ライフサイエンスコーパス: neutrophil recruitment

1 XCL1 in the interstitium effectively reduced neutrophil recruitment.

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

3 nary inflammation, characterized by enhanced neutrophil recruitment.

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

5 the blockade of which resulted in increased neutrophil recruitment.

6 ignificant increases in mucin production and neutrophil recruitment.

7 dida albicans infection due to impairment in neutrophil recruitment.

8 is in driving CXCL5 expression and pulmonary neutrophil recruitment.

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

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

11 attenuating lung injury caused by excessive neutrophil recruitment.

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

13 are key mechanisms facilitating appropriate neutrophil recruitment.

14 f 5 cytokines and chemokines associated with neutrophil recruitment.

15 e bone marrow into circulation and increased neutrophil recruitment.

16 the blockade of which significantly reduced neutrophil recruitment.

17 and CXCL5 expression, thereby restoring the neutrophil recruitment.

18 role during sepsis by negatively regulating neutrophil recruitment.

19 ections, excess mucus production, and robust neutrophil recruitment.

20 tokine levels, lymphocyte proliferation, and neutrophil recruitment.

21 Cxcl8-l2 signaled through Cxcr2 for inducing neutrophil recruitment.

22 downstream cytokine/chemokine production and neutrophil recruitment.

23 e the radius of highly directed interstitial neutrophil recruitment.

24 ded similar reductions in lung autophagy and neutrophil recruitment.

25 fied CXCL5 and MIP-2 as important factors in neutrophil recruitment.

26 nophil values and cytokine levels related to neutrophil recruitment.

27 PDI is critical for its regulatory effect on neutrophil recruitment.

28 e and sagA deletions synergistically enhance neutrophil recruitment.

29 idase in myeloid cells suppresses intestinal neutrophil recruitment.

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

31 ispensable for beta2 integrin activation and neutrophil recruitment.

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

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

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

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

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

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

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

39 At the peak of infection, we observed neutrophil recruitment accompanied by induction of KC, m

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

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

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

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

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

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

46 bated IL-17 production that causes increased neutrophil recruitment and associated lung pathology.

47 Faster neutrophil recruitment and bacterial clearance were obse

48 Neutrophil recruitment and bacterial clearance were rest

49 . aeruginosa lung infection despite enhanced neutrophil recruitment and bacterial clearance.

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

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

52 , at gingival sites was sufficient to induce neutrophil recruitment and bone resorption.

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

54 his study examines the role of Fer kinase in neutrophil recruitment and chemotaxis to various chemoat

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

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

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

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

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

60 penia did not influence lung inflammation or neutrophil recruitment and did not attenuate local or sy

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

62 Neutrophil recruitment and directional movement toward c

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

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

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

66 nd Cx3cr1(-/-) mice, respectively, abolished neutrophil recruitment and endothelial killing.

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

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

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

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

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

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

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

74 nt in vivo in orchestrating LPS-induced lung neutrophil recruitment and inflammation.

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

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

77 jejuni-induced PI3K-gamma signaling mediates neutrophil recruitment and intestinal inflammation in Il

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

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

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

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

82 tion lipid mediators that inhibit phlogistic neutrophil recruitment and promote wound-healing macroph

83 integrin activation contributed to decreased neutrophil recruitment and reduced kidney damage in P-Re

84 of acute inflammation requires cessation of neutrophil recruitment and removal of tissue neutrophils

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

86 local mast cells (MCs), resulting in limited neutrophil recruitment and restricting outflow of vascul

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

88 Neutrophil recruitment and SpeB(A-)% among recovered GAS

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

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

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

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

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

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

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

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

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

98 Furthermore, neutrophil recruitment and the neutrophil cytokines, CXC

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

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

101 l challenge with Hsp70 resulted in increased neutrophil recruitment and TNF-alpha levels in the MCPT4

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

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

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

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

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

107 disease severity and progression, increased neutrophil recruitment, and delayed pathogen elimination

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

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

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

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

112 induced tubular damage, cytokine expression, neutrophil recruitment, and renal failure.

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

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

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

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

117 We recently observed rapid and sustained neutrophil recruitment at a primary site of infection (p

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

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

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

121 function of DBP appears to be selective for neutrophil recruitment, but, in contrast to previous in

122 se 1 (HPK1) participates during signaling of neutrophil recruitment by acting as a regulator of the a

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

124 We hypothesized that increased neutrophil recruitment by keratinocytes may contribute t

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

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

127 the vasculature, initiate an early phase of neutrophil recruitment by releasing the chemoattractants

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

129 roduced by serotype M1 GAS (SsE(M1)) reduces neutrophil recruitment by targeting platelet-activating

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

131 -MEK, G-CSF, and Ets expression and enhanced neutrophil recruitment compared with normal pancreata.

132 These changes in neutrophil recruitment could be explained by regulation

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

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

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

136 ACh-producing B-cells reduce peritoneal neutrophil recruitment during sterile endotoxemia indepe

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

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

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

140 Neutrophil recruitment from blood to extravascular sites

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

142 l insult but until now the role of Cxcl8s in neutrophil recruitment has not been studied.

143 lium mediates blood vessel tone, hemostasis, neutrophil recruitment, hormone trafficking, and fluid f

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

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

146 ted cell death and prevented NLRP3-dependent neutrophil recruitment in a monosodium urate crystal inf

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

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

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

150 s in monocyte/macrophage, dendritic cell, or neutrophil recruitment in dblGATA1-deficient mice, sugge

151 ominent increase in macrophage/microglia and neutrophil recruitment in GFAPcre p38alpha(-/-) mice com

152 that appear essential for polymorphonuclear neutrophil recruitment in IC disease.

153 hether absence of platelet serotonin affects neutrophil recruitment in inflammatory responses.

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

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

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

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

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

159 We find that neutrophil recruitment in response to virulent L. pneumo

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

161 9, was infected, lack of galectin-3 impaired neutrophil recruitment in the footpads and the draining

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

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

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

165 7, but not CXCL1 and CCL2, had a key role in neutrophil recruitment in this model.

166 Prevention of neutrophil recruitment in Tlr7(host+/+BM-/-) mice or by

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

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

169 Increased neutrophil recruitment in vivo was associated with incre

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

171 yp1 triple-knockout mice exhibited increased neutrophil recruitment in zymosan-treated peritoneal exu

172 o several cytoskeletal regulators that guide neutrophil recruitment including Lyn, Rac2, and SHIP.

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

174 During acute inflammation, neutrophil recruitment into extravascular tissue require

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

176 First, gene ablation of CD99L2 impairs neutrophil recruitment into inflamed cremaster and perit

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

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

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

180 c-E) functions to selectively regulate early neutrophil recruitment into the lung.

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

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

183 Neutrophil recruitment into the neonatal lungs was inhib

184 ynergistically mainly at the initial step of neutrophil recruitment into the peritoneal cavity.

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

186 beta2 integrins play a crucial role during neutrophil recruitment into the site of vascular inflamm

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

188 Neutrophil recruitment is an important early step in con

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

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

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

192 These age-mediated defects in early neutrophil recruitment may alter the dynamics of the inf

193 IL-17A-driven neutrophil recruitment may participate in this process.

194 1 antagonist treatment significantly reduced neutrophil recruitment (mean difference 26.7 x 10(3) cel

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

196 Neutrophil recruitment, mediated by beta2 integrins, com

197 mine whether immunity to OPC is mediated via neutrophil recruitment, mice lacking CXCR2 were subjecte

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

199 cell autophagy that correlated with reduced neutrophil recruitment, myeloperoxidase activity, and ai

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

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

202 o, administration of Slit2 did not attenuate neutrophil recruitment or bacterial clearance in mice wi

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

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

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

206 , which facilitate macrophage activation and neutrophil recruitment, respectively.

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

208 Studies on neutrophil recruitment revealed its complexity, especial

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

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

211 l IL-1beta-mediated lymphangiogenesis but no neutrophil recruitment, suggesting that neutrophils are

212 (-/-) mouse colon showed less macrophage and neutrophil recruitment than in WT mice.

213 ammatory cytokines KC and TNF-alpha and less neutrophil recruitment than Muc18(+/+) mice.

214 protein may have a more significant role in neutrophil recruitment than previously recognized.

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

216 iglec-E-deficient mice exhibited exaggerated neutrophil recruitment that was reversed by blockade of

217 production that is correlated with pulmonary neutrophil recruitment; the second step occurs when anti

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

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

220 presence of podocytes significantly reduced neutrophil recruitment to GEnCs by up to 50% when cultur

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

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

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

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

225 ognized role for perivascular macrophages in neutrophil recruitment to inflamed skin and indicate tha

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

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

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

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

230 disclose the molecular pattern that controls neutrophil recruitment to LNs.

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

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

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

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

235 ligands, which results in the inhibition of neutrophil recruitment to neuronal tissue.

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

237 Neutrophil recruitment to sites of injured tissue or inf

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

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

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

241 ecognition of conidia, resulting in impaired neutrophil recruitment to the cornea and increased funga

242 ficantly increased CXC chemokine production, neutrophil recruitment to the corneal stroma, and bacter

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

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

245 g lymph node of infected mice, and there was neutrophil recruitment to the infection site.

246 tured (budding) particles induced more rapid neutrophil recruitment to the injection site.

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

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

249 glec-E is an important negative regulator of neutrophil recruitment to the lung and beta2 integrin-de

250 gative regulator of beta2-integrin-dependent neutrophil recruitment to the lung following exposure to

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

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

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

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

255 neumonia and associated acute lung injury is neutrophil recruitment to the lung.

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

257 P(-/-) mice had significantly reduced (~50%) neutrophil recruitment to the lungs compared with their

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

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

260 y, we find no essential role for IL-1beta in neutrophil recruitment to the lungs in response to L. pn

261 ow that IL-1alpha is a critical initiator of neutrophil recruitment to the lungs of L. pneumophila-in

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

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

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

265 mutant bone marrow chimeras exhibit reduced neutrophil recruitment to the peritoneum on induction of

266 Although VWF-mediated neutrophil recruitment to the peritoneum was described t

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

268 e was found to be associated with diminished neutrophil recruitment to the site of bacterial infectio

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

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

271 Neutrophil recruitment to the site of inflammation plays

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

273 vasculature and extracellular matrix mediate neutrophil recruitment to the site of microbial infectio

274 mma promoted ELR(+) chemokine expression and neutrophil recruitment to the spinal cord.

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

276 imulus, and that both are crucial for normal neutrophil recruitment to the wound and normal resolutio

277 Neutrophil recruitment to tissues and effective neutroph

278 s revealed a specific reduction in ATF3(-/-) neutrophil recruitment to wild-type lungs.

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

280 This study reveals a novel role for CXCL1 in neutrophil recruitment via modulating T cell function an

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

282 2alpha-overexpressing mice demonstrated that neutrophil recruitment was a direct response to increase

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

284 Neutrophil recruitment was assessed based on adhesion an

285 Additionally, neutrophil recruitment was dependent on CXCR2.

286 At 24 h, neutrophil recruitment was greater.

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

288 ecently, the contribution of the PC layer to neutrophil recruitment was largely ignored.

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

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

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

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

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

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

295 se (MAPK) activation was required to trigger neutrophil recruitment, which is influenced by extrinsic

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

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

298 acteria: here, IL-1alpha was dispensable for neutrophil recruitment, while IL-1beta was required.

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

300 10 produced through TLR2 activation prevents neutrophil recruitment, WT pups were treated with the TL