ライフサイエンスコーパス: neutrophil recruitment

1 ction which then enhances reparative hepatic neutrophil recruitment.

2 the blockade of which resulted in increased neutrophil recruitment.

3 Ang-1 resulted in a significant reduction in neutrophil recruitment.

4 the blockade of which significantly reduced neutrophil recruitment.

5 nophil values and cytokine levels related to neutrophil recruitment.

6 CL1 chemokine by keratinocytes, resulting in neutrophil recruitment.

7 e and sagA deletions synergistically enhance neutrophil recruitment.

8 idase in myeloid cells suppresses intestinal neutrophil recruitment.

9 d MSCs promote tumor metastasis via CXCR2(+) neutrophil recruitment.

10 ispensable for beta2 integrin activation and neutrophil recruitment.

11 -inflammatory role for Ang-1 with respect to neutrophil recruitment.

12 effect of IL-1beta in bitten mice abrogates neutrophil recruitment.

13 ratory distress syndrome (ARDS) by enhancing neutrophil recruitment.

14 ired for fMLF-triggered Mac-1 activation and neutrophil recruitment.

15 s, decreased IL-10 production, and increased neutrophil recruitment.

16 ed MD2-dependent and CD14-independent innate neutrophil recruitment.

17 XCL1 in the interstitium effectively reduced neutrophil recruitment.

18 ytes have been shown to involve promotion of neutrophil recruitment.

19 nary inflammation, characterized by enhanced neutrophil recruitment.

20 he absence of SP-A and is not dependent upon neutrophil recruitment.

21 ignificant increases in mucin production and neutrophil recruitment.

22 dida albicans infection due to impairment in neutrophil recruitment.

23 is in driving CXCL5 expression and pulmonary neutrophil recruitment.

24 bitory factor (MIF) have additive effects in neutrophil recruitment.

25 e production, and promoted calcium-dependent neutrophil recruitment.

26 attenuating lung injury caused by excessive neutrophil recruitment.

27 ors at the IL-36gamma promoter, resulting in neutrophil recruitment.

28 are key mechanisms facilitating appropriate neutrophil recruitment.

29 chemokines responsible for inflammation and neutrophil recruitment.

30 y for the inhibitory effect of colchicine on neutrophil recruitment.

31 rtant mediators of the processes involved in neutrophil recruitment.

32 creased levels of chemokine CCL2 and greater neutrophil recruitment.

33 ammatory diseases characterized by excessive neutrophil recruitment.

34 nsforming growth factor (TGF) beta-dependent neutrophil recruitment.

35 or 2 deficiency exacerbates inflammation and neutrophil recruitment.

36 bial-induced COPD exacerbations by promoting neutrophil recruitment.

37 ctions impact bacterial-induced acute airway neutrophil recruitment.

38 DR has a proinflammatory profile and promote neutrophil recruitment.

39 ing mucin 5AC and reduced LPS-induced airway neutrophil recruitment 6 and 24 hours after challenge.

40 acillus subtilis with the ability to trigger neutrophil recruitment across human-cultured monolayers.

41 t factor in promoting hepoxilin A3-dependent neutrophil recruitment across pulmonary epithelium in a

42 or without bacterial LPS stimulation, affect neutrophil recruitment, activation, and the formation of

43 d following challenge with CI 79, indicating neutrophil recruitment/activation associated with signif

44 in the sensitization phase of CHS regulating neutrophil recruitment and accumulation in the skin thro

45 Hence, CFP-10 may contribute specifically to neutrophil recruitment and activation during M. tubercul

46 igh levels of CXCL2, which further amplified neutrophil recruitment and activation in an autocrine an

47 A key driver of neutrophil recruitment and activation is the complement

48 We propose that, during infection, neutrophil recruitment and activation may neutralize pat

49 These findings confirm that neutrophil recruitment and activation play an essential

50 hese interactions allow monocytes to promote neutrophil recruitment and activation within the glomeru

51 ion as a promising treatment option to block neutrophil recruitment and activation.

52 t that CCRL2-deficient mice have a defect in neutrophil recruitment and are protected in 2 models of

53 m patients with acute appendicitis confirmed neutrophil recruitment and bacterial capture at FALCs.

54 Macrophage FABP4 is required for neutrophil recruitment and bacterial clearance in Pseudo

55 Faster neutrophil recruitment and bacterial clearance were obse

56 Neutrophil recruitment and bacterial clearance were rest

57 ell (DC)-induced T-helper 17 (Th17)-mediated neutrophil recruitment and bacterial clearance.

58 eversed the siglec-E-mediated suppression of neutrophil recruitment and blocked neutrophil ROS produc

59 lent group A streptococcus (GAS) can inhibit neutrophil recruitment and cause systemic infection in a

60 selective cytokine hypersecretion, increased neutrophil recruitment and clinical exacerbation by expo

61 sembling nonsmoked mice, with a reduction in neutrophil recruitment and CXCL1 chemokine expression.

62 CXCL8 is able to induce intestinal zebrafish neutrophil recruitment and cxcl8-l1 expression, demonstr

63 e in the host by B. dolosa strains, and yet, neutrophil recruitment and cytokine production were lowe

64 matory response during infection by reducing neutrophil recruitment and cytokine production, resultin

65 airspaces which, in turn, results in reduced neutrophil recruitment and diminished Th2 response.

66 yte depletion also resulted in reductions in neutrophil recruitment and dwell time in glomerular capi

67 nd lymphocytes, accompanied by a significant neutrophil recruitment and early interleukin-10 (IL-10)

68 nduce the pathologic process associated with neutrophil recruitment and EC damage.

69 By contrast, CXCL5 was dispensable for neutrophil recruitment and effective bacterial clearance

70 activation of NF-kappaB (RelA) and increased neutrophil recruitment and elastase activity.

71 ecreased proinflammatory cytokine levels and neutrophil recruitment and enhanced T-cell recruitment i

72 ur data reveal that ecSOD activity modulates neutrophil recruitment and function in a cell-extrinsic

73 he enzymes that control their production, on neutrophil recruitment and function is not well understo

74 To further investigate the role of CD45 in neutrophil recruitment and function, we analyzed transge

75 ossess a microenvironment that may influence neutrophil recruitment and function.

76 multiple Mac-1 activation events involved in neutrophil recruitment and functions during sterile infl

77 a demonstrate a key role for candidalysin in neutrophil recruitment and fungal virulence during disse

78 Here, we summarize existing models of neutrophil recruitment and highlight recent discoveries

79 influenza A-induced STAT1 signaling inhibits neutrophil recruitment and increases susceptibility to p

80 ist ameliorated the effects of LTA, blocking neutrophil recruitment and increasing the expression of

81 that NLRP3 inflammasome activation promotes neutrophil recruitment and inflammation during infection

82 XCR2 is necessary for Brucella-induced focal neutrophil recruitment and inflammation.

83 cumulate in inflamed skin where they augment neutrophil recruitment and inflammation.

84 t C. gattii infection could dampen pulmonary neutrophil recruitment and inflammatory cytokine product

85 fic T-cell responses, yet how VACV modulates neutrophil recruitment and its significance in the immun

86 ing as both effector cells and regulators of neutrophil recruitment and life span.

87 sser extent, the promotion of adipose tissue neutrophil recruitment and M1 polarization of gene expre

88 Neutrophil recruitment and neutrophil extracellular trap

89 resses bacterial endotoxin-induced pulmonary neutrophil recruitment and neutrophil extracellular trap

90 ction and suggest that AKT2 is important for neutrophil recruitment and neutrophil-platelet interacti

91 asal pneumococcal colonization rescued nasal neutrophil recruitment and prevented invasive disease in

92 d-type, a finding associated with diminished neutrophil recruitment and reduced fluid accumulation in

93 Here we review the mechanisms that regulate neutrophil recruitment and resolution at sites of tissue

94 -specific knockout of Cx43 enhanced alveolar neutrophil recruitment and secretion of proinflammatory

95 dothelial cell-derived CD95L in induction of neutrophil recruitment and support the use of therapeuti

96 ed the expression of important regulators of neutrophil recruitment and survival by oral epithelial c

97 Both inhibition of SDF-1-mediated neutrophil recruitment and systemic depletion of neutrop

98 that neither is sufficient for inhibition of neutrophil recruitment and systemic infection by hypervi

99 e synergistic contributions to inhibition of neutrophil recruitment and systemic infection in subcuta

100 Severe asthma (SA) is associated with neutrophil recruitment and T helper (TH )17 chemokine ov

101 the receptor antagonist (anakinra) decreases neutrophil recruitment and T helper 17 responses and pro

102 acute and chronic inflammation by targeting neutrophil recruitment and that this effect, at least in

103 ssue-specific responses in the regulation of neutrophil recruitment and the initiation and resolution

104 Furthermore, neutrophil recruitment and the neutrophil cytokines, CXC

105 The commensal-specific response drove neutrophil recruitment and the release of antimicrobials

106 ceptor (FcalphaRI) on neutrophils results in neutrophil recruitment and the release of neutrophil ext

107 ition of this chemotaxis abolished increased neutrophil recruitment and tumor metastasis.

108 onary inflammation, which is associated with neutrophil recruitment and weight loss.

109 ction in GAS skin invasion and inhibition of neutrophil recruitment and whether SsE is a viable targe

110 R12) dampens myocardial inflammation, limits neutrophils recruitment and monocyte chemoattractant pro

111 factor (TNF) and interleukin-6 (IL-6), more neutrophil recruitment, and a lower bacterial load in lu

112 cant reduction of bacterial burden, enhanced neutrophil recruitment, and ameliorated lung histopathol

113 icantly reduced systemic inflammation, liver neutrophil recruitment, and hepatotoxicity.

114 red the production of IL-1beta and CXCL1 and neutrophil recruitment, and increased fungal proliferati

115 led to activation of coagulation, increased neutrophil recruitment, and increased PAR-1 expression.

116 RAM-dependent production of CXCL2, increased neutrophil recruitment, and led to PGD, which was indepe

117 associated with reduced lung injury, reduced neutrophil recruitment, and lower cytokine levels.

118 sequently promoting inflammasome activation, neutrophil recruitment, and M1-macrophage polarization i

119 is factor (TNF)-alpha and IL-17A, pathologic neutrophil recruitment, and microvascular remodeling.

120 respect to bacterial clearance, weight loss, neutrophil recruitment, and MIP-2 production.

121 de novo synthesis of Cxcl2, amplification of neutrophil recruitment, and potentiation of their antiba

122 CovS mutants in skin invasion, inhibition of neutrophil recruitment, and virulence in subcutaneous in

123 disease; however, the signals driving early neutrophil recruitment are poorly known.

124 tive regulation of integrin adhesiveness and neutrophil recruitment are poorly understood.

125 gnaling axis identified HIF-2alpha-dependent neutrophil recruitment as an essential mechanism to incr

126 ly, suppressing IL-1beta expression to limit neutrophil recruitment as each phagocyte eliminated nume

127 ults explain how early H2O2 signal regulates neutrophil recruitment at all phases, directly via Lyn o

128 is functional to finely tune CXCR2-mediated neutrophil recruitment at sites of inflammation.

129 lar V. cholerae DNases were not required for neutrophil recruitment, but DNase-deficient V. cholerae

130 Neutrophil recruitment by dermal cDC1s was also observed

131 Metoprolol acts during early phases of neutrophil recruitment by impairing structural and funct

132 Dampening early neutrophil recruitment by neutralization of IL-1alpha, G

133 at, in inflammation, Lp(a)/apo(a) suppresses neutrophil recruitment by plasminogen-independent cytoki

134 gs revealed a dual mechanism of monocyte and neutrophil recruitment by T cells relying on overlapping

135 erleukin-1- and 12/15-lipoxygenase-dependent neutrophil recruitment cascade that promotes bacterial r

136 The neutrophil recruitment cascade to inflamed tissues invol

137 tivating chemokines in vitro, and diminishes neutrophil recruitment, causing significant mortality in

138 These changes in neutrophil recruitment could be explained by regulation

139 tion, we show in this study that MVA-induced neutrophil recruitment depends on complement component C

140 ion marker, can drive innate IL-1R-dependent neutrophil recruitment during infection with the lung-mi

141 The small GTPase Rac is required for neutrophil recruitment during inflammation, but its guan

142 and pathogen factors that promote protective neutrophil recruitment during invasion of the CNS by Can

143 factors, plays a crucial role in regulating neutrophil recruitment during lung inflammation.

144 ing to the selective activation of Mac-1 and neutrophil recruitment during sterile inflammation.

145 In this study, we investigated Nrf2 role in neutrophil recruitment during the sensitization phase of

146 her plasma CXCL1/KC levels and enhanced lung neutrophil recruitment early after infection, and lower

147 reduces cardiomyocyte cell death and blocks neutrophil recruitment following heart transplantation.

148 In contrast, in vivo neutrophil recruitment following thioglycollate-induced

149 inflammatory disorders in which dysregulated neutrophil recruitment, function, and elimination serve

150 bacterial infections, its role in regulating neutrophil recruitment, granulopoiesis, and neutrophil m

151 ial cells was associated with suppression of neutrophil recruitment, IgA secretions, Th2 responses, a

152 increased survival, ii) increased pulmonary neutrophil recruitment, iii) increased bacterial clearan

153 PLY triggered neutrophil recruitment in a 12-LOX-dependent manner in v

154 on in kidney macrophage IL-1beta and reduced neutrophil recruitment in a murine model of antibody-med

155 CD37-deficient mice showed impaired neutrophil recruitment in a peritonitis model.

156 RtxA and HlyA played no discernible role in neutrophil recruitment in a wild-type background.

157 Reconstitution of CXCL1 or CXCL2 restored neutrophil recruitment in apo(a)tg mice.

158 eceptor after zymosan challenge reduced lung neutrophil recruitment in CGD to WT levels.

159 , but provoked a cooperative intraperitoneal neutrophil recruitment in mice when co-injected with CXC

160 down-regulation in vivo promoted LPS-induced neutrophil recruitment in mouse lung but delayed neutrop

161 decreases lung IL-17A expression and airway neutrophil recruitment in response to acute K. pneumonia

162 or coreceptor CD14 on donor TRAMs prevented neutrophil recruitment in response to endotoxin and amel

163 dent alveolar macrophages (TRAMs) attenuated neutrophil recruitment in response to endotoxin as shown

164 on, which serves to amplify the magnitude of neutrophil recruitment in response to epithelial infecti

165 nds reduces neutrophil velocity and inhibits neutrophil recruitment in response to inflammation in a

166 clock protein Bmal1 was required to regulate neutrophil recruitment in response to inflammatory chall

167 e for IL-1beta, CXCL1, and CCL7 in mediating neutrophil recruitment in response to S. pneumoniae infe

168 ive oxygen and nitrogen species release, and neutrophil recruitment in the ears of CD1 mice.

169 e of enhanced plasma CXCL1 levels as well as neutrophil recruitment in the KO mice.

170 Neutrophil recruitment in the lung of superinfected mice

171 These phenotypic changes may promote rapid neutrophil recruitment in the presence of pathogens but

172 strate that IL-36gamma is a key regulator of neutrophil recruitment in the vaginal microenvironment a

173 ophilic inflammation, and the mechanisms for neutrophil recruitment in this context are poorly unders

174 7, but not CXCL1 and CCL2, had a key role in neutrophil recruitment in this model.

175 changes induced by IFN-gamma priming reduce neutrophil recruitment in vitro and in vivo.

176 Hes1 negatively regulated neutrophil recruitment in vivo in a manner that was depe

177 hat CXC ELR+ chemokines might be involved in neutrophil recruitment in vivo To test that hypothesis,

178 Increased neutrophil recruitment in vivo was associated with incre

179 Candidalysin induces immune activation and neutrophil recruitment in vivo, and it promotes mortalit

180 main is critical for integrin activation and neutrophil recruitment in vivo.

181 be dispensable for beta2 integrin-dependent neutrophil recruitment in vivo.

182 LPS-stimulated FMs further augmented neutrophil recruitment, inflammatory cytokine/chemokine

183 ed to induce robust vaginal immunopathology (neutrophil recruitment, interleukin-1beta [IL-1beta] sec

184 lear disruption of lung epithelia, decreased neutrophil recruitment into infected lungs, and increase

185 y enhancing both circulating neutrophils and neutrophil recruitment into infected lungs, by reducing

186 e showed recently that this activity dampens neutrophil recruitment into inflamed tissue and is requi

187 deactivation of integrins and regulation of neutrophil recruitment into inflamed tissue.

188 gh pannexin-1, a process that may facilitate neutrophil recruitment into metabolic tissues during obe

189 rol mice after pIVCL and bile-duct ligation; neutrophil recruitment into sinusoidal lumen of liver mi

190 her Aspergillus fumigatus burden and reduced neutrophil recruitment into the airways.

191 model, CD45E613R mice displayed a decreased neutrophil recruitment into the alveolar compartment, wh

192 with these findings, we observe that in vivo neutrophil recruitment into the inflamed peritoneum of m

193 with wild-type mice, including reduction of neutrophil recruitment into the joint cavity and IL-1bet

194 of cytokines (PTX3, CXCL1, and IL-1beta) and neutrophil recruitment into the joint cavity.

195 ggered by integrin engagement is involved in neutrophil recruitment into the lung and bacterial clear

196 BP4(-/-) mice were associated with a delayed neutrophil recruitment into the lungs and were followed

197 Allergen airway exposure induced higher neutrophil recruitment into the lungs of Sema3e(-/-) mic

198 ant Sema3E markedly reduced allergen-induced neutrophil recruitment into the lungs, which was associa

199 Thioglycollate-induced neutrophil recruitment into the peritoneum was more seve

200 Our results suggest that impaired neutrophil recruitment is an important contributor to th

201 Neutrophil recruitment is delayed in early wounds (12 ho

202 In an air-pouch model, CS-induced neutrophil recruitment is dependent on LTB4 production b

203 d postinfection and that KC-mediated mature neutrophil recruitment is impaired in IL-36gamma(-/-) mi

204 Neutrophil recruitment is key for initiating immune defe

205 Neutrophil recruitment is not only vital for host defens

206 Neutrophil recruitment is regulated by a multistep proce

207 le of Skap2 in beta2 integrin activation and neutrophil recruitment is unknown.

208 emotaxis toward bacteria induced superfluous neutrophil recruitment, leading to inappropriate inflamm

209 vidual animals revealed that the blocking of neutrophil recruitment leads to rapid mortality in this

210 1 antagonist treatment significantly reduced neutrophil recruitment (mean difference 26.7 x 10(3) cel

211 evant models of necrosis, HMGB1/RAGE-induced neutrophil recruitment mediated subsequent amplification

212 Neutrophil recruitment, mediated by beta2 integrins, com

213 e lung of ANDV-infected hamsters but altered neutrophil recruitment, MIP-1alpha and MIP-2 chemokine e

214 mmation as measured by footpad thickness and neutrophil recruitment occurred independent of adoptive

215 n vivo function, we characterized peritoneal neutrophil recruitment of a trapped monomer and trapped

216 n, secretion of antimicrobial cathelicidins, neutrophil recruitment, or provision of extracellular DN

217 To advance our understanding of neutrophil recruitment, organ-specific intravital micros

218 that Staphylococcus aureus infection induced neutrophil recruitment, platelet aggregation, and neutro

219 m lymph nodes to the infected skin to induce neutrophil recruitment, proinflammatory cytokines IL-1al

220 d GAG heparin binding affinities and reduced neutrophil recruitment, providing compelling evidence th

221 ta from IL-17-treated donors induced reduced neutrophil recruitment, reduced IL-6 and RANKL, and less

222 However, the mechanisms of neutrophil recruitment remain enigmatic, and there is no

223 Type I NKT cell-induced inflammation and neutrophil recruitment results in liver tissue damage wh

224 e reduced levels of chemokines important for neutrophil recruitment, such as the chemokine (C-X-C mot

225 ncreased bacterial burden, despite increased neutrophil recruitment, suggesting Die-P phagocytes have

226 cord did not exhibit the same dependence on neutrophil recruitment that was observed for the brain.

227 we show that C57BL/6J mice have a defect in neutrophil recruitment to a range of inflammatory stimul

228 ls and connective protein expression enhance neutrophil recruitment to a stimulus that may contribute

229 n of a biofilm infection in which a delay in neutrophil recruitment to an abiotic surface allows surf

230 TLR2-expressing cells involved in this early neutrophil recruitment to be of nonhematopoietic origin.

231 rate that HIF-2alpha is a novel regulator of neutrophil recruitment to colon tumors and that it is es

232 CXCR2 is an essential regulator of neutrophil recruitment to inflamed and damaged sites and

233 eveal that podocytes can negatively regulate neutrophil recruitment to inflamed GEnCs by modulating I

234 that Rap1b-deficient mice exhibited enhanced neutrophil recruitment to inflamed lungs and enhanced su

235 Basal lymphocyte homing and neutrophil recruitment to inflamed sites are normal.

236 ys inflammation resolution, without altering neutrophil recruitment to inflammatory sites in vivo.

237 toire of macrophages, leading to a change in neutrophil recruitment to inflammatory sites.

238 ts, we uncover that ferroptosis orchestrates neutrophil recruitment to injured myocardium by promotin

239 However, immune pathways that regulate neutrophil recruitment to injured tissues during noninfe

240 ish, we report that H2O2 also contributes to neutrophil recruitment to injuries at the late phase as

241 pretreatment synergistically increases human neutrophil recruitment to LPS-stimulated human endotheli

242 and VCAM-1 and inhibited BMP9-induced human neutrophil recruitment to LPS-stimulated human endotheli

243 tribution for PAR-1 signaling in influencing neutrophil recruitment to lung airspaces in response to

244 that lipopolysaccharide (LPS) induces early neutrophil recruitment to lungs and increases pulmonary

245 g by L. major phosphoglycans is critical for neutrophil recruitment to negatively affect disease deve

246 ed lower bacterial load but no impairment in neutrophil recruitment to peritoneum.

247 orobenzene-induced xenoinflammation, notably neutrophil recruitment to sensitized skin.

248 Neutrophil recruitment to sites of injured tissue or inf

249 Colchicine decreases neutrophil recruitment to sites of vascular injury.

250 Similarly, neutrophil recruitment to specific organs can rely on di

251 A in AECOPD may thus be beneficial to reduce neutrophil recruitment to the airways.

252 , with no expansion of peripheral T cells or neutrophil recruitment to the brain and no severe tissue

253 N-gamma inhibited, ELR(+) chemokine-mediated neutrophil recruitment to the brain, and that neutrophil

254 activation, expansion of CD4(+) T cells, and neutrophil recruitment to the brain.

255 ditional knockout mice exhibit impairment of neutrophil recruitment to the colon mucosa as a result o

256 BMP9 alone did not induce neutrophil recruitment to the endothelium.

257 itulated the loss of monocyte/macrophage and neutrophil recruitment to the heart following myocardial

258 destly impaired CXC chemokine expression and neutrophil recruitment to the infected tongue but not to

259 e to proinflammatory mediators and following neutrophil recruitment to the inflamed lung.

260 P. acnes in the murine dermis by controlling neutrophil recruitment to the inflamed site and survival

261 provides a novel imaging technique to target neutrophil recruitment to the intestinal wall, especiall

262 n intestinal IR by inhibiting C5aR1-mediated neutrophil recruitment to the ischemic tissue.

263 arthritis and regulates activation and early neutrophil recruitment to the joints, without general in

264 l inflammatory cytokine/chemokine levels and neutrophil recruitment to the kidneys after the acute in

265 eased IL-17 production in vivo and decreased neutrophil recruitment to the lung in a murine model of

266 These drive circadian neutrophil recruitment to the lung via the chemokine CXC

267 bacterial burden, 2.2-fold higher levels of neutrophil recruitment to the lung, and a 2.25-fold high

268 Remarkably, we find that C5 mediates neutrophil recruitment to the lung, even in the absence

269 w a pulmonary epithelial cell clock controls neutrophil recruitment to the lungs and provides insight

270 The mechanisms responsible for neutrophil recruitment to the lungs during bacterial pne

271 MIIG mice also exhibited reduced neutrophil recruitment to the lungs following infection.

272 L-1beta/IL-1R actions account for oedema and neutrophil recruitment to the lungs, leading to TsV-indu

273 se reconnaissance cells, there is a delay in neutrophil recruitment to the lymph node and a reduction

274 n A mice exhibited striking EG and amplified neutrophil recruitment to the lymph nodes (LNs) that was

275 of CXC chemokines and concomitantly impaired neutrophil recruitment to the oral mucosa.

276 Using various strategies to block neutrophil recruitment to the pre-metastatic site, we de

277 nt improves microbial clearance and enhances neutrophil recruitment to the site of infection.

278 he IL-1 receptor was associated with reduced neutrophil recruitment to the site of infection; and cle

279 Neutrophil recruitment to the site of inflammation plays

280 f classical monocytes alone had no effect on neutrophil recruitment to the site of injury, implicatin

281 increased IL-10 secretion, and repression of neutrophil recruitment to the spleen, were all observed

282 Neutrophil recruitment to tissues and effective neutroph

283 cteria or lipopolysaccharide, as assessed by neutrophil recruitment to, and cytokine induction in, th

284 ncy significantly heightened macrophages and neutrophils recruitment to the site of inflammation.

285 erexpression of Th17 cytokines, which induce neutrophil recruitment via neutrophil-mobilizing cytokin

286 2alpha-overexpressing mice demonstrated that neutrophil recruitment was a direct response to increase

287 As platelets slowly dissipated, neutrophil recruitment was also halted.

288 Additionally, neutrophil recruitment was dependent on CXCR2.

289 At 24 h, neutrophil recruitment was greater.

290 the ganglia, Cxcl2 expression and subsequent neutrophil recruitment was inhibited by type I interfero

291 The reduction in interstitial and airway neutrophil recruitment was not due to a cell-intrinsic m

292 let-paved endothelium given that very little neutrophil recruitment was noted in thrombocytopenic or

293 fically, Cxcl1/2/3, which in turn controlled neutrophil recruitment, was up-regulated in the skin but

294 s coding for multiple chemokines involved in neutrophil recruitment were more highly expressed in IPS

295 tor alpha (TNF-alpha) protein expression and neutrophil recruitment were strikingly higher in neonata

296 A chemotaxis model demonstrated decreased neutrophil recruitment when stimulated with perfusate fr

297 helial cells by tumor exosomal RNAs triggers neutrophil recruitment, which contributes to PMN formati

298 GPVI deficiency did not modify neutrophil recruitment, which was reduced by thrombocyto

299 duced lung injury in a manner independent of neutrophil recruitment, which we postulate instead arise

300 These data identify a pathway of neutrophil recruitment within glomerular capillaries fol