ライフサイエンスコーパス: lung inflammation

1 mice exhibited a severe symptom of allergic lung inflammation.

2 del with concomitantly reduced virus-induced lung inflammation.

3 s breathing activity did not increase global lung inflammation.

4 ar epithelial regeneration and resolution of lung inflammation.

5 s increased house-dust-mite-specific IgE and lung inflammation.

6 allenged with IL-33 and assessed for AHR and lung inflammation.

7 mately 92 cluster in ILC2s displayed reduced lung inflammation.

8 rden and histopathologic evidence of chronic lung inflammation.

9 neumoniae to induce either lung infection or lung inflammation.

10 d with IRF4 and NFAT1 expression in allergic lung inflammation.

11 - and Alternaria-induced ILC2 activation and lung inflammation.

12 irrespective of aggregation during skin and lung inflammation.

13 Nippostrongylus brasiliensis or induction of lung inflammation.

14 gregation, stronger and prolonged anemia and lung inflammation.

15 ILC2 development and restores IL-33-mediated lung inflammation.

16 tial of VLA-4 as a surrogate marker of acute lung inflammation.

17 no signs of hemorrhage in models of skin or lung inflammation.

18 the effects of IL-33 on ILC2 activation and lung inflammation.

19 C2-mediated airway hyperreactivity (AHR) and lung inflammation.

20 e recruitment and ultimately contributing to lung inflammation.

21 act (HDE), to test their role in maintaining lung inflammation.

22 es isolated from aged blood into mice caused lung inflammation.

23 ysis, in vitro proinflammatory activity, and lung inflammation.

24 ultiple adverse clinical sequelae, including lung inflammation.

25 rentiating K. pneumoniae lung infection from lung inflammation.

26 les were unaffected by the presence of acute lung inflammation.

27 el in mice, and blocked papain-induced acute lung inflammation.

28 this can lead to susceptibility to asthmatic lung inflammation.

29 crease in metabolic activity associated with lung inflammation.

30 t and activation of specific immune cells in lung inflammation.

31 nd IL-1RI upregulation on the development of lung inflammation.

32 ncy attenuates atherosclerosis but not acute lung inflammation.

33 -/-) mice, including increased mortality and lung inflammation.

34 urther showed that AM pyroptosis exaggerates lung inflammation.

35 PEG-PTX conjugates induced lung inflammation.

36 ring influenza infection to limit widespread lung inflammation.

37 e end of the imaging period was unaltered by lung inflammation.

38 innate lymphoid cell (ILC) 2 during allergic lung inflammation.

39 luding increased mortality, weight loss, and lung inflammation.

40 c target for treating ILC2-mediated allergic lung inflammation.

41 ection, but they also contribute to allergic lung inflammation.

42 ultiple adverse clinical sequelae, including lung inflammation.

43 lonella, bacteria previously associated with lung inflammation.

44 aB inhibitor) markedly mitigated mouse acute lung inflammation.

45 only attenuated RV-induced CXCL-10, but also lung inflammation.

46 are resistant to the development of allergic lung inflammation.

47 h HMPV displayed less airway dysfunction and lung inflammation.

48 mproved histologic lung injury, and dampened lung inflammation.

49 nto nascent alveoli at sites of interstitial lung inflammation.

50 role for autophagy as negative regulator of lung inflammation.

51 nous pathways that help to control excessive lung inflammation.

52 tion between platelets and AECs during acute lung inflammation.

53 d interaction in human ILC2s reduced AHR and lung inflammation.

54 oimmunity in systemic lupus erythematosus or lung inflammation.

55 denosine aggravated ragweed-induced allergic lung inflammation.

56 mast cell accumulation in models of allergic lung inflammation.

57 ms also operated during HDM-induced allergic lung inflammation.

58 expression, neutralization of which reduced lung inflammation.

59 clearance and facilitate resolution of acute lung inflammation.

60 elper 2 (Th2) cytokines that promote AHR and lung inflammation.

61 ng of ovalbumin- and house dust mite-induced lung inflammation.

62 treatment option for HDM-induced allergy and lung inflammation.

63 etabolic change in the lung affects allergic lung inflammation.

64 ce, indicating that type III IFN exacerbates lung inflammation.

65 environment and increases offspring allergic lung inflammation.

66 ar fraction which corresponded to protracted lung inflammation.

67 responsiveness in a murine model of allergic lung inflammation.

68 t for four consecutive days to induce innate lung inflammation.

69 as well as reversal of established allergic lung inflammation.

70 s, and plays an important role in infectious lung inflammation.

71 bese people are more susceptible to allergic lung inflammation.

72 nce resolution of lipopolysaccharide-induced lung inflammation.

73 and assessed for airway hyperreactivity and lung inflammation.

74 hyperactivation and consequent experimental lung inflammation.

75 ment significantly alleviated both joint and lung inflammation.

76 elays the recovery process from neutrophilic lung inflammation.

77 Similarly, in mice with lung inflammation, (64)Cu-alphaCD11b PET/CT readily dete

78 dust mite (HDM)-induced asthma-like allergic lung inflammation, a collagen-induced arthritis, an indu

79 sculin significantly suppressed neutrophilic lung inflammation, a hallmark of acute lung injury (ALI)

80 mpaired chloride permeability and persistent lung inflammation, a multidrug approach is required for

81 We investigated quantitatively whether lung inflammation affects the clearance of 50nm lipid na

82 n airway epithelial cells led to exacerbated lung inflammation after allergen exposure.

83 er time and have been shown to contribute to lung inflammation after transfusion.

84 acked red blood cells (pRBCs) and subsequent lung inflammation after transfusion.

85 Mice were exposed to ozone, and lung inflammation, airway hyperresponsiveness (AHR), and

86 infection, ovalbumin (OVA)-induced allergic lung inflammation (ALI) was induced in mice followed by

87 Influenza induced persistent parenchymal lung inflammation, alveolar epithelial metaplasia, and e

88 of blocking IgG induction and suppression of lung inflammation and airway hyperresponsiveness, but SC

89 tigated whether focal ischemic stroke causes lung inflammation and ALI in mice.

90 and sufficient for B. cenocepacia-triggered lung inflammation and also protects mice from lethal B.

91 te (HDM) and infected with RV1B to determine lung inflammation and antiviral response.

92 eases associated with ILC2s such as allergic lung inflammation and asthma.

93 oxP/loxP) SPC Cre(+) mice confirmed elevated lung inflammation and attenuated alveolar fluid clearanc

94 t in DC homeostasis, is required to modulate lung inflammation and bacterial burden in TB.

95 ils in TLR2KO mice by targeting Ly6G reverts lung inflammation and bacterial burden to levels compara

96 er understanding of the interactions between lung inflammation and barrier framework could lead to th

97 )) is produced in the airway during allergic lung inflammation and both promotes and inhibits feature

98 on of the ambient air pollutant ozone causes lung inflammation and can suppress host defense mechanis

99 gnaling via this receptor results in reduced lung inflammation and cellular recruitment as well as re

100 activates the NLRP3 inflammasome and induces lung inflammation and cellular recruitment that is NLRP3

101 ptible to bacterial infections, which worsen lung inflammation and contribute to lung function declin

102 tenance of alveolar macrophages, and reduced lung inflammation and damage.

103 to examine the role of FABP5 in the allergic lung inflammation and demonstrated that the expression o

104 - mice also show viral persistence, enhanced lung inflammation and elevated pro-inflammatory cytokine

105 ction faster than controls and had decreased lung inflammation and endoplasmic reticulum stress.

106 te respiratory distress syndrome by reducing lung inflammation and enhancing alveolar fluid clearance

107 a of investigation aimed at curbing allergic lung inflammation and exacerbation.

108 This study provides insights into lung inflammation and fibrosis and suggests that vimenti

109 reveals a hierarchy of immune abnormalities, lung inflammation and fibrosis, which do not depend on e

110 f the SHIP-1 gene in mice caused spontaneous lung inflammation and fibrosis.

111 ulmonary artery thrombosis because of severe lung inflammation and hypercoagulability rather than thr

112 n IP(-/-) mice restored both the HDM-induced lung inflammation and ILC2 numbers, whereas transfer of

113 cal role in alveolar macrophage homeostasis, lung inflammation and immunological disease.

114 et activation, which is a major driver of CF lung inflammation and impaired bacterial clearance.

115 Despite the different accumulation, the lung inflammation and inflammatory T cell responses were

116 in myeloid cells also led to elevated basal lung inflammation and influenza resistance.

117 Mechanical ventilation caused significant lung inflammation and injury that was prevented in the p

118 r lavage (BAL) fluid showed that LPS-induced lung inflammation and injury were significantly inhibite

119 sgene overexpression reduced E. coli-induced lung inflammation and injury, decreased nuclear factor-k

120 Chronic asthma is associated with persistent lung inflammation and long-term remodelling of the airwa

121 improve our understanding and management of lung inflammation and lung disease throughout the natura

122 early half of subjects experienced worsening lung inflammation and lung function at Week 4 of ART.

123 cases of an HDM-induced asthma-like allergic lung inflammation and of a collagen-induced arthritis, t

124 trophil infiltration, leading to exacerbated lung inflammation and oxidative stress.

125 CFTR in platelets produced exaggerated acute lung inflammation and platelet activation after intratra

126 Pgam5 (-/-) mice showed exacerbated lung inflammation and proinflammatory cytokines in an oz

127 ral factor in the pathogenesis of persistent lung inflammation and protein-rich edema formation, the

128 Worsening Week 4 lung inflammation and pulmonary function were both assoc

129 )Cu-alphaCD11b PET/CT readily detected acute lung inflammation and recruitment of CD11b(+) myeloid ce

130 Bronchiectasis is a disorder of persistent lung inflammation and recurrent infection, defined by a

131 ciated with higher viral loads and increased lung inflammation and reduced influenza A virus-specific

132 and potential links among diabetes, O3, and lung inflammation and remodeling are currently unknown.

133 -biased airway inflammation that can develop lung inflammation and remodeling of the respiratory trac

134 -targeted molecular imaging for detection of lung inflammation and remodeling.

135 e-4 inhibitor roflumilast prevents COPD-like lung inflammation and remodelling.

136 laying a role in dampening LPS-induced acute lung inflammation and suggest that C1P could be a valuab

137 PPP1R11 in mouse lungs significantly affects lung inflammation and the clearance of Staphylococcus au

138 e sought to address the role of autophagy in lung inflammation and the pathogenesis of corticosteroid

139 nfected with influenza demonstrated enhanced lung inflammation and tissue damage.

140 ognized role for MMP-28 in promoting chronic lung inflammation and tissue remodeling induced by cigar

141 was to assess the variation in AgNP-induced lung inflammation and toxicity across multiple inbred mo

142 rodent studies indicate that AgNPs can cause lung inflammation and toxicity in a strain- and particle

143 efore sensitization exacerbated eosinophilic lung inflammation and type 2 cytokine production in resp

144 d infiltration of neutrophils during sterile lung inflammation and were less sensitive to bacterial s

145 ne innate immune cellular and cytokine-based lung inflammation and were resistant to lethal influenza

146 neutrophil accumulation in a model of acute lung inflammation and, at 0.001 mg/kg, alleviates pulmon

147 In the immature lung, inflammation and injury disrupt the epithelial-mes

148 ice have increased bacterial load, increased lung inflammation, and accelerated mortality.

149 induced airway hyperresponsiveness (AHR) and lung inflammation, and bleomycin-induced lung fibrosis;

150 and emerging PET techniques for quantifying lung inflammation, and discuss potential clinical applic

151 stimulates cardiac fibroblast proliferation, lung inflammation, and fibrosis.

152 th increased airway and tissue eosinophilia, lung inflammation, and IL-4, IL-5, IL-13, and IgE produc

153 T mice, sensitized PHIL mice maintained AHR, lung inflammation, and increased levels of IL-4, IL-5, a

154 mediating airway hyperresponsiveness (AHR), lung inflammation, and mucus metaplasia in a dual Th2/Th

155 rp78 deletion caused weight loss, mortality, lung inflammation, and spatially heterogeneous fibrosis

156 c improvement in pulmonary function, reduced lung inflammation, and the rapid clearance of the Pneumo

157 s of genetic susceptibility to ozone-induced lung inflammation are not completely understood.

158 Most significantly, lung inflammation as a consequence of virus persistence

159 ed no significant toxicity or indications of lung inflammation, as assessed by cell population count

160 duction also decreased viral replication and lung inflammation, as evidenced by a reduced neutrophil

161 Global lung inflammation assessed by specific [F]fluorodeoxyglu

162 ng antigen doses, we observed an increase in lung inflammation associated with an upregulation of pro

163 e cytokine milieu holds promise in resolving lung inflammation associated with COVID-19.

164 finally allows prediction of the spectrum of lung inflammation associated with materials of interest

165 mice exhibited exacerbated protease-induced lung inflammation associated with reduced numbers of reg

166 reus pneumonia is characterized by extensive lung inflammation associated with severe morbidity and m

167 d pulmonary pathology in a model of allergic lung inflammation but also reduced ability to combat inf

168 It caused mild fetal lung inflammation but had a more profound effect on the

169 lone is necessary and sufficient to regulate lung inflammation but it has no direct antiviral activit

170 lating basal airway function and LPS-induced lung inflammation, but does not play a role in bleomycin

171 Thus, it appears that lung inflammation, but not ALI, occurs after experimenta

172 ic cells enhances resolution of experimental lung inflammation by incompletely understood mechanisms.

173 at ACE2 inhibits neutrophil infiltration and lung inflammation by limiting IL-17 signaling by reducin

174 of mouse ILC-intrinsic Arg1 abrogated type 2 lung inflammation by restraining ILC2 proliferation and

175 inflammation in a mouse model of LPS-induced lung inflammation by significantly reducing the release

176 er inflammation-related diseases such as the lung inflammation caused by the newly identified COVID-1

177 We analyzed lung inflammation, cellular infiltrate, and airway hyper

178 inhalation of SplD without adjuvant induced lung inflammation characterized by TH2 cytokines and eos

179 Persistent lung inflammation, characterized by increasing polymorph

180 Molecular imaging revealed intense lung inflammation coincident with massive increases in p

181 n vivo, CO(2) -RWE induced stronger allergic lung inflammation compared to control-RWE, as indicated

182 cted in mice with lipopolysaccharide-induced lung inflammation compared to healthy controls.

183 ed viral RNA shedding and substantially more lung inflammation compared with macaques.

184 ental allergens and less severe IL-33-driven lung inflammation, correlating with an impaired expansio

185 ) on CD4 T cells is required for OVA-induced lung inflammation, DCs have also been shown to be target

186 ocomotor activity in parallel with increased lung inflammation, disrupted rhythms of pulmonary functi

187 th Haemophilus influenzae resulted in lethal lung inflammation due to massive production of proinflam

188 (TNF-alpha), a protein biomarker that causes lung inflammation due to RCS exposure.

189 Lung inflammation due to sarcoidosis is characterized by

190 e of host IL-6 response in the regulation of lung inflammation during AA and the control of S. pneumo

191 abilize dependent lung regions reduce global lung inflammation during mechanical ventilation, indepen

192 e-signaling pathways to reduce or ameliorate lung inflammation during respiratory viral infections is

193 n AA model, IL-6 deficiency led to increased lung inflammation, eosinophil recruitment, tissue pathol

194 esolving lipid mediators, thereby prolonging lung inflammation evoked by E. coli Genetic deletion of

195 and that mice and humans with NEC-associated lung inflammation express higher levels of pulmonary TLR

196 ngs of mice challenged with HDM allergen and lung inflammation, expression of suppressive molecules,

197 In zymosan-induced lung inflammation, focal neutrophil infiltrates were inc

198 timal viral clearance and prevents excessive lung inflammation following RV infection.

199 ited exacerbation of cardiac dysfunction and lung inflammation, greater increases in levels of plasma

200 s might dampen house dust mite (HDM)-induced lung inflammation has not been shown.

201 diopulmonary mortality via macrophage-driven lung inflammation; however, the mechanisms are incomplet

202 To analyze allergen-induced gut and lung inflammation, immunodeficient mice were engrafted w

203 We found that severe lung inflammation impairs the autophagy pathway, particu

204 ked the same direction of change in regional lung inflammation in 98.6% and 84.3% of measurements, re

205 ow that it can ameliorate AHR and suppresses lung inflammation in a humanized mouse model.

206 ne cells to inflamed tissues, in quantifying lung inflammation in a mouse model of lipopolysaccharide

207 ET) radiotracer for noninvasive detection of lung inflammation in a mouse model of lung injury and in

208 ion to aeroallergens and consequent allergic lung inflammation in a murine model of chronic asthma.

209 -4-targeted PET in quantification of ongoing lung inflammation in a murine model.

210 entiation of effector TH2 cells and adaptive lung inflammation in a T cell-intrinsic manner.

211 have emerged as major mediators of allergic lung inflammation in animal models as well as humans.

212 ndritic cells (DC) are critical mediators of lung inflammation in asthma, but the characteristics of

213 ography can be useful to identify and target lung inflammation in asthmatic patients.

214 Intranasal bleomycin challenge exacerbated lung inflammation in autophagy-deficient mice and produc

215 s the major driver of excessive neutrophilic lung inflammation in CGD mice in the early response to f

216 Lung inflammation in dorsal regions correlated with tran

217 auma and atelectrauma on the distribution of lung inflammation in experimental acute respiratory dist

218 sessed airways hyperresponsiveness (AHR) and lung inflammation in germline and airway smooth muscle-s

219 ntify iNOS expression from endotoxin-induced lung inflammation in healthy volunteers.

220 suggest that adiponectin inhibits excessive lung inflammation in invasive aspergillosis.

221 B cells, dramatically ameliorates kidney and lung inflammation in lupus-prone MRL.Fas(lpr) mice.

222 nted the exaggerated airway eosinophilia and lung inflammation in mice given HDM-pulsed Map3k8(-/-) D

223 PLA2 isoform cPLA2alpha dramatically reduced lung inflammation in mice upon high-dose pulmonary chall

224 ibility to silver nanoparticle-induced acute lung inflammation in mice.

225 rway hyperreactivity and severe neutrophilic lung inflammation in mice.

226 n soluble TNF in vivo, producing significant lung inflammation in mice.

227 ermine the role of IL-6 in the regulation of lung inflammation in murine AA caused by Aspergillus fum

228 ver, FPS-ZM1 treatment significantly reduced lung inflammation in Nrf2(+/+) , but not in Nrf2(-/-) mi

229 S-1 showed lower IL-33 levels and attenuated lung inflammation in response to repetitive Alternaria i

230 Lung inflammation in tissue from subjects with nondiseas

231 timal intracellular mycobacteria control and lung inflammation in vivo.

232 ay hyperreactivity and significantly reduces lung inflammation in vivo.

233 ed the severity of OVA/alum-induced allergic lung inflammation in WT BALB/c mice to mice that lack ex

234 y properties in a model of DEP-induced acute lung inflammation, in contrast to anti-inflammatory effe

235 he full therapeutic potential of curcumin in lung inflammation, in this study we utilized a novel wat

236 ion, neutrophil migration into the lung, and lung inflammation induced by LPS.

237 from Cpn 60.1, named IRL201104, on allergic lung inflammation induced by ovalbumin (OVA) in mice and

238 Pik3cg(-/-) mice exhibited persistent lung inflammation induced by sepsis and sustained increa

239 O-1) on hRSV replication and pathogenesis on lung inflammation induced by this virus.

240 y is characterized by rapid alveolar injury, lung inflammation, induced cytokine production, neutroph

241 mmation, p52 overexpression caused increased lung inflammation, injury, and mortality following intra

242 creased neutrophilic alveolitis, and greater lung inflammation/injury compared with WT mice.

243 me arginase-1 (Arg1) during acute or chronic lung inflammation is a conserved trait of mouse and huma

244 However, its role in virus-induced lung inflammation is currently unknown.

245 Robust lung inflammation is one of the prominent features in th

246 Host-mediated lung inflammation is present(1), and drives mortality(2)

247 ction of Wnt/beta-catenin signaling in acute lung inflammation is unknown.

248 Moreover, lung inflammation leads to increased IL-5 production by

249 puncture (CLP)-induced sepsis by inhibiting lung inflammation, leukocyte apoptosis, and the producti

250 anscript activity was highly correlated with lung inflammation (lung [(18)F]fluorodeoxyglucose [FDG]

251 In patients with neutrophilic lung inflammation, mature CatC is found in large amounts

252 In mouse allergic lung inflammation MCTRs were present with temporally reg

253 skin inflammation model based on an allergic lung inflammation model.

254 -phosphorylated in vivo in acute and chronic lung inflammation models and this response is required t

255 3 have exaggerated neutrophilic/eosinophilic lung inflammation, mucus production, and airway hyperres

256 iate and maintain responses to pneumonia and lung inflammation, often playing a role in resolution, t

257 o effect on MAV-1 replication, virus-induced lung inflammation, or adaptive immunity compared to C57B

258 umor inflammatory stage, TNF-alpha-dependent lung inflammation plays an important role in MHC-II upre

259 ammatory biomarkers to delineate the type of lung inflammation present in asthmatic subjects is incre

260 investigated the effects of human MSC MVs on lung inflammation, protein permeability, bacterial clear

261 review the clinical techniques used to image lung inflammation, provide an overview of clinical and e

262 ruct TH2 responses in patients with allergic lung inflammation remains unknown.

263 tion of this normal homeostatic dampening of lung inflammation results in increased resistance to inf

264 ietic deletion of Ship1 leads to spontaneous lung inflammation, selective deletion of Ship1 in T cell

265 deregulation of host erythropoiesis, and the lung inflammation signature was linked to increased neut

266 Acute lung inflammation slightly shortened the residence time

267 targets Tregs and ILC2s to restrain allergic lung inflammation, suggesting MaR1 as the basis for a ne

268 istress syndrome, volutrauma promoted higher lung inflammation than atelectrauma at comparable low ti

269 in type I IFN signaling had lower levels of lung inflammation than wild-type mice.

270 Rationale: In addition to the overwhelming lung inflammation that prevails in COVID-19, hypercoagul

271 didate susceptibility genes for AgNP-induced lung inflammation that warrant additional exploration in

272 dontis and Altenaria alternata induced acute lung inflammation, that inflammation of the pleural cavi

273 monary delivery into mouse models with acute lung inflammation, the volatile reporters are released a

274 staining exhibited goblet cell hyperplasia, lung inflammation, thickening of smooth muscle layer on

275 atopoietic AR expression limits IL-33-driven lung inflammation through a cell-intrinsic inhibition of

276 esearch need for noninvasive ways to monitor lung inflammation through targeting of immunoregulatory

277 es: To test the hypothesis that during acute lung inflammation tissue production of proresolution typ

278 progression of allergen-induced eosinophilic lung inflammation to corticosteroid-refractory neutrophi

279 mouse model of house dust mite (HDM)-induced lung inflammation to explore the potential of laser-faci

280 an be used to understand the contribution of lung inflammation to loss in lung function.

281 hese results suggested that the reduction in lung inflammation together with a more robust antiviral

282 Gprc5a-knockout (ko) mice are susceptible to lung inflammation, tumorigenesis and metastasis, which r

283 inflammatory responses in poly(I:C)-induced lung inflammation using a tamoxifen-inducible versican-d

284 ions after 4 weeks of high-fat diet, whereas lung inflammation was assessed after inhalation of lipop

285 The severity of lung inflammation was assessed histologically and by mea

286 Lung inflammation was associated with increase in severa

287 Acute lung inflammation was induced by intratracheal lipopolys

288 Lung inflammation was induced with intratracheal adminis

289 Fetal lung inflammation was mild, with elevations in CXCL8, tu

290 Allergic lung inflammation was modeled in mice sensitized and cha

291 om acid sphingomyelinase-deficient mice, and lung inflammation was studied in mice receiving transfus

292 In a murine model of lung inflammation, we found that integrin-independent mi

293 nstrate that signals governing resolution of lung inflammation were altered in Yap/Taz mutant mice, w

294 n of inflammatory cells into the airway, and lung inflammation were enhanced in AT2CC(-/-) mice relat

295 Anaphylaxis and allergic lung inflammation were restored in ADAM10(DC)(-/-) with

296 ell trafficking in animal models of allergic lung inflammation, which are known to be platelet depend

297 sc(-/-) mice spontaneously developed gut and lung inflammation with age.

298 bone marrow-derived dendritic cells augments lung inflammation with increased IL-17A levels in the lu

299 Zc3h12a(-/-) mice have spontaneous severe lung inflammation, with an increase in mainly IL-5- and

300 find that myeloid BCL6 deficiency diminished lung inflammation without affecting viral loads.