ライフサイエンスコーパス: neutrophilia

1 evaluation was notable for leukocytosis and neutrophilia.

2 witch from a mild lymphophilia to a moderate neutrophilia.

3 on of pro-inflammatory mediators and reduced neutrophilia.

4 me frame as AhR-mediated increased pulmonary neutrophilia.

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

6 ive alveolar macrophages that enhance airway neutrophilia.

7 t may still be active during inflammation or neutrophilia.

8 plenomegaly and lymphomegaly associated with neutrophilia.

9 oE (COG1410) mimetic peptides reduces airway neutrophilia.

10 els of carboxyhemoglobin and enhanced airway neutrophilia.

11 nduce and exacerbate eosinophilia as well as neutrophilia.

12 s and collaborating with it to induce airway neutrophilia.

13 granulocytic hyperplasia does not result in neutrophilia.

14 pressing cells was primarily attributable to neutrophilia.

15 ich occurs in the absence of eosinophilia or neutrophilia.

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

17 mmatory responses were suppressed, including neutrophilia.

18 1 cytokine responses without affecting acute neutrophilia.

19 y increased hepatic, peritoneal, and splenic neutrophilia.

20 elial damage, hemolysis, leukocytopenia, and neutrophilia.

21 sponses to respiratory infections and airway neutrophilia.

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

23 inophilia and AHR to mannitol but not airway neutrophilia.

24 in vivo function for this cytokine in airway neutrophilia.

25 ch have defective neutrophil trafficking and neutrophilia.

26 odelling in central airways and intraluminal neutrophilia.

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

28 portant to the development of AHR and airway neutrophilia.

29 ptor-positive neutrophils and in SCW-induced neutrophilia.

30 urine anti-IL-17 Ab inhibited the late phase neutrophilia.

31 neutralization significantly reduced airway neutrophilia.

32 molecules display altered hematopoiesis and neutrophilia.

33 d that IL-8 is an important mediator of this neutrophilia.

34 a and were positively associated with sputum neutrophilia.

35 T cells and, consequently, increased airway neutrophilia.

36 environments favoring interleukin-17-driven neutrophilia.

37 to produce this dichotomous eosinophilia or neutrophilia.

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

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

40 deletion also normalized JAK2-V617F-induced neutrophilia.

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

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

43 rsing the hematopoietic changes and systemic neutrophilia.

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

45 as well as with lavage and peripheral blood neutrophilia.

46 athways that promote allograft rejection and neutrophilia.

47 ut the spleens lacked necrosis and displayed neutrophilia.

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

49 ng lung tissue inflammation score and tissue neutrophilia.

50 ne is effective in driving alveolar airspace neutrophilia.

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

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

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

54 c mice had increased serum G-CSF and exhibit neutrophilia, a property shared by IL-17.

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

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

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

58 Bronchoalveolar lavage (BAL) fluid neutrophilia after O3 exposure was significantly decreas

59 Importantly, neutrophilia also correlates with asthma that is refract

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

61 GlcNAcT exhibit a restricted phenotype with neutrophilia and a partial deficiency of selectin ligand

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

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

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

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

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

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

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

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

70 Bronchoalveolar lavage neutrophilia and cytokine levels were measured.

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

72 ered, including severe bone marrow and blood neutrophilia and elevated G-CSF and GM-CSF levels.

73 decline in anticoagulants; thrombocytopenia; neutrophilia and endotoxemia.

74 wild type mice with PVM results in pulmonary neutrophilia and eosinophilia accompanied by local produ

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

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

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

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

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

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

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

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

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

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

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

86 NTHi-exacerbated neutrophilia and induction of neutrophil chemoattractant

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

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

89 or IL-17F resulted in bronchoalveolar lavage neutrophilia and inflammatory gene expression in the lun

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

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

92 Induction of BCR-ABL resulted in neutrophilia and leukocytosis, and the mice became morib

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

110 nstrated a biphasic phenotype, consisting of neutrophilia and subsequent B-cell lymphoblastic disease

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

112 insight into the lack of correlation between neutrophilia and the outcome of infection.

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

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

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

120 in their hematopoietic progenitors developed neutrophilia, and bone marrow cells were hyperresponsive

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

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

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

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

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

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

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

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

132 and sudden asthma is associated with airway neutrophilia, and that O(3) oxidative stress is likely t

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

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

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

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

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

143 wed that hydrocortisone spared the pulmonary neutrophilia but resulted in ablation of the pulmonary e

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

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

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

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

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

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

150 Resolution of neutrophilia characteristic of acute inflammation requir

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

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

153 pretreatment significantly diminished airway neutrophilia compared with placebo.

154 vivo, it stimulates hematopoiesis and causes neutrophilia consisting of mature granulocytes.

155 Neutrophilia could be restored by co-administering ricin

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

157 levels were increased during the late phase neutrophilia (day 2), and this was concomitant with an i

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

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

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

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

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

163 We suggest that neutrophilia during tuberculosis indicates failed Th1 im

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

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

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

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

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

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

170 and impressive bronchoalveolar lavage (BAL) neutrophilia followed by a smaller but significant eosin

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

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

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

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

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

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

177 Postallergen neutrophilia in airway subepithelium and epithelial lini

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

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

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

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

182 interleukin (IL)-8, which was accompanied by neutrophilia in blood and nasal secretions.

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

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

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

186 These data show that the neutrophilia in CD18(-/-) mice is not caused by enhanced

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

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

189 that chronic stress induced monocytosis and neutrophilia in humans.

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

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

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

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

194 cytokine, and its in vivo expression induces neutrophilia in mice.

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

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

197 ervations may have relevance in induction of neutrophilia in severe asthma.

198 intestinal inflammatory response similar to neutrophilia in systemic infection.

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

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

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

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

203 ) completely inhibited both eosinophilia and neutrophilia in the late-phase reaction.

204 uggest a role for IL-17F in the induction of neutrophilia in the lungs and in the exacerbation of Ag-

205 with a reduced eosinophilia and an increased neutrophilia in the peritoneal exudate cells.

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

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

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

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

210 Bronchoalveolar lavage neutrophilia in uninjured and infected mice was increase

211 ycin in lipopolysaccharide-induced pulmonary neutrophilia in vivo.

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

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

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

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

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

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

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

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

220 Neutrophilia is a characteristic of hemolytic uremic syn

221 However, neutrophilia is also prominent during severe exacerbatio

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

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

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

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

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

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

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

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

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

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

232 o be a marker of poor prognosis; conversely, neutrophilia may not be a determinant of a better progno

233 cruitment in a guinea pig LPS-induced airway neutrophilia model and decreased paw edema in a rat adju

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

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

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

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

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

239 FX(-/-) adults suffer from an extreme neutrophilia, myeloproliferation, and absence of leukocy

240 been observed to reduce to normal levels the neutrophilia observed after exhaustive exercise and to d

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

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

249 O3-induced neutrophilia (p = 0.04) was present in lavage fluid.

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

254 r of metalloproteinases rescued the enhanced neutrophilia phenotype.

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

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

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

258 e defects were reflected in vivo by baseline neutrophilia, reduced inflammatory peritoneal exudate fo

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

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

261 The neutrophilia resulted from PKCalpha-mediated upregulatio

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

263 rophils was sufficient to prevent the severe neutrophilia seen in mice reconstituted with CD18(-/-) b

264 7 (IL-17) were elevated in proportion to the neutrophilia seen in these mice, regardless of the under

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

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

267 These mice develop severe neutrophilia, splenomegaly, extramedullary hematopoiesis

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

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

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

271 hil infiltration is not enhanced by systemic neutrophilia suggests that the ability of GCSF-stimulate

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

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

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

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

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

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 Except for modest airway neutrophilia, these effects all were blocked by treatmen

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

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

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

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

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

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

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

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

290 The neutrophilia was directly associated with B cells, since

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

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

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

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

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

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

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

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

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

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