T4SS-de

158 nocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) secretion from 3T3-L1 adipocytes.

159 occal supernatants and tended to induce less interleukin-8 (IL-8) secretion in primary human fallopia

160 A significantly dysregulated interleukin-8 (IL-8) signaling network was identified in

161 from a C. jejuni 11168H cdtA mutant induced interleukin-8 (IL-8) to the same extent as did wild-type

162 lost T4SS function, defined as a normalized interleukin-8 (IL-8) value of <0.3 relative to the input

163 trial of cerebral palsy, the level of plasma interleukin-8 (IL-8) was increased, correlated with moto

164 y detecting the approximately 8 kDa cytokine interleukin-8 (IL-8) with a limit of detection and dynam

165 genously produced chemokines (in particular, interleukin-8 (IL-8)).

166 ctant protein-1 (MCP-1), a CC chemokine, and interleukin-8 (IL-8), a CXC chemokine, along with their

167 Interleukin-8 (IL-8), a key modulator of neutrophil func

168 igh-affinity receptors for the CXC chemokine interleukin-8 (IL-8), a major mediator of immune and inf

169 CXCR1 is a receptor for the chemokine interleukin-8 (IL-8), a mediator of immune and inflammat

170 d sensor for the detection in serum of human interleukin-8 (IL-8), a pro-angiogenic chemokine implica

171 had increased production of MIG (CXCL9) and interleukin-8 (IL-8), and decreased production of IL-10,

172 Fibronectin, interleukin-8 (IL-8), biotin, and neutrophil gelatinase-

173 Expression of interleukin-8 (IL-8), cyclooxygenase-2 (COX-2), and heme

174 interferon gamma-induced protein 10 (IP-10), interleukin-8 (IL-8), epidermal growth factor (EGF), mat

175 f vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), human beta-defensin 1 (hBD-1), and

176 uction of several cellular factors including interleukin-8 (IL-8), in both, normal and tumorigenic ce

177 activating factors for phagocytes, including interleukin-8 (IL-8), monocyte chemotactic protein 1 (MC

178 WF levels of angiopoietin-2, interleukin-8 (IL-8), tumor necrosis factor-alpha (TNF-a

179 increase GBM invasiveness and growth through interleukin-8 (IL-8)-mediated enrichment of CSCs.

180 secretion, and suppresses hypersecretion of interleukin-8 (IL-8).

181 roduction of the pro-inflammatory chemokine, interleukin-8 (IL-8).

182 l secretion of the proinflammatory chemokine interleukin-8 (IL-8).

183 shedding and the production of the cytokine interleukin-8 (IL-8).

184 expression of inflammatory genes, including interleukin-8 (IL-8).

185 of fibronectin, fibrinogen, and the cytokine interleukin-8 (IL-8).

186 mutated DNA damage pathway and the chemokine interleukin-8 (IL-8).

187 is factor-alpha (TNF-alpha) or the chemokine interleukin-8 (IL-8, CXCL8) compared to controls.

188 Proinflammatory and pro-angiogenic chemokine interleukin-8 (IL-8, CXCL8) contributes to ovarian cance

189 y response characterized by the secretion of interleukin-8 (IL-8; also called CXCL8) and the expressi

190 The human chemokine interleukin-8 (IL-8; CXCL8) is a key mediator of innate

191 by strong CXCL2 (mouse functional homolog of interleukin-8 [IL-8]) and tumor necrosis factor alpha (T

192 rum leptin, adiponectin, KC (mouse analog of interleukin-8 [IL-8]), monokine induced by interferon-ga

193 s in MDS, AML, and control samples and found interleukin 8 (IL8) to be consistently overexpressed in

194 Plasma levels of interleukin 8 (IL8), IL13, chemokine (C-C motif) ligand

195 dinucleotide (NAAD) inside endolysosomes of interleukin 8 (IL8)-treated lymphokine-activated killer

196 e tumor necrosis factor alpha (TNFalpha) and interleukin 8 (IL8).

197 chemokine (C-C motif) ligand 20 (CCL20) and interleukin 8 (IL8).

198 Interleukin-8 (IL8) receptors IL8RA and IL8RB on neutrop

199 Studying the regulation of interleukin-8 (IL8), a newly identified AML1-ETO-activat

200 ered genes include humanin-like-8 (MTRNRL8), interleukin-8 (IL8), and serpin peptidase inhibitor, cla

201 pressing gingipain-associated degradation of interleukin-8 (IL8).

202 production of the neutrophil-chemoattractant interleukin 8 in the lungs.

203 lating endogenous DNA as well as ammonia and interleukin-8 in a synergistic manner inducing systemic

204 crosis factor -alpha, interleukin-1beta, and interleukin-8 in a temporal manner may indicate early ba

205 ession of monocyte chemotactic protein-1 and interleukin-8 in porcine jugular vein ECs.

206 lpha were reduced in the injured lung and of Interleukin-8 in the contralateral lung, respectively.

207 or necrosis factor alpha, interleukin-6, and interleukin-8 in the respiratory tract and central nervo

208 rulent strains to translocate CagA or induce interleukin 8, indicating that hypervirulent phenotypes

209 agellin and lipopolysaccharide are the major interleukin-8 inducers.

210 Interleukin-8 induction by wood smoke extract in lung ep

211 and activator of transcription protein 3 and interleukin-8 induction.

212 in 3 activation by inhibitors attenuated the interleukin-8 induction.

213 and activator of transcription protein 3 and interleukin-8 induction.

214 AMP-activated protein kinase activation, and interleukin-8 induction.

215 ulated kinase and Jun N-terminal kinase, and interleukin-8 induction.

216 ge colony-stimulating factor, interleukin-6, interleukin-8, interferon-inducible protein-10, monocyte

217 decreased interleukin 1beta, interleukin 6, interleukin 8, interleukin 10, and tumor necrosis factor

218 cytokines (interleukin 1beta, interleukin 6, interleukin 8, interleukin 17, interferon gamma, and tum

219 A group consisting of interleukin-6, interleukin-8, interleukin-10, and fractalkine was ident

220 mponent 1, mainly loaded with interleukin-6, interleukin-8, interleukin-10, and fractalkine, was sign

221 statistically significant increase in plasma interleukin-8, interleukin-10, and interleukin-1 recepto

222 interleukin-4, interleukin-5, interleukin-6, interleukin-8, interleukin-10, interleukin-12/interleuki

223 in-1beta, interleukin-1alpha, interleukin-6, interleukin-8, interleukin-10, interleukin-15, eotaxin-3

224 rations of interleukin-1beta, interleukin-6, interleukin-8, interleukin-10, interleukin-18, and tumor

225 Interleukin-6, interleukin-8, interleukin-10, interleukin-18, and tumor

226 eukin-1ra, interleukin-1beta, interleukin-6, interleukin-8, interleukin-10, interleukin-18, monocyte

227 With ubiquitin treatment, tissue levels of Interleukin-8, Interleukin-10, Tumor Necrosis Factor alp

228 rleukin-1beta, interleukin-4, interleukin-6, interleukin-8, interleukin-10, tumor necrosis factor-alp

229 ls of tissue necrosis factor, interleukin-6, interleukin-8, interleukin-17A, and interleukin-10 were

230 nt protein D, angiopoietin-2, interleukin-6, interleukin-8, interleukin-33, and soluble suppression o

231 ases, bronchoalveolar lavage fluid levels of interleukin-8, interleukin-6, and elastase-alpha1-antitr

232 Interleukin-8 level (bronchoalveolar lavage) did not dif

233 ut human beta-defensin 2 (HBD-2), HBD-3, and interleukin 8 levels decreased after unprotected sex.

234 Clara cell secretory protein (CCSP) and interleukin 8 levels were assessed in the bronchoalveola

235 Bronchoalveolar lavage CCSP and CCSP/interleukin 8 levels were low and decreasing early after

236 own syndrome had increased interleukin-6 and interleukin-8 levels compared to males with Down syndrom

237 alpha, interleukin-1beta, interleukin-6, and interleukin-8 levels were detected as early as 4 days pr

238 alpha, interleukin-1beta, interleukin-6, and interleukin-8 levels were observed within patients with

239 ion, microvesicle tissue factor activity and interleukin-8 levels were significantly and positively c

240 y end point was bronchoalveolar lavage fluid interleukin-8 levels.

241 There was no difference in interleukin-8 levels.

242 conditions regarding the capture of an anti-interleukin 8 mAb, using a multimodal ligand (2-benzamid

243 those measured after placebo treatment) and interleukin-8 (mean peak levels of 57.0% [p<0.05 vs plac

244 of tumor necrosis factor alpha (TNFalpha) or interleukin-8 messenger RNA.

245 a-B (NF-kappaB) activation and production of interleukin-8, monocyte chemoattactrant protein-1, and i

246 ivariable analysis included higher levels of interleukin-8, monocyte chemoattractant protein-1, resis

247 lial cell (EC) expression of chemokines (eg, interleukin-8, monocyte chemotactic protein-1) and other

248 Betalains dampened cyclooxygenase-2 and interleukin-8 mRNA expression after lipopolysaccharide i

249 CFA treatment induced CXCL1 and interleukin-8 mRNA in BEAS-2B and primary human bronchia

250 Ks), p38 activation, and a superinduction of interleukin-8 mRNA.

251 PBP induced interleukin 8 or CXCL2, tumor necrosis factor alpha, int

252 (n = 9) presented with a 10-fold increase in interleukin-8 over extracorporeal membrane oxygenation p

253 gnificantly associated with plasma levels of interleukin 8 (P = .001), monocyte chemotactic protein 1

254 concentrations of interleukin 6 (p<0.0001), interleukin 8 (p=0.002), and osteopontin (p<0.0001) were

255 high concentrations (relative to median) of interleukin 8 (p=0.006), osteopontin (p=0.0004), HGF (p=

256 differentiate PGD3 cases from controls were interleukin-8 (P < 0.001, AUC = 0.93) and growth-regulat

257 ses were reduced, and leukocyte recruitment (interleukin-8 pathway, P = 1.41E-5) and extravasation pr

258 ction efficiency) and short interfering RNA (interleukin-8, PCNA, and Bax), as a validation of effect

259 Although elevated plasma interleukin-8 (pIL-8) has been associated with poor outc

260 s of interest-angiopoietin 2, interleukin 6, interleukin 8, placental growth factor, soluble TIE-1, s

261 ed LPS-induced inflammation, as monitored by interleukin 8 production.

262 E. faecalis MN1 inhibited interleukin-8 production from human vaginal epithelial c

263 ed nuclear factor-kappaB activation, reduced interleukin-8 production, and decreased epithelial injur

264 s which appear responsible for inhibition of interleukin-8 production, as well as inhibition of T cel

265 owed similar inhibition (35.5% and 35.9%) of interleukin-8 production, due to PEF treatment and heati

266 mmatory actions, which include reductions in interleukin-8 production, neutrophil migration and/or fu

267 d are capable of inducing AEC activation and interleukin-8 production.

268 ng the top of the lamellipodium, whereas the interleukin 8 receptors CXCR1 and CXCR2 and the integrin

269 on was also shown to manifest an increase in interleukin 8 release from A549 lung epithelial cells bu

270 hagocytosis promotes killing of S aureus and interleukin-8 release by neutrophils.

271 apoptosis and inhibition of cell growth and interleukin-8, RHAMM, HAS2, CD44, and MMP-9 expression.

272 n of TLR10 completely abrogated TLR2-induced interleukin 8 secretion by HEK-293 cells in response to

273 region and CagA expression levels influence interleukin 8 secretion by the host gastric epithelial c

274 RIP1 kinase triggered JNK3/MAPK10-dependent interleukin-8 secretion and FADD-mediated proapoptotic c

275 gA EPIYA and CRPIA domains, V225d stimulates interleukin-8 secretion and the hummingbird phenotype in

276 nce, biofilm formation, and pro-inflammatory interleukin-8 secretion compared with ST31 isolates.

277 and induce caspase-9-mediated apoptosis and interleukin-8 secretion.

278 tion of a JAK2-dependent pathway, leading to interleukin-8 secretion.

279 A reduced set of three biomarkers (interleukin-8, soluble tumor necrosis factor receptor-1,

280 thrombomodulin, endocan, interleukin-6, and interleukin-8 than those without acute respiratory distr

281 1/CCL-2, MIP-1alpha/CCL-3, RANTES/CCL-5, and interleukin 8) than SARS-CoV.

282 -inflammatory factors including the cytokine interleukin-8, the chemokines (C-X-C motif) ligand 1 and

283 hase: granulocyte colony-stimulating factor, interleukin-8, tissue necrosis factor-alpha, interleukin

284 The ratio of proinflammatory (interleukin-8) to anti-inflammatory (interleukin-10) pla

285 attractant protein-1, interleukin-1beta, and interleukin-8 transcripts levels compared with control.

286 on of nuclear factor kappa B, interleukin-6, interleukin-8, transforming growth factor beta, and vasc

287 tor-alpha, interleukin-1beta, interleukin-6, interleukin-8, transforming growth factor-beta, and proc

288 T-cells (NFAT) pathway and the production of interleukin 8 triggered by histamine in HUVECs.

289 (IL-1alpha), IL-1beta, interleukin 6 (IL-6), interleukin 8, tumor necrosis factor alpha, and interleu

290 report that the procancerous cytokine IL-8 (interleukin-8) upregulates CXCR7 expression along with l

291 es identified associations of interleukin 6, interleukin 8, VEGF, osteopontin, E-selectin, and HGF wi

292 dhesion molecule-1, and leptin and decreased interleukin-8 versus controls.

293 The protein level of interleukin-8 was also increased.

294 Interleukin-8 was quantified in serum and bronchoalveola

295 n addition, neutrophil chemotaxis induced by interleukin-8 was significantly enhanced when cells were

296 Interleukin-8 was significantly higher in nonsurvivors c

297 In interleukin-8, we substituted Pro for each of the three

298 ocan, C-reactive protein, interleukin-6, and interleukin-8 were different between sepsis and noninfec

299 kers (C-reactive protein, interleukin-6, and interleukin-8) were measured from peripheral plasma coll

300 ncreased synthesis of the secreted chemokine interleukin 8, which contributes to metastasis, inflamma