ライフサイエンスコーパス: neutrophilia

1 d significantly associated with a low sputum neutrophilia.

2 ivation of the IL-23/IL-17 axis and systemic neutrophilia.

3 ar Th2 responses, as well as Th17-associated neutrophilia.

4 rsing the hematopoietic changes and systemic neutrophilia.

5 lease HNP 1-3, which further enhances airway neutrophilia.

6 athways that promote allograft rejection and neutrophilia.

7 ut the spleens lacked necrosis and displayed neutrophilia.

8 ause a P2X7 dependent increase in LPS-driven neutrophilia.

9 order presenting with cutaneous and systemic neutrophilia.

10 ng lung tissue inflammation score and tissue neutrophilia.

11 ne is effective in driving alveolar airspace neutrophilia.

12 tal lung epithelium attenuated IL-17-induced neutrophilia.

13 evaluation was notable for leukocytosis and neutrophilia.

14 witch from a mild lymphophilia to a moderate neutrophilia.

15 on of pro-inflammatory mediators and reduced neutrophilia.

16 me frame as AhR-mediated increased pulmonary neutrophilia.

17 y 1/88 had a combined blood eosinophilia and neutrophilia.

18 ive alveolar macrophages that enhance airway neutrophilia.

19 t may still be active during inflammation or neutrophilia.

20 plenomegaly and lymphomegaly associated with neutrophilia.

21 oE (COG1410) mimetic peptides reduces airway neutrophilia.

22 els of carboxyhemoglobin and enhanced airway neutrophilia.

23 nduce and exacerbate eosinophilia as well as neutrophilia.

24 ith test characteristics similar to alveolar neutrophilia.

25 s and collaborating with it to induce airway neutrophilia.

26 granulocytic hyperplasia does not result in neutrophilia.

27 pressing cells was primarily attributable to neutrophilia.

28 mice, but did not decrease mucus plugging or neutrophilia.

29 mmatory responses were suppressed, including neutrophilia.

30 1 cytokine responses without affecting acute neutrophilia.

31 y increased hepatic, peritoneal, and splenic neutrophilia.

32 elial damage, hemolysis, leukocytopenia, and neutrophilia.

33 sponses to respiratory infections and airway neutrophilia.

34 and T helper 17 (Th17 cell)-mediated airway neutrophilia.

35 in vivo function for this cytokine in airway neutrophilia.

36 ch have defective neutrophil trafficking and neutrophilia.

37 of blood-borne leukocytes, mirrored by blood neutrophilia.

38 ycemia-driven myelopoiesis, monocytosis, and neutrophilia.

39 to produce this dichotomous eosinophilia or neutrophilia.

40 as well as with lavage and peripheral blood neutrophilia.

41 ich occurs in the absence of eosinophilia or neutrophilia.

42 inophilia and AHR to mannitol but not airway neutrophilia.

43 odelling in central airways and intraluminal neutrophilia.

44 a and were positively associated with sputum neutrophilia.

45 T cells and, consequently, increased airway neutrophilia.

46 environments favoring interleukin-17-driven neutrophilia.

47 P(-/-) mice completely reversed the systemic neutrophilia.

48 signaling was required for IL-17A-dependent neutrophilia.

49 deletion also normalized JAK2-V617F-induced neutrophilia.

50 for: sputum eosinophilia (3% cut-off) 0.69; neutrophilia (65% cut-off) 0.88; asthma control (cut-off

51 alysis of peripheral blood revealed a modest neutrophilia, a loss of reticulocytes, and a massive lym

52 Despite overt T-cell expansion and neutrophilia, a reduction in conventional DC frequency a

53 Indeed, Ube2w KO mice displayed sustained neutrophilia accompanied by increased G-CSF signaling an

54 icient mice did not exhibit increased airway neutrophilia after LPS challenge.

55 Importantly, neutrophilia also correlates with asthma that is refract

56 ate that Ada(-/-) mice exhibit OPN-dependent neutrophilia, alveolar air-space enlargement, and increa

57 on of these receptors correlates with airway neutrophilia and AHR in COPD patients.

58 t TLR4 signalling may protect against airway neutrophilia and AHR in COPD.

59 (-/-) mice were protected against CS-induced neutrophilia and AHR.

60 on of these receptors correlates with airway neutrophilia and airway hyperresponsiveness (AHR) in COP

61 As expected, inhalation of LPS induced neutrophilia and an up-regulation of inflammatory mediat

62 me plays a major role in the pathogenesis of neutrophilia and anemia of chronic diseases and reveal d

63 h altered hematopoiesis that could result in neutrophilia and anemia.

64 rom EVs; these cytokines are associated with neutrophilia and are increased during exacerbations.

65 evere asthmatics and controls in relation to neutrophilia and asthma exacerbations.

66 due, at least in part, to basal circulating neutrophilia and basal TLR4/MyD88-dependent serum cytoki

67 zed by viscous, dehydrated mucus, persistent neutrophilia and chronic infections.

68 s, showing a novel link between coagulation, neutrophilia and complement activation.

69 reater baseline and allergen-provoked airway neutrophilia and concentrations of myeloperoxidase than

70 ic Ab completely prevented Th17 cell-induced neutrophilia and CXCL5 expression, whereas Abs specific

71 Bronchoalveolar lavage neutrophilia and cytokine levels were measured.

72 ack leukocyte adhesion molecules, which have neutrophilia and defective neutrophil trafficking.

73 decline in anticoagulants; thrombocytopenia; neutrophilia and endotoxemia.

74 responsiveness and airway inflammation (both neutrophilia and eosinophilia) in a mouse model of sever

75 ice, infected Nlrp3 (-/-) mice had increased neutrophilia and eosinophilia, correlating with enhanced

76 ry responses, as evidenced by reduced airway neutrophilia and eosinophilia, respectively.

77 ) mice were not protected against CS-induced neutrophilia and had more severe CS-induced AHR.

78 ion, IL-10(-/-) mice had a pronounced airway neutrophilia and heightened levels of pro-inflammatory c

79 Neutrophilia and higher levels of CD4 and CD8 T-cell act

80 hallenge in nasally sensitized mice promoted neutrophilia and higher levels of lung MAC-1(+) I-A(b lo

81 echanisms underlying hyperlipidemia-mediated neutrophilia and how neutrophils may enter atherosclerot

82 stinal cancer, we find a correlation between neutrophilia and hypercoagulation.

83 sitive CXC chemokines, for RV-induced airway neutrophilia and hyperresponsiveness.

84 ry inflammation due to loss of IL-17-induced neutrophilia and IL-25-induced eosinophilia, respectivel

85 hage inflammatory protein 2, and severe lung neutrophilia and immunopathology were linked to the poor

86 -challenged Mgat5(-/-) mice developed airway neutrophilia and increased airway reactivity with persis

87 of severe asthma in humans, including airway neutrophilia and increased lung IFN-gamma.

88 NTHi-exacerbated neutrophilia and induction of neutrophil chemoattractant

89 HVs and accompanied by reductions in airway neutrophilia and inflammasome-dependent cytokine product

90 of the S1P4 receptor partially decreased the neutrophilia and inflammation in S1P lyase-deficient mic

91 The IL-1 pathway might contribute to airway neutrophilia and is a potential therapeutic target in pa

92 Compared to WT mice, airway neutrophilia and keratinocyte chemoattractant production

93 the marked reduction in postinfection airway neutrophilia and lung expression of Th17 cytokines, alle

94 airway infections that were associated with neutrophilia and lymphopenia.

95 Stx type 2-triggered neutrophilia and monocytosis and polymorphonuclear neutr

96 Interleukin-17A induces airway neutrophilia and mucin production associated with Pseudo

97 In vivo, poly(I.C)-induced neutrophilia and mucosal chemokine production are blocke

98 racterized by persistent airflow limitation, neutrophilia and oxidative stress from endogenous and ex

99 lony stimulating factor 3, (Csf3)] prevented neutrophilia and partially ameliorated the inflamed skin

100 ENMs produced similar patterns of neutrophilia and pathology in rats and mice.

101 nd gammadelta(+) T cells induced significant neutrophilia and pulmonary fibrosis.

102 olecules in primary airway epithelial cells, neutrophilia and pulmonary inflammation.

103 ence of AAMPhi was associated with increased neutrophilia and reduced eosinophilia, suggesting that A

104 and elevated IL-1alpha, but abrogated airway neutrophilia and reduced mortality, mucus obstruction, a

105 ent in beta2 integrins transiently decreases neutrophilia and reduces levels of serum IL-17.

106 blocks Toll-like receptor 3 (TLR3)-dependent neutrophilia and RSV-induced inflammation, demonstrating

107 ostasis, as Cxcr2(-/-) mice demonstrate mild neutrophilia and severe neutrophil hyperplasia in the bo

108 thogenesis, predominantly in asthmatics with neutrophilia and severe refractory disease.

109 not prevent circadian variation in pulmonary neutrophilia and showed reduced neutrophilic inflammatio

110 ess one CRTC3 allele (CRTC2/3m mice) develop neutrophilia and splenomegaly in adulthood due to the up

111 ase, triggers the release of IL-1beta/IL-18, neutrophilia and subsequent disease exacerbations.

112 y cytokines were associated with both tissue neutrophilia and symptomatic bacterial infection/coloniz

113 expression in the lung as well as pulmonary neutrophilia and the reduction in exercise tolerance.

114 antly greater reticulocytosis, leukocytosis, neutrophilia and thrombocytosis, marked expansion of ery

115 tend to the bone marrow and are reflected by neutrophilia and thrombocytosis.

116 The intrinsic factors that drive reactive neutrophilias and emergency granulopoiesis have been inf

117 tory response syndrome, hypoxia, tachypnoea, neutrophilia) and the absence of diabetes mellitus and p

118 response to systemic corticosteroid therapy, neutrophilia, and abrupt onset of erythematous cutaneous

119 yperinflammatory response, massive pulmonary neutrophilia, and an increase in neutrophil-associated i

120 evated C-reactive protein, leukocytosis with neutrophilia, and anemia.

121 ed pulmonary eosinophilia without augmenting neutrophilia, and decreased lung IL-4, IL-5, and IL-13 p

122 However, unlike in adults, there was no neutrophilia, and despite the wide range in eosinophil c

123 ly activated macrophages, prevents cachexia, neutrophilia, and endotoxemia during acute schistosomias

124 s MPD that is characterized by splenomegaly, neutrophilia, and extramedullary hematopoiesis, despite

125 17A and CXCL9 in the lungs, induced a tissue neutrophilia, and increased the frequency of iBALT to th

126 t production of IL-1beta in the lung, airway neutrophilia, and increases in CD11c(+hi)/MHC class II(+

127 kedly decreased IL-17A and G-CSF expression, neutrophilia, and marrow myeloid hyperplasia.

128 n of the 3 miRNAs was associated with sputum neutrophilia, and miR-223-3p and miR-142-3p expression w

129 to control HSPC proliferation, monocytosis, neutrophilia, and monocyte accumulation in atherosclerot

130 ne-induced asthma is characterized by airway neutrophilia, and not eosinophilia, it is nevertheless a

131 b/db mice exhibited disorganized granulomas, neutrophilia, and reduced B cell migration to the lungs,

132 ficant MPN, characterized by thrombocytosis, neutrophilia, and splenomegaly.

133 that heparin induced both lymphocytosis and neutrophilia, and the effects required heparin to be 6-O

134 of acute alcoholic hepatitis such as fever, neutrophilia, and wasting, interfering with the IL-1 pat

135 However, whether hypercoagulation and neutrophilia are linked and involved in cancer developme

136 domonas, infection, and BAL eosinophilia and neutrophilia are risk factors for the later development

137 monary barrier function and excessive airway neutrophilia are thought to contribute to the enhanced t

138 Meanwhile, identifying intense airway neutrophilia as an indicator of airway infection and air

139 s a potential therapeutic agent for treating neutrophilia-associated inflammatory skin disorders.

140 atic subgroups based on sputum eosinophilia, neutrophilia, asthma control and inhaled corticosteroid

141 All MWCNT types caused neutrophilia at 1 day in three of four mouse labs and in

142 development of leucocytosis with concurrent neutrophilia at end-stage disease; and possible damage t

143 erentiation, and Ceacam1(-/-) mice developed neutrophilia because of loss of the Src-homology-phospha

144 numbers, and neutralizing IL-17 reduces the neutrophilia but does not affect numbers of bacteria det

145 ) mice were not protected against CS-induced neutrophilia but were partially protected against CS-ind

146 enhanced the levels of Ag-induced pulmonary neutrophilia, but not eosinophilia, goblet cell hyperpla

147 CXCL12 activity significantly reduced blood neutrophilia by inhibiting bone marrow release of granul

148 Siat1DeltaP1 mice exhibited 3-fold greater neutrophilia by thioglycollate, greater pools of epineph

149 essive cyclosporine A analog) reduced tissue neutrophilia by up to 50%, with a concurrent decrease in

150 ndirect, role in the support of alum-induced neutrophilias by expanding both pluripotent and myeloid

151 To determine whether the absence of alveolar neutrophilia can exclude bacterial pneumonia in critical

152 atory variability was found in the degree of neutrophilia caused by the three types of TiO2 nanoparti

153 Resolution of neutrophilia characteristic of acute inflammation requir

154 However, the mice developed extensive neutrophilia compared to CD40wt/Ldlr(-/-) (CD40wt) chime

155 L-12, and IL-23 showed significantly blunted neutrophilia compared with Itgb2-/- mice.

156 l growth factor) were overexpressed with BAL neutrophilia compared with nonneutrophilic asthma, and t

157 pretreatment significantly diminished airway neutrophilia compared with placebo.

158 STAT2 did not change fungal burden or airway neutrophilia compared with wild-type mice.

159 Neutrophilia could be restored by co-administering ricin

160 o, and host defense within all loci, because neutrophilia, cytokine induction, and bacterial clearanc

161 t exacerbations, airway (sputum and mucosal) neutrophilia, decreased lung microbiota diversity, and u

162 chow or Western- type diet, monocytosis and neutrophilia developed in association with the prolifera

163 Airway neutrophilia developed in RAG-deficient and CD4-depleted

164 ckout models showed distinct lymphopenia and neutrophilia, different from the full SGPL1 knockout.

165 as able to colonize the joints and triggered neutrophilia during dissemination.

166 tes directly to the development of pulmonary neutrophilia during pneumonia and acute lung injury.

167 sly undetermined role of MGL1 in controlling neutrophilia during pneumonic infection, thus playing an

168 We suggest that neutrophilia during tuberculosis indicates failed Th1 im

169 majority of these subjects (>83%) had sputum neutrophilia either alone or with concurrent sputum eosi

170 estinal inflammation associated with chronic neutrophilia, elevated CXCL1, and G-CSF.

171 Lack of NE significantly reduced airway neutrophilia, elevated mucin expression, goblet cell met

172 icantly to the antigen (Ag)-dependent airway neutrophilia elicited in ovalbumin-specific T-cell recep

173 (MMP-9)] and lung inflammatory cell burden (neutrophilia/eosinophilia).

174 the formation of sterile cutaneous pustules, neutrophilia, fever and features of systemic inflammatio

175 thology that was characterized by early lung neutrophilia, followed by subsequent pneumonia.

176 ermined the test characteristics of alveolar neutrophilia for the diagnosis of bacterial pneumonia in

177 Conclusions: The absence of alveolar neutrophilia has a high negative predictive value for ba

178 ell-associated cytokine IFN-gamma and airway neutrophilia have been implicated in severe asthma.

179 t that NLRP3 has a role in constraining lung neutrophilia, helminth killing, and type 2 immune respon

180 ity (HR, 1.37; 95% CI, 1.02-1.84), and blood neutrophilia (HR, 1.06 per 109 neutrophils/L increase; 9

181 nts with an increased bronchoalveolar lavage neutrophilia (i.e., 15%-20% or more), AZI treatment coul

182 along with a striking reduction in pulmonary neutrophilia, IL-6, MIP-1alpha, MIP-1beta, CXCL1, and CX

183 ting G-CSF release, contributed to augmented neutrophilia in Adipo(-/-) mice.

184 The eosinophilia was gradually replaced by neutrophilia in adult mice, while eotaxin-1 levels decre

185 Postallergen neutrophilia in airway subepithelium and epithelial lini

186 ing (IL-17 receptor A(-/-)) prevented airway neutrophilia in allergic mice with SD.

187 c link between GSTM1 polymorphism and airway neutrophilia in atopic asthma.

188 ight be informative on bronchial IL17-driven neutrophilia in atopic SA.

189 NOMID mice exhibit neutrophilia in blood and many tissues, including knee j

190 BAL neutrophilia in BOS and RAS were elevated at days 360, 5

191 in increased airway hyper-reactivity (AHR), neutrophilia in bronchoalveolar lavage and airway inflam

192 t to promote neutrophil apoptosis and reduce neutrophilia in bronchoalveolar lavage fluid, while IL-6

193 Exacerbated airway neutrophilia in cigarette smoke-exposed mice infected wi

194 ls in peritonitis in mixed chimeric mice and neutrophilia in Crel(-/-)Nfkappab1(-/-)Rela(+/-) mice.

195 that chronic stress induced monocytosis and neutrophilia in humans.

196 ministration, whereas bronchoalveolar lavage neutrophilia in infected leptin-resistant mice was decre

197 The neutrophilia in Kit(W-sh/W-sh) mice might influence the

198 Although IL-6 diminishes neutrophilia in mast cell-deficient mice, TGF-beta1 is i

199 -A, TiO2-P25, and TiO2-NB caused significant neutrophilia in mice at 1 day in three of four labs.

200 sceptibility to CDI in humans, but increased neutrophilia in mouse models correlates with host pathol

201 TiO2-NB caused neutrophilia in rats at 1 day in two of three labs, and

202 IL-17F, but not IL-17, had defective airway neutrophilia in response to allergen challenge.

203 intestinal inflammatory response similar to neutrophilia in systemic infection.

204 challenge normalized eosinophils and reduced neutrophilia in the Abcg1(-/-) airway.

205 ted Ldlr(-/-) mice displayed monocytosis and neutrophilia in the absence of hematopoietic stem and mu

206 ppression of eosinophilia and enhancement of neutrophilia in the airway following allergen sensitizat

207 ve transfer model characterized by increased neutrophilia in the airways.

208 aling promoted systemic wasting, anemia, and neutrophilia in the FMF-KI mice.

209 nd lung Arthus reactions and agonist-induced neutrophilia in the peritoneum, whereas Galpha(i3) plays

210 ntly attenuates late but not early pulmonary neutrophilia in this model.

211 nificantly suppressed IL-17-dependent airway neutrophilia in this setting.

212 L-6 was increased in serum with accompanying neutrophilia in tissues of an inducible mouse model of M

213 Bronchoalveolar lavage neutrophilia in uninjured and infected mice was increase

214 ycin in lipopolysaccharide-induced pulmonary neutrophilia in vivo.

215 icantly to Ag- and Th17 cell-mediated airway neutrophilia in vivo.

216 signaling in vivo prolonged zymosan-induced neutrophilia in wild-type mice, whereas having no effect

217 re, we show that alum cannot elicit reactive neutrophilias in IL-1R type I (IL-1RI)(-/-) mice, wherea

218 ophage progenitor proliferation and reactive neutrophilias in radiation chimeric mice.

219 exposed to 100 ppm Cl2 for 5 min had airway neutrophilia, increased cysLT production, and pulmonary

220 and required for NTHi-exacerbated pulmonary neutrophilia induced by cigarette smoke.

221 A is required for NTHi-exacerbated pulmonary neutrophilia induced by cigarette smoke.

222 retention by CXCL12 blockade prevented blood neutrophilia, inhibited peritoneal neutrophil accumulati

223 Neutrophilia is a characteristic of hemolytic uremic syn

224 However, neutrophilia is also prominent during severe exacerbatio

225 tokine production by T cells and that airway neutrophilia is primarily an innate response to allergen

226 protected from neutrophilia, suggesting that neutrophilia is primarily because of extrinsic defects t

227 on, we observed that elastase-induced airway neutrophilia is steroid resistant.

228 While BRP-39 did not influence neutrophilia, it was required for IL-17 production in ga

229 in the IMDC model (anaemia, thrombocytosis, neutrophilia, Karnofsky performance status [KPS] <80, an

230 , hypertension, obtundation, seizures, and a neutrophilia lasting 18 hours.

231 Proximal reflux events correlated with neutrophilia, linked to allograft dysfunction and mortal

232 mice display enhanced type I IFN production, neutrophilia, lung injury, and lethality, while therapeu

233 Polytrauma was the only model to induce neutrophilia (Ly6G (+)CD11b(+) cells) on days 1 and 3 (p

234 release (IL-1beta/MMP-9) or cellular burden (neutrophilia/lymphomononuclear cells).

235 ro potencies were demonstrated in a rat lung neutrophilia model by administration of a suspension wit

236 maT treatment, focusing on changes in sputum neutrophilia, mucins, and cytokines.

237 milarly, BRD4 inhibition reduces RSV-induced neutrophilia, mucosal CXC chemokine expression, activati

238 ating mucus plugs; and 3) in Scnn1b-Tg mice, neutrophilia, mucus obstruction, and airspace enlargemen

239 manifested by significant leukocytosis with neutrophilia, myeloid hyperproliferation, and myeloid ce

240 asthma has different immune features: airway neutrophilia, obesity-related systemic inflammation, or

241 However, neutrophilia occurred in a mouse strain-selective fashio

242 Overall mortality was associated with neutrophilia on BAL (hazard ratio 2.23 [95% confidence i

243 Early mortality was associated with neutrophilia on BAL (hazard ratio 8.40 [95% confidence i

244 Neutrophilia on BAL is linked to early mortality, but BA

245 The presence of neutrophilia on BAL was not associated with time to decl

246 Late mortality was not associated with neutrophilia on BAL.

247 n induces bronchial mucosal eosinophilia and neutrophilia only in patients with COPD and monocytes/ma

248 patients who had active ILD, as evidenced by neutrophilia or eosinophilia on BAL fluid analysis befor

249 icasone/salmeterol decreased bronchoalveolar neutrophilia (p = 0.03) to the same extent as antigen av

250 Airway neutrophilia (P=0.047) and systemic C-reactive protein (

251 n exclusion of underlying causes of reactive neutrophilia particularly if evidence of myeloid clonali

252 lls was also enhanced, but without increased neutrophilia/pathology.

253 Surprisingly, rhythmic pulmonary neutrophilia persisted, despite nonrhythmic CXCL5 respon

254 We now show that clock control of pulmonary neutrophilia persists without rhythmic glucocorticoid av

255 er of CRTC2/3m BM conferred the splenomegaly/neutrophilia phenotype in WT recipients.

256 r of metalloproteinases rescued the enhanced neutrophilia phenotype.

257 s with severe asthma in which chronic airway neutrophilia predicts a poor outcome.

258 n existed between proximal reflux events and neutrophilia (r = 0.52, P = 0.03).

259 icted to CD11c-expressing DCs develop airway neutrophilia rather than allergic airway inflammation.

260 the mechanisms underlying plerixafor-induced neutrophilia remain poorly defined.

261 mmation and infection, which often result in neutrophilia, remains ambiguous.

262 The neutrophilia resulted from PKCalpha-mediated upregulatio

263 hR-mediated elevations in iNOS and pulmonary neutrophilia reveal that although they are contemporaneo

264 -/-) mice exhibited reduced thrombocythemia, neutrophilia, splenomegaly, and neoplastic stem cell poo

265 Neutrophil CD18 silencing resulted in neutrophilia, splenomegaly, and significant defects in n

266 These mice develop severe neutrophilia, splenomegaly, extramedullary hematopoiesis

267 m IgE and eosinophilia but diminished airway neutrophilia, suggesting a protective role for TLR2.

268 but not IL-1R signaling in vivo rescues this neutrophilia, suggesting that a G-CSF-dependent, IL-1bet

269 nts who succumb exhibit a 2-fold increase in neutrophilia, suggesting that exaggerated innate immunit

270 2(-/-) fetal liver cells were protected from neutrophilia, suggesting that neutrophilia is primarily

271 ain AhR ligands, also developed greater lung neutrophilia than controls, and bronchoalveolar lavage c

272 y cytokines in results from 32 biopsies with neutrophilia than in those from 12 biopsies without acut

273 TRA exhibit increased intraepithelial airway neutrophilia that correlated with better lung function.

274 The IL-22R1 transgenic animals developed neutrophilia that correlated with increased levels of ci

275 iesis, a response that supports the reactive neutrophilia that follows infection.

276 cells, secretion of WNT ligands and systemic neutrophilia that potentiates metastatic progression.

277 d IL-17A and proinflammatory monocytosis and neutrophilia that precedes development of carotid artery

278 ditionally, TLR-dependent signals stimulated neutrophilia that promoted rejection.

279 a airway infection induces a G-CSF-dependent neutrophilia that stimulates acute rejection.

280 Infections and inflammation trigger neutrophilias that are supported by a hematopoietic prog

281 lood and serum analysis of these mice showed neutrophilia, thrombocytopenia, red cell hemolysis, and

282 e characterized by elevated eosinophilia and neutrophilia, tissue inflammation, mucus metaplasia, and

283 PGD2 receptor resulted in aggravated airway neutrophilia, tissue myeloperoxidase activity, cytokine

284 Resveratrol reduced lung tissue neutrophilia to a similar magnitude as that achieved by

285 alization of IL-17 greatly reduces pulmonary neutrophilia, underscoring a key role for IL-17 in promo

286 ose-dependently prevented LPS-induced airway neutrophilia (up to ~60%) and AHR (up to ~90%).

287 In these studies, airway neutrophilia was associated with asthma severity.

288 e of thymocytes from the thymus, whereas the neutrophilia was caused primarily by neutrophil release

289 Non-cartilaginous airways neutrophilia was inversely correlated with blood H2S, an

290 Neutrophilia was preserved when Crel(-/-)Nfkappab1(-/-)R

291 ig model of lipopolysaccharide (LPS)-induced neutrophilia, we demonstrated that Sul-121 inhalation do

292 e GC frass inhalation usually induces airway neutrophilia, we queried the effect of neutrophil deplet

293 50% mouse serum, while inducing a transient neutrophilia, we suggest that RTD-1 mediates its antifun

294 od neutrophil levels and LPS-elicited tissue neutrophilia were equal in Kit(W-sh) and Kit+ mice, both

295 ermal neutrophilic inflammation and systemic neutrophilia when PKCalpha is activated by topical 12-O-

296 n a significant increase in plasma G-CSF and neutrophilia, whereas these responses are ablated in G-C

297 evels of systemic G-CSF increased peripheral neutrophilia, which amplified neutrophilic peritoneal in

298 ed bacterial clearance and reduced pulmonary neutrophilia, which we predicted were due to accelerated

299 nfection, resulting in substantial pulmonary neutrophilia with enhanced lung pathology and disease.

300 The association of early indexes of neutrophilia with major adverse cardiovascular events wa