ライフサイエンスコーパス: eosinophil

1 ey lung morphogenetic event associating with eosinophils.

2 in basophils and by IL-3, IL-5, and IL-33 in eosinophils.

3 ochondrial metabolism in cytokine-stimulated eosinophils.

4 rticoids induced rapid bone marrow homing of eosinophils.

5 resulting in >= 99% purity and >= 95% viable eosinophils.

6 decreased IL-5 and IL-13 production and BAL eosinophils.

7 h 1-NM-PP1 in TrkA(F592A)-knock-in (TrkA-KI) eosinophils.

8 PD-L1 checkpoint expression in basophils and eosinophils.

9 t not PMX-53 was functional on basophils and eosinophils.

10 leukin-5 (IL-5), IL-13, immunoglobulin E and eosinophils.

11 tently suppresses effector cell functions in eosinophils.

12 ly glucocorticoid-induced reduction in blood eosinophils.

13 %), monocytes (7.99%), neutrophils (59.03%), eosinophils (2.84%), and basophils (71.88%).

14 bjects who demonstrated low peripheral blood eosinophils accompanied by increased expression of the s

15 /macrophages with B cells, plasma cells, and eosinophils accounting for <5%.

16 rare allergic disease associated with marked eosinophil accumulation in the esophagus.

17 y esophageal dysfunction and intraepithelial eosinophil accumulation.

18 ergic disease associated with marked mucosal eosinophil accumulation.

19 o several pro-inflammatory events, including eosinophil activation and migration, release of the type

20 be a driver of mitochondrial metabolism upon eosinophil activation.

21 reviously unknown role for mitochondria upon eosinophil activation.

22 ent increase in eosinophilia and evidence of eosinophil activation.

23 asia, airway hyperresponsiveness, and airway eosinophil activation.

24 vealed that genes associated with neutrophil/eosinophil activities were up-regulated in non-responder

25 e bone marrow-derived and human blood-sorted eosinophil activity against FITC-linked fibrinogen subst

26 Eosinophil activity was adhesion dependent, as a blockin

27 receded cytolysis, which was associated with eosinophil adhesion and reduced migration.

28 l processes underlying airway recruitment of eosinophils after birth remain unexplored.

29 e tumors are infiltrated by large numbers of eosinophils also exhibit robust CD8 T cell infiltrates a

30 istically, type 2 immune responses involving eosinophil and basophil granulocytes, mast cells and hum

31 ignited perivascular inflammation to promote eosinophil and CD4+ T cell recruitment.

32 In the descending colon, eosinophil and mast cell densities both correlated with

33 flammation as defined by antral and duodenal eosinophil and mast cell densities.

34 eviously reported increased bronchial mucosa eosinophil and neutrophil inflammation in patients with

35 ts significance, the functional link between eosinophils and fibrinogen is not understood.

36 There was a baseline imbalance in tissue eosinophils and high variability between treatment group

37 the presence of IL-13, with infiltration of eosinophils and IgE-coated mast cells in clinical specim

38 Muc5b, and Muc5ac mRNA; increased numbers of eosinophils and IL-13-producing ILC2s; and exaggerated m

39 .007) and an association between epithelial eosinophils and IL-5 concentrations in nasal secretion (

40 Nasal tissue eosinophils and IL-5 in nasal secretion increased signif

41 nomial regression models were used to assess eosinophils and IL-6 as predictive biomarkers.Measuremen

42 of eosinophils and local recruitment of both eosinophils and IL33-expressing M2 macrophages into corp

43 n increased number of bronchoalveolar lavage eosinophils and increased expression of IL-13 mRNA but n

44 y is a plausible strategy to decrease sputum eosinophils and inhibit lung mast cells in asthma.

45 ) is an anti-Siglec-8 antibody that depletes eosinophils and inhibits mast cells and that has shown p

46 s and % of CD4(+) T cells expressing CRTh2), eosinophils and innate lymphoid cells (ILC2).

47 Robust peripheral (bone marrow) expansion of eosinophils and local recruitment of both eosinophils an

48 ry receptor Siglec-8 on the surface of human eosinophils and mast cells binds to sialic acid-containi

49 Siglec-8 is highly expressed on eosinophils and mast cells in asthmatic sputum and targe

50 8 is prominently expressed on the surface of eosinophils and mast cells in sputum.

51 thma and correlates with gene expression for eosinophils and mast cells.

52 mplete suppression of bronchoalveolar lavage eosinophils and mucous metaplasia.

53 n increased the numbers of bronchial mucosal eosinophils and neutrophils only in COPD and CD8(+) T ly

54 D15+CD33+HLADR- cells overlapped with common eosinophils and neutrophils, which were not expanded in

55 CD8 T cells and resident macrophages; fewer eosinophils and SiglecF+ macrophages.

56 munity pathways and, finally, on the role of eosinophils and Staphylococcus aureus in the persistence

57 t age-related alterations in neutrophils and eosinophils and systemic cytokine and chemokine response

58 ed better lung functions and lower levels of eosinophils and T(H) 2 cytokines.

59 onships between inflammation (mast cells and eosinophils) and depression have been reported in adults

60 differently methylated in asthma in isolated eosinophils, and 10 were replicated in respiratory epith

61 had decreased IL-5 and IL-13 production, BAL eosinophils, and IL-33 release compared to WT mice.

62 was most potent for promoting resolution of eosinophils, and MCTR3 potently decreased airway hyperre

63 uited inflammatory cells (e.g., neutrophils, eosinophils, and monocytes), high rates of oxidative met

64 eased ILC2 proliferation, the percentages of eosinophils, and mucus production in the lung.

65 (1) assess densities of colonic mast cells, eosinophils, and TH17 cells in youth with IBS; and, (2)

66 s, densities were determined for mast cells, eosinophils, and TH17 cells, respectively, in 37 youth w

67 flammation; recruitment of platelet-adherent eosinophils; and increases in IL-33, IL-4, IL-5, and IL-

68 ng ligands in the local milieu, resulting in eosinophil apoptosis, inhibition of mast cell degranulat

69 We demonstrate for the first time that eosinophils are capable of metabolic plasticity, evidenc

70 Eosinophils are circulating and tissue-resident leukocyt

71 Eosinophils are effectors of immunity to tissue helminth

72 Eosinophils are evolutionarily conserved, pleotropic cel

73 Type 2 immune cells and eosinophils are transiently present in the lung tissue n

74 We determined that in mice, mature eosinophils are transiently recruited to the lung during

75 Finally, we present emerging data regarding eosinophils as predictive biomarkers and effector cells

76 eatment, association of platelets with blood eosinophils, as reported by CD41, predicted esophageal e

77 hil cationic protein (RNS3), and with murine eosinophil-associated RNases.

78 This response resulted in fewer eosinophil-attracting chemokines and reduced eosinophil

79 distinguishing eosinophilic N-ERD (for blood eosinophils, AUC = 0.72; for periostin, AUC = 0.75).

80 in murine models and inhibited IL-13-induced eosinophil binding to endothelial cells.

81 We measured eosinophil binding with a Sykes-Moore adhesion chamber.

82 ein, we aim to comprehensively outline basic eosinophil biology that is directly related to their act

83 ners of CLC/Gal-10 and elucidate its role in eosinophil biology.

84 The number of eosinophils (both resting and activated) and chemoattrac

85 tokine combinations synergistically affected eosinophils but failed to enhance IL-13-driven effects o

86 ces on counts of monocytes, neutrophils, and eosinophils but not lymphocytes or basophils.

87 was significantly expressed by basophils and eosinophils but not neutrophils.

88 in (Siglec)-8 is expressed on mast cells and eosinophils, but information about Siglec-8 expression a

89 sion by T cells, monocytes, macrophages, and eosinophils, but it is not known if glucocorticoids regu

90 -derived expansion and local infiltration of eosinophils, but markedly decreased M2 macrophages and S

91 Eosinophils can readily respond to diverse stimuli and a

92 Isolation techniques for tissue-derived eosinophils can result in unwanted cell or ribonuclease

93 to the levels of eosinophil granule proteins eosinophil cationic protein (ECP) and eosinophil peroxid

94 llected before and after the NACs to measure eosinophil cationic protein (ECP).

95 ly, eosinophil-derived neurotoxin (RNS2) and eosinophil cationic protein (RNS3), and with murine eosi

96 eveal changes in blood eosinophil counts and eosinophil cationic proteins that may serve as risk fact

97 ltrate in the neuromuscular layers including eosinophils, CD3-positive T cells, and CD68-positive mac

98 The human eosinophil Charcot-Leyden crystal (CLC) protein is a mem

99 f GM-CSF signaling or IRF5 expression in the eosinophil compartment phenocopies the loss of the entir

100 o the biology of these cells has illustrated eosinophils contribute to homeostatic functions in healt

101 Third, do eosinophils contribute to the lung pathology induced dur

102 monstrating that tissue, but not circulating eosinophils, contributes to disease pathology.

103 We demonstrated that the isolated eosinophils could undergo epigenetic analysis to determi

104 imary endpoint was the reduction in absolute eosinophil count (AEC) during the first week of DEC trea

105 f IL-6 (non-Type 2 asthma) and FeNO or blood eosinophil count (Type 2 asthma) identified asthma endot

106 ures of EoE (peak esophageal intraepithelial eosinophil count and EoE histologic scores), endoscopica

107 reduced the peak esophageal intraepithelial eosinophil count by a mean 86.8 eosinophils per high-pow

108 end point was the change in gastrointestinal eosinophil count from baseline to 2 weeks after the fina

109 revious 12 months, and had a screening blood eosinophil count greater than or equal to 1000 cells/muL

110 sthma symptoms worsened and peripheral blood eosinophil count increased to 813/muL.

111 ic rhinitis aOR = 1.96 [95% CI = 1.58-2.42]; eosinophil count of at least 150 cells per microliter aO

112 her prevalence of asthma, allergic rhinitis, eosinophil count of at least 150 cells per microliter, a

113 actors, including asthma, allergic rhinitis, eosinophil count of at least 150 cells per microliter, a

114 Asthma, allergic rhinitis, eosinophil count of at least 150 cells per microliter, a

115 % CI, 1.02-7.43) for those with a peripheral eosinophil count of greater than 436 cells/muL.

116 (worsening of HES-related symptoms or blood eosinophil count requiring therapeutic escalation) in th

117 ma symptoms and reduced the peripheral blood eosinophil count to 0/muL.

118 e mean percentage change in gastrointestinal eosinophil count was -86% in the combined AK002 group, a

119 score and >75% reduction in gastrointestinal eosinophil count) and the change in total symptom score.

120 determine the relationship between the blood eosinophil count, clinical characteristics and gene expr

121 s, as reported by CD41, predicted esophageal eosinophil count.

122 Seropositive patients had higher absolute eosinophil counts (AECs) than seronegative patients (P =

123 Clinical studies reveal changes in blood eosinophil counts and eosinophil cationic proteins that

124 rushings transcriptional signal versus blood eosinophil counts as well as differential expression usi

125 een genes and pathways associated with blood eosinophil counts in asthma versus COPD.

126 Here we report an increase of blood or heart eosinophil counts in humans and mice after myocardial in

127 risons of symptoms, lung function, and blood eosinophil counts revealed differences that were more pr

128 Blood eosinophil counts showed a positive relationship with pe

129 orticosteroids effectively reduce esophageal eosinophil counts to <15 per high-power field over a sho

130 gies may be effective in reducing esophageal eosinophil counts to <15 per high-power field over a sho

131 LRTSs and blood eosinophil counts were augmented and lung function was r

132 re is no evidence that it reduces esophageal eosinophil counts.

133 determined by RNA-seq analysis, naive murine eosinophils cultured with ECM enriched in TNC significan

134 terfering with these pathways would modulate eosinophil cytolysis and subsequent eosinophil-driven ti

135 ism of CD32- and alphaMB2 integrin-dependent eosinophil cytolysis of IL3-primed blood eosinophils see

136 ic asthma, but the consequences of prolonged eosinophil deficiency for human health remain poorly und

137 correct exacerbated cardiac dysfunctions in eosinophil-deficient DeltadblGATA mice.

138 brinogen is a specific trigger for cytolytic eosinophil degranulation with implications in human dise

139 to lung tissue without affecting circulating eosinophils, demonstrating that tissue, but not circulat

140 Together with results for eosinophil density and clinical end points from the main

141 as associated with higher anxiety scores and eosinophil density correlated with depression scores.

142 sodes of dysphagia/week with peak esophageal eosinophil density of 15 or more eosinophils per high-po

143 IL33 promotes metaplasia and the sequelae of eosinophil-dependent downstream infiltration of IL33-pro

144 t to control filarial adult infection via an eosinophil-dependent effector response prior to patency.

145 ased M2 macrophages and SPEM features, while eosinophil depletion caused a significant reduction in b

146 ading to metaplasia was evaluated, including eosinophil depletion studies using anti-IL5/anti-CCR3 tr

147 ule cationic ribonucleases (RNases), namely, eosinophil-derived neurotoxin (RNS2) and eosinophil cati

148 nule proteins (major basic protein [MBP] and eosinophil-derived neurotoxin [EDN]; Spearman's r = 0.30

149 the rapid colocalization of CLC/Gal-10 with eosinophil-derived neurotoxin/RNS2 and CD63.

150 ntration of IL-5, a cytokine associated with eosinophil differentiation and recruitment, and IL-4, a

151 so affect neutrophil differentiation and the eosinophil-directed bias of murine bone marrow stem cell

152 treatment of allergic inflammation and other eosinophil-driven disorders.

153 nt of diseases associated with mast cell and eosinophil-driven inflammation.

154 modulate eosinophil cytolysis and subsequent eosinophil-driven tissue damage.

155 underlying signaling pathways of ApoA-IV on eosinophil effector function in vitro and in vivo.

156 Genetic or inducible depletion of eosinophils exacerbates cardiac dysfunction, cell death,

157 B2 integrin-dependent adhesion model, lysing eosinophils exhibit reduced migration and ROCK signallin

158 Although adhered, eosinophils exhibited no proteolytic activity on collage

159 d to investigate whether human basophils and eosinophils express functional MRGPRX2.

160 activation in type 2 CRSwNP, associated with eosinophil extracellular traps cell death and Charcot-Le

161 T mice or recombinant mEar1 protein, but not eosinophils from IL4-deficient mice, effectively correct

162 In vitro-cultured eosinophils from WT mice or recombinant mEar1 protein, b

163 nflammation, as demonstrated by an influx of eosinophils, goblet cell hyperplasia, elevated serum Igs

164 CLC/Gal-10 interacts with both human eosinophil granule cationic ribonucleases (RNases), name

165 ration and vesicular transport of the potent eosinophil granule cationic RNases during both different

166 IFABP was positively related to the 2 other eosinophil granule proteins (major basic protein [MBP] a

167 C was positively correlated to the levels of eosinophil granule proteins eosinophil cationic protein

168 Cell-free eosinophil granules are found in tissues in eosinophilic

169 ood-derived CD34(+) progenitor cells impairs eosinophil granulogenesis.

170 ell as differential expression using a blood eosinophil > 200 cells/muL as a cut-off.

171 h asthma (subgroups including baseline blood eosinophils >=150/300 cells/uL and/or fractional exhaled

172 ement by AZD9412 in patients with high blood eosinophils (>0.3 x 10(9) /L) at screening and low serum

173 Eosinophils have been long implicated in antiparasite im

174 Eosinophils have been widely investigated in asthma and

175 This suggests that eosinophils have lysed and released cellular content, li

176 ory disease on one end, type 2 inflammatory, eosinophil-heavy disease on the other and an overlap of

177 correlated positively with disease severity (eosinophils/high-power field) and BZH.

178 We discuss the mechanisms of eosinophil homing to the TME and examine their diverse p

179 ociated with increased expression of TrkA by eosinophils; however, the functional role of TrkA in reg

180 fection (CBI), reduced number of circulating eosinophils, ICS treatment, and the risk of pneumonia in

181 data indicate that in addition to targeting eosinophils, IL-5 and anti-IL-5 biologics may have a dir

182 Mechanistic studies reveal roles of eosinophil IL4 and cationic protein mEar1 in blocking H(

183 s were analyzed, alone or in combination, on eosinophils in blood and other compartments and on the d

184 IL-5 increased the number of eosinophils in BM and lung tissue but failed to affect s

185 activation state, and migratory behavior of eosinophils in bone marrow (BM), blood, lung, and bronch

186 ase, and other markers typical for activated eosinophils in development and allergic inflammatory res

187 rotein levels, consistently associating with eosinophils in development and disease in mice and human

188 etter understand the role of tissue resident eosinophils in different context.

189 6), with a notable influx of neutrophils and eosinophils in KK and KKAy mice.

190 and BM, whereas IL-5 and IL-4 only increased eosinophils in lung and BM.

191 ection and support a key role for intestinal eosinophils in mitigating C. difficile-mediated disease

192 es in interleukin 5-expressing Th2 cells and eosinophils in perigonadal and inguinal AT, and enhanced

193 study establishes a cardioprotective role of eosinophils in post-MI hearts.

194 d to determine whether an S8mAb can decrease eosinophils in sputum from asthma patients ex vivo.

195 S8mAbs decrease eosinophils in sputum from patients with asthma and inhi

196 The presence of eosinophils in the airway is associated with asthma seve

197 bined results demonstrate a critical role of eosinophils in tumor control in CRC and introduce the GM

198 ing immune cell lung infiltration, including eosinophils, increasing cytokine/chemokine expression an

199 cluster, and cluster D (29.5%) was a "T(H)2/eosinophil-inferior" cluster.

200 Nonetheless, eosinophils infiltrate multiple tumours and are equipped

201 bly, only dual IL-4/IL-13 blockade prevented eosinophil infiltration into lung tissue without affecti

202 EGE causes eosinophil infiltration into the gastrointestinal (GI) t

203 The GI mucosa showed eosinophil infiltration of more than 40/high-power field

204 n was associated with epidermal hyperplasia, eosinophil infiltration, less large-cell transformation,

205 Basal zone hyperplasia and eosinophil inflammation were greater in V-EoE (P < .05).

206 omoting a functional role for CCR3-dependent eosinophil influx in immune control in the absence of IL

207 Percentage CD41+ circulating eosinophils is a potential non-invasive biomarker for Eo

208 Here we focused on comparing eosinophils isolated from human peripheral blood vs huma

209 their tissue environment, relying instead on eosinophils isolated from peripheral blood.

210 re frequent exacerbations (P = .0042), blood eosinophil level less than or equal to 100 cells/muL (P

211 curve >= 0.91), (2) correlated with gastric eosinophil levels (plasma: r = 0.72, P = .0002; serum: r

212 d (4) inversely correlated with gastric peak eosinophil levels (r = -0.83, P < .0001), periglandular

213 Eosinophil levels vary dramatically in a number of clini

214 al tagged by rs992969 associating with blood eosinophil levels, asthma, and eosinophilic asthma.

215 nostic panel score (P < 1.08E-30) but not in eosinophil levels.

216 Loss of H1.2 and H1.4 induced an eosinophil-like transcriptional program, thereby negativ

217 ed nitric oxide (<35 and >=35 ppb) and blood eosinophil (<250 and >=250 cells/uL) subgroups.

218 (glycosylated hemoglobin), serum creatinine, eosinophils, lymphocyte, monocytes, neutrophils, and pla

219 Symptoms and duodenal eosinophils, mast cells (all, P < .0001), and paracellul

220 Duodenal mucosal eosinophils, mast cells and permeability were quantified

221 ng and IgE-mediated activation controlled by eosinophils, mast cells, T(H)2 cells, group 2 innate lym

222 metabolism may be of therapeutic benefit in eosinophil-mediated diseases and regulation of tissue ho

223 Selective targeting of eosinophil metabolism may be of therapeutic benefit in e

224 Eosinophil metabolism was elucidated using pharmacologic

225 aling mechanisms of MRGPRX2 on basophils and eosinophils might enable the development of new therapeu

226 ibited eotaxin-1-induced TrkA activation and eosinophil migration, additively with 1-NM-PP1, indicati

227 M-1 but inhibited eotaxin-1 (CCL11)-mediated eosinophil migration, calcium flux, cell polarization, a

228 naling pathway activated by eotaxin-1 during eosinophil migration.

229 rnible change in adjusted mean subepithelial eosinophils/mm(2) in response to lebrikizumab (95% CI, -

230 with CBI (hazard ratio [HR], 1.635) and <100 eosinophils/mul (HR, 1.975) being independently associat

231 isk of pneumonia in those patients with <100 eosinophils/mul and CBI (HR, 2.925).Conclusions: Less th

232 .925).Conclusions: Less than 100 circulating eosinophils/mul combined with the presence of CBI increa

233 had bronchiectasis, and 20.9% had <100 blood eosinophils/mul.

234 Combined elevated sputum eosinophils+neutrophils in asthma associated with lowest

235 microenvironment and mediated recruitment of eosinophils, neutrophils, and inflammatory monocytes to

236 lymphocytes [normal range, 20%-40%], and 2% eosinophils [normal range, 1%-4%]), and an erythrocyte s

237 ole can reduce both esophageal mast cell and eosinophil numbers and attenuate type 2 inflammation in

238 obal Initiative for Asthma guidelines, blood eosinophil numbers are one marker that helps to guide tr

239 We did not observe reduced tissue eosinophil numbers in association with lebrikizumab trea

240 IL-5 and IL-13 markedly increased eosinophil numbers locally in lung and airways and dista

241 ghly purified peripheral blood basophils and eosinophils of atopic and nonatopic donors.

242 Severe asthma patients with high blood eosinophils or low serum interleukin-18 response are pot

243 apping inflammatory pathways while increased eosinophils or neutrophils alone show less effect.

244 sputum, or the absence (or normal levels) of eosinophils or other T2 markers in sputum (paucigranuloc

245 ic IgE and intestinal mucosal mast cells and eosinophils over sham treatments.

246 The metabolic processes that govern eosinophils, particularly upon activation, are unknown.

247 Developmental eosinophils peaked during P10-14 and exhibited Siglec-F(

248 raepithelial eosinophil count by a mean 86.8 eosinophils per high-power field (reduction of 107.1%; P

249 agnosis requires greater than or equal to 15 eosinophils per high-power field on light microscopy.

250 esophageal eosinophil density of 15 or more eosinophils per high-power field), from May 12, 2015, th

251 was relative change in airway subepithelial eosinophils per mm(2) of basement membrane (cells/mm(2)

252 t was significantly associated with AIS/CES, eosinophil percentage of white cells with LAS, and throm

253 oteins eosinophil cationic protein (ECP) and eosinophil peroxidase (EPO) (P < .05), while IFABP was p

254 a was quantified by using Congo red and anti-eosinophil peroxidase staining.

255 antly induced expression of Siglec-F, CD11c, eosinophil peroxidase, and other markers typical for act

256 oteolytic reactions detected the presence of eosinophil peroxidase, MBP, and fibrin alpha-, beta-, an

257 low blood basophil (r = .414, P = .021) and eosinophil (r = .623, P < .001) counts.

258 r, the functional role of TrkA in regulating eosinophil recruitment and contributing to AAI is poorly

259 ctivation of TrkA and its role in regulating eosinophil recruitment by using a chemical-genetic appro

260 er TrkA-activating mediators, contributes to eosinophil recruitment during AAI and suggests that targ

261 lung transcriptome and proteome during peak eosinophil recruitment in postnatal development, we iden

262 eosinophil-attracting chemokines and reduced eosinophil recruitment into the lung, which was benefici

263 geting the TrkA signaling pathway to inhibit eosinophil recruitment may serve as a therapeutic strate

264 TNC knockout mice had an altered eosinophil recruitment profile in development.

265 filarial nematode infection, optimum tissue eosinophil recruitment was coordinated by local macropha

266 that SATB1 upregulated the genes involved in eosinophil recruitment, including signal transducer and

267 have significantly increased neutrophil and eosinophil recruitment, mucin production and asthma-asso

268 ficiency led to increased lung inflammation, eosinophil recruitment, tissue pathology, and collagen d

269 inhibit recruitment and activation of airway eosinophils, reducing airway inflammation.

270 e provide the first prospective evidence for eosinophil-reducing effects as a therapeutic mechanism o

271 The depletion of eosinophils represents an efficient strategy to alleviat

272 Recombinant ApoA-IV potently inhibited eosinophil responsiveness in vitro as measured by Ca(2+)

273 philic esophagitis (EoE) is characterized by eosinophil-rich inflammation, basal zone hyperplasia (BZ

274 Eosinophilic esophagitis (EoE) is an eosinophil-rich, T(H)2 antigen-mediated disease of incre

275 ent eosinophil cytolysis of IL3-primed blood eosinophils seeded on heat-aggregated immunoglobulin G (

276 We show here that the ablation of eosinophils severely compromises antitumor immunity in s

277 Blockade of TrkA by 1-NM-PP1 enhanced eosinophil spreading on VCAM-1 but inhibited eotaxin-1 (

278 ne fractional exhaled nitric oxide and blood eosinophil subgroups (207 mL [95% CI: -283, 698];133 mL

279 ne fractional exhaled nitric oxide and blood eosinophil subgroups, respectively) and were sustained t

280 We assessed eosinophils, T cells, Tregs, and innate lymphoid cells (

281 r of clinical settings, especially following eosinophil-targeted therapy, which is now available to s

282 Eosinophils tethered to esophageal fibroblasts after LIG

283 rate multiplicity of Th2-cytokine control of eosinophil tissue recruitment during chronic filarial in

284 Eosinophils, tissue-dwelling granulocytes with several h

285 we first studied the response of circulating eosinophils to in vivo glucocorticoid administration in

286 with IRL201104 inhibits the infiltration of eosinophils to the lung, cytokine release, and in guinea

287 Endothelial miR-1 regulates eosinophil trafficking in the setting of allergic airway

288 RS), and the endothelium plays a key role in eosinophil trafficking.

289 respectively, except in patients with >= 300 eosinophils/uL in phase 2b study (24%/50% (P = .52/0.15)

290 e presence and activation of neutrophils and eosinophils was analyzed in CRS without NP and CRSwNP by

291 Cytolysis of IL3-primed eosinophils was dependent on the production of reactive

292 flux and apoptosis of human peripheral blood eosinophils were assessed in vitro.

293 icant deficits in intestinal neutrophils and eosinophils were detected in aged mice, with a correspon

294 No eosinophils were found in the esophageal mucosa.

295 Peripheral blood eosinophils were isolated for the analysis of metabolic

296 Eosinophils were labeled with major basic protein (MBP)

297 act human adipose tissue, greater than 10(4) eosinophils were purified by fluorescence-activated cell

298 actions between these scaffolds and adhering eosinophils were quantified using three-dimensional lase

299 Activation of eosinophils with INF-gamma induces the rapid colocalizat

300 ient, profound decrease in circulating human eosinophils within hours of administration.