ライフサイエンスコーパス: bronchiolar

1 Bronchiolar abnormalities are relatively common and occu

2 protein-expressing (CE) cells in renewal of bronchiolar airway epithelium following injury.

3 of the pulmonary epithelium to bronchial and bronchiolar airway lineages occurs during the transition

4 lial cells shedding into the narrow-diameter bronchiolar airway lumens resulted in rapid accumulation

5 to significant virus-induced alterations in bronchiolar airway wall thickness and mast cell increase

6 cluding fibrosis-associated occlusion of the bronchiolar airways in all allografts of long-term survi

7 The C57BL/6 mice showed prominent lesions at bronchiolar-alveolar duct (BAD) junctions where asbestos

8 led asbestos fibers deposit initially at the bronchiolar-alveolar duct regions and alveolar macrophag

9 the peptide were clearly up-regulated at the bronchiolar-alveolar duct regions by 24 hours after the

10 reduction of growth factor expression by the bronchiolar-alveolar epithelium and lung macrophages.

11 In each patient, a stereotyped bronchiolar-alveolar pattern of lung remodeling was iden

12 d into gas-exchange tissue to form long-term bronchiolar-alveolar remodeling regions.

13 renew and contribute descendents to both the bronchiolar and alveolar compartments.

14 eolar duct junction, BASCs were resistant to bronchiolar and alveolar damage and proliferated during

15 Single BASCs had bronchiolar and alveolar differentiation potential in lu

16 Stat3 was selectively deleted from bronchiolar and alveolar epithelial cells in Stat3(Delta

17 e most marked at 30 days and co-localized in bronchiolar and alveolar epithelial cells using an antib

18 Within 24 h, the H5N1 virus produced severe bronchiolar and alveolar lesions.

19 ion of NA alone resulted in desialylation of bronchiolar and alveolar surfaces and induction of TNF-a

20 howed that remodeling and destruction of the bronchiolar and alveolar tissue is associated with macro

21 emphysematous destruction, remodeling of the bronchiolar and alveolar tissue, and the infiltration of

22 adducin were almost exclusively expressed in bronchiolar and alveolar type II (ATII) epithelial cells

23 at both HNF-3beta and TTF-1 were detected in bronchiolar and alveolar type II cells in the human lung

24 d in cell lines and are co-expressed in lung bronchiolar and alveolar type II cells.

25 ratinocyte chemoattractant CXCL1 staining in bronchiolar and alveolar type II epithelial cells and al

26 was localized at the apical cell surface of bronchiolar and alveolar type II epithelial cells expose

27 ion, RAR and TTF-1 were colocalized in mouse bronchiolar and alveolar type II epithelial cells, the c

28 Isolated bronchiolar and bronchial basal cell responses to IL13 w

29 Bronchiolar and bronchioalveolar duct junction hyperplas

30 earance of plasma membrane disruptions, both bronchiolar and parenchymal, the latter to a much greate

31 was detected by in situ hybridization in the bronchiolar and peribronchiolar areas and the vascular e

32 5 hours after IA endotoxin) and later in the bronchiolar and peribronchiolar areas and vascular endot

33 The presence of skin lesions and lung bronchiolar and vascular inflammation was also dramatica

34 of virus antigen within tracheal, bronchial, bronchiolar, and alveolar epithelium.

35 for further migration of the cells into the bronchiolar area.

36 MUC5AC-high niche bronchiolar basal cells expressed reduced FOXA2 and elev

37 In cultured bronchiolar basal cells, IL13 suppressed FOXA2 and DASC

38 elial cells were obtained from bronchial and bronchiolar brushing performed under radiological guidan

39 ysis and immunohistochemistry, we found that bronchiolar cell density remained stable with aging, but

40 pletion increased chromatin accessibility of bronchiolar cell genes, increased BASC frequency, and ac

41 s, increased BASC frequency, and accelerated bronchiolar cell injury repair.

42 Alp1 damages bronchiolar cell junctions, which triggers a calcium flu

43 ting a functional link for BOA formation via bronchiolar cell migration.

44 nt significantly inhibited NNK-induced early bronchiolar cell proliferation on day 5.

45 e alveolar type II cells and the nonciliated bronchiolar cells (Clara cells) of the lungs; these cell

46 Although bronchiolar cells and alveolar cells are proposed to be

47 identified immunohistochemically in terminal bronchiolar cells and bronchiolized cells 7 and 14 days

48 ck gene Bmal1 (also called Arntl or MOP3) in bronchiolar cells disrupts rhythmic Cxcl5 expression, re

49 ilitating migration of Clara cells and other bronchiolar cells into the regions of alveolar injury.

50 Following injury, bronchiolar cells undergo rapid squamous metaplasia, fol

51 were assessed by the transfection of murine bronchiolar cells with a reporter containing 1.1 kb of t

52 eolar lavage fluid (BALF) and in nonciliated bronchiolar cells, alveolar type II epithelial cells, an

53 estores host translation in infected hamster bronchiolar cells, and leads to an enrichment in methyla

54 sentative of the trachea versus small airway bronchiolar cells.

55 re a stem cell population that maintains the bronchiolar Clara cells and alveolar cells of the distal

56 arker, SP-C, shows normal differentiation of bronchiolar Clara cells but a reduction in the number of

57 in lung tumors growing in wild-type mice and bronchiolar Clara cells isolated from normal mouse lungs

58 teration in the distribution and function of bronchiolar Clara cells.

59 ype 2 cells from less complete processing in bronchiolar Clara cells.

60 hat it is also secreted tonically from human bronchiolar Clara cells.

61 specific manner by the alveolar type II and bronchiolar (Clara) epithelial cells of the lung and is

62 -specific manner by the alveolar type II and bronchiolar (Clara) epithelial cells of the lung and is

63 protein (Clara) (CC16) is produced mainly by bronchiolar club cells and has been shown to have protec

64 a that is initiated by the rapid response of bronchiolar club cells to Alp1.

65 ned stable with aging, but inferred rates of bronchiolar club progenitor cell self-renewal and differ

66 els, reduced pulmonary eosinophilia and peri-bronchiolar collagen deposition.

67 induced an improvement in the mean terminal bronchiolar density (2.5 +/- 0.8 br/mm vs 3.5 +/- 0.9 br

68 induced an improvement in the mean terminal bronchiolar density (2.5 +/- 0.8 br/mm2 vs 3.5 +/- 0.9 b

69 , the molecular pathophysiology of asthmatic bronchiolar disease is poorly defined.

70 separating (1) those disorders in which the bronchiolar disease is the predominant abnormality (prim

71 Some histopathologic patterns of bronchiolar disease may be relatively unique to a specif

72 Primary bronchiolar disorders include constrictive bronchiolitis

73 ease is the predominant abnormality (primary bronchiolar disorders) from (2) parenchymal disorders wi

74 reas mature mice exhibited a more restricted bronchiolar distribution of infection that produced a di

75 Bronchiolar dysfunction is associated with asthma exacer

76 ll proliferation were observed at 30 days in bronchiolar epithelia and at 4, 14, and 30 days in the a

77 XII protein was localized apically in human bronchiolar epithelia and basolaterally in the reabsorpt

78 tions in histologically normal bronchial and bronchiolar epithelia from lung adenocarcinomas bearing

79 gh niches were identified heterogeneously in bronchiolar epithelia independent of immune cell localiz

80 ere and FA excised tissues demonstrated that bronchiolar epithelia were populated by MUC5AC-expressin

81 In excised tissues, severe and FA bronchiolar epithelia, depleted of distal airway secreto

82 in the apical cytoplasm of the bronchial and bronchiolar epithelia, in the cytoplasm of pulmonary end

83 -Flu to virion aggregation at the surface of bronchiolar epithelia.

84 buted to either type II cells or nonciliated bronchiolar epithelial (Clara) cells.

85 ial hyperplasia, and also exhibited enhanced bronchiolar epithelial and type II pneumocyte proliferat

86 However, bronchiolar epithelial cell and interstitial cell labeli

87 s strengthen the potential importance of the bronchiolar epithelial cell as a source of production of

88 ion, Stard7 expression was knocked down in a bronchiolar epithelial cell line (BEAS-2B) and specifica

89 minal airways and vessels, the appearance of bronchiolar epithelial cell necrosis, and necrotizing va

90 s developed atypical hyperplastic lesions of bronchiolar epithelial cell origin at 3 and 6 months.

91 Pulmonary nonciliated bronchiolar epithelial cells (Clara cells) and alveolar

92 These proliferating bronchiolar epithelial cells (Clara cells) may be the in

93 ted to alveolar type II epithelial cells and bronchiolar epithelial cells (Clara cells) of adult lung

94 ow that osteopontin (OPN) is up-regulated by bronchiolar epithelial cells after chrysotile asbestos e

95 asbestos caused increased numbers of distal bronchiolar epithelial cells and peribronchiolar cells i

96 me, the virus also replicated efficiently in bronchiolar epithelial cells and spread extensively in b

97 4PBA treatment of IB3-1 CF bronchiolar epithelial cells caused transiently increase

98 al antigen and nucleic acid were detected in bronchiolar epithelial cells during peak viral replicati

99 fferential display RT-PCR screen on IB3-1 CF bronchiolar epithelial cells exposed to 4PBA.

100 Nuclear STAT3 staining was induced in bronchiolar epithelial cells following naphthalene-media

101 heral epithelium and on luminal membranes of bronchiolar epithelial cells in the proximal lung, a pat

102 t PVM-positive pneumocytes and bronchial and bronchiolar epithelial cells in wt PVM- and DeltaNS1-inf

103 Knockdown of MIG-6 in H441 human bronchiolar epithelial cells increased phospho-EGFR and

104 orylated PKD (p-PKD) were observed in distal bronchiolar epithelial cells of mice inhaling asbestos.

105 ding with significantly increased numbers of bronchiolar epithelial cells staining positively for muc

106 Clara cells are non-ciliated, secretory bronchiolar epithelial cells that serve to detoxify harm

107 um, studies were performed in NCI-H441 human bronchiolar epithelial cells transfected with the human

108 rential display RT-PCR on mRNA from IB3-1 CF bronchiolar epithelial cells treated for 0-24 h with 1 m

109 P protein in a range of cell types including bronchiolar epithelial cells, macrophages and type II pn

110 GGL is also expressed in thymic lymphocytes, bronchiolar epithelial cells, pulmonary interstitial cel

111 in the proliferation and differentiation of bronchiolar epithelial cells, resulting in dramatic expa

112 were not associated with alveolar type II or bronchiolar epithelial cells, the cellular sites of SP-C

113 and villi of the small and large intestine, bronchiolar epithelial cells, the epidermis and hair fol

114 ty was limited to the luminal border of rare bronchiolar epithelial cells.

115 CL1 in the bronchoalveolar lavage fluid, and bronchiolar epithelial necrosis.

116 To investigate the role of bronchiolar epithelial NF-kappaB activity in the develop

117 the function of hepatocytes, intestinal and bronchiolar epithelial, and pancreatic acinar cells.

118 In marked contrast, the bronchiolar epithelium after infection with the mutant P

119 enabling them to localize near the infected bronchiolar epithelium and airway lumen to function as t

120 ip' containing a differentiated, mucociliary bronchiolar epithelium and an underlying microvascular e

121 lusters of positive cells in the respiratory bronchiolar epithelium and associated subepithelial regi

122 ated with higher viral antigen levels in the bronchiolar epithelium and greater histopathologic chang

123 ion of nuclear factor (NF)-kappaB within the bronchiolar epithelium and increased luciferase activity

124 te bronchiolitis with occasional necrosis of bronchiolar epithelium and mild to moderate peribronchio

125 inct epithelial subpopulations: the proximal bronchiolar epithelium and the distal respiratory epithe

126 Mechanisms that regulate the repair of bronchiolar epithelium are of considerable relevance for

127 interactions between molds and the bronchial/bronchiolar epithelium at the early steps after inhalati

128 nlikely to contribute to renewal of terminal bronchiolar epithelium because of the paucity of NEBs at

129 rated at areas of the H1N1pdm virus-infected bronchiolar epithelium by 1 day postinfection (dpi).

130 From E18.5 to PN20, Clara cells in the bronchiolar epithelium co-expressed Clara cell secretory

131 shape and numbers required for repair of the bronchiolar epithelium following injury.

132 ber of BrdUrd-labeled cells increased in the bronchiolar epithelium from day 2 to day 14, with the hi

133 tation, and 90 sites of normal bronchial and bronchiolar epithelium from the same surgical specimens.

134 sed in myofibroblasts and basal cells of the bronchiolar epithelium in lungs of patients with IPF, wh

135 n as regional progenitor cells to repair the bronchiolar epithelium in response to lung damage.

136 dentified putative HFH-4 target genes in the bronchiolar epithelium including the clara cell secretor

137 spores in vivo cannot explain the bronchial/bronchiolar epithelium invasion observed in some invasiv

138 Surprisingly, K-ras activation in the bronchiolar epithelium is associated with a robust infla

139 Bronchiolar epithelium is postulated to play a critical

140 CR analysis for levels of c-jun and c-fos in bronchiolar epithelium isolated by laser capture microdi

141 of mucus and increased mClca3 protein in the bronchiolar epithelium of asbestos-exposed mice at all t

142 f 25 cases of DAD but was only identified in bronchiolar epithelium of control lungs.

143 0 and MIG receptor CXCR3 was detected in the bronchiolar epithelium of preterm lambs by immunostainin

144 ein expression was detected diffusely in the bronchiolar epithelium of rats receiving Ad5-HO-1, as as

145 e that activation of Wnt/beta-catenin in the bronchiolar epithelium of the adult mouse lung does not

146 ivin expression was restricted to the distal bronchiolar epithelium of the lung and neural-crest-deri

147 e small intestine, white pulp of the spleen, bronchiolar epithelium of the lung, myocardium, adrenal

148 e splenic reticuloendothelial system and the bronchiolar epithelium of the lung.

149 in the lamina propria of the gut and in the bronchiolar epithelium of the lungs.

150 otype, resulting in a phenotypic switch from bronchiolar epithelium to the highly proliferative dista

151 Whereas nearly complete repair of the bronchiolar epithelium was observed in control mice with

152 oss of alveolar septae, and sloughing of the bronchiolar epithelium were observed in Stat3(DeltaDelta

153 in the apical cytoplasm of the bronchial and bronchiolar epithelium yet no staining was seen in the a

154 in the apical cytoplasm of the bronchial and bronchiolar epithelium yet robust staining was seen in t

155 ent at alveolar duct bifurcations and within bronchiolar epithelium, alveolar macrophages, and the vi

156 and eotaxin were predominantly expressed in bronchiolar epithelium, in contrast to distal regions of

157 onal sites as well as in the esophagus, lung bronchiolar epithelium, kidney glomerular epithelium, ol

158 e of foci of hyperproliferative cells in the bronchiolar epithelium, particularly in the bronchiolalv

159 t virus showed widespread destruction of the bronchiolar epithelium, with extensive distribution of v

160 markers of cell cycle reentry, in the distal bronchiolar epithelium.

161 s perinatal expression was restricted to the bronchiolar epithelium.

162 Viral RNA localized to bronchial and bronchiolar epithelium.

163 B) and contribute to renewal of the proximal bronchiolar epithelium.

164 al organization, or organelle composition in bronchiolar epithelium.

165 club cells, a major component of the murine bronchiolar epithelium.

166 nd exhibits abundant expression in the adult bronchiolar epithelium.

167 s of goblet cell metaplasia in bronchial and bronchiolar epithelium.

168 e transcriptional regulation of genes in the bronchiolar epithelium.

169 anges and epithelial necrosis of bronchi and bronchiolar epithelium.

170 pism to ciliated cells and club cells of the bronchiolar epithelium.

171 tive NF-kappaB pathway, respectively, in the bronchiolar epithelium.

172 STAT3 signaling pathway during repair of the bronchiolar epithelium.

173 iated with severe injury of the alveolar and bronchiolar epithelium.

174 ning and fibrosis may be caused by increased bronchiolar expression of cytokines such as TGF-beta 1 i

175 distal epithelial progenitors first produce bronchiolar-fated and subsequently alveolar-fated progen

176 Treated rats had fewer proliferating bronchiolar fibroblasts, as detected by bromodeoxyuridin

177 ha is an important mediator of virus-induced bronchiolar fibrosis, and 3) TNF-alpha has a critical ro

178 important regulatory event in virus-induced bronchiolar fibrosis, pulmonary TNF-alpha mRNA and prote

179 nza type I (Sendai) virus is associated with bronchiolar fibrosis.

180 sistant (Fischer 344; F344) to virus-induced bronchiolar fibrosis.

181 terestingly, alveolar gas NO (estimated from bronchiolar gases at end-expiration) was near zero, sugg

182 synthesis in the static lung was measured in bronchiolar gases during an expiratory breath-hold in no

183 ARS-CoV infection demonstrated bronchial and bronchiolar hyperplasia and perivascular cuffing in ferr

184 e localized to regions of mucus and alveolar-bronchiolar hyperplasia, proliferations of type 2 epithe

185 al for the development of K-Ras(G12V)-driven bronchiolar hyperplasias and adenomas, but not for the g

186 -induced structural abnormalities, including bronchiolar hypoplasia, alveolar dysplasia, bronchiolar

187 al sequelae, the IFN-gamma group having less bronchiolar inflammation (p = 0.025) and fibrosis (p = 0

188 on lung transplantation, is characterized by bronchiolar inflammation and tissue remodeling.

189 was concordant with increased bronchial and bronchiolar inflammation.

190 fficient to suppress airway hyperreactivity, bronchiolar inflammatory infiltrate and allergen-specifi

191 Previous studies of naphthalene-induced bronchiolar injury and repair in the mouse have shown th

192 We compared acute bronchiolar injury and repair in three strains of mice u

193 Various histopathologic patterns of bronchiolar injury have been described and have led to c

194 immunochemically during repair of this acute bronchiolar injury.

195 rom (2) parenchymal disorders with prominent bronchiolar involvement and (3) bronchiolar involvement

196 th prominent bronchiolar involvement and (3) bronchiolar involvement in large airway diseases.

197 Prominent bronchiolar involvement may be seen in several interstit

198 spiratory Distress Syndrome (CARDS) toxin in bronchiolar lavage fluid (BALF) and lung.

199 the total number of cells and macrophages in bronchiolar lavage fluid (BALF), as well infiltrating in

200 Metabolomics of bronchiolar lavage fluid and fibroblast infection, growt

201 -dependent inhibition of eosinophilia in the bronchiolar lavage fluid, when compound A was given intr

202 ung tissue substantiated the findings in the bronchiolar lavage fluid.

203 rom fungi and bacteria in DNA extracted from bronchiolar lavage samples and oropharyngeal wash.

204 The clinical relevance of a bronchiolar lesion is best determined by identifying the

205 tic foci (subpleural, peri-vascular and peri-bronchiolar lesions) and destruction of alveolar archite

206 f BOS and is characterized by a perivascular/bronchiolar leukocyte infiltration.

207 isk factor, is characterized by perivascular/bronchiolar leukocyte infiltration.

208 ow end-expiratory lung volume, mainly at the bronchiolar level.

209 Conclusions: EB-OCT demonstrated marked bronchiolar loss in early IPF (between 30% and 50%), eve

210 A levels (P < 0.05) and increased numbers of bronchiolar macrophages and fibroblasts expressing TNF-a

211 BN rats also had greater numbers of bronchiolar macrophages expressing TGF-beta 1 protein th

212 t by increased TGF-beta 1 gene expression by bronchiolar macrophages in genetically susceptible indiv

213 bronchiolar mural fibrosis, and increases in bronchiolar mast cells, were associated with virus-induc

214 The bronchial thickening and bronchiolar micronodules regressed after allo-HSCT, wher

215 bronchiolar hypoplasia, alveolar dysplasia, bronchiolar mural fibrosis, and increases in bronchiolar

216 rmalities were most strongly associated with bronchiolar mural thickening and fibrosis as well as wit

217 We also determined whether bronchiolar mural thickening and fibrosis may be caused

218 immuno-proteomics of these MUC5AC-expressing bronchiolar niches identified increased goblet, suprabas

219 n multiorgan system cGVHD model that induces bronchiolar obliterans (BO).

220 tent bronchioalveolar stem cells (BASCs) and bronchiolar progenitor club cells.

221 The factors that regulate bronchiolar regeneration after Clara cell injury are not

222 collagen deposition in the alveolar and the bronchiolar region.

223 ithelial cell interfaces in the alveolar and bronchiolar regions of the lung parenchyma and was assoc

224 proliferative population in initial terminal bronchiolar repair and include a population of label-ret

225 RP-expressing neuroendocrine cells reside in bronchiolar SCPC niches, we hypothesized that the glandu

226 to type I and type II pneumocytes as well as bronchiolar secretory cells following transplantation to

227 ytes and abundant expression in vascular and bronchiolar smooth muscle cells.

228 achments to the outer wall of small airways: bronchiolar smooth muscle is increased also.

229 r prostaglandin E(2) (PGE(2)) production and bronchiolar smooth muscle relaxation.

230 observed in the respiratory epithelium, the bronchiolar smooth muscle, and the pulmonary vasculature

231 rk, bacteria and hemorrhages in alveolar and bronchiolar spaces, and hypoxic foci in the lung (endoth

232 The bronchial/bronchiolar spores decreased between 1 and 18 hours afte

233 alysis revealed a higher number of bronchial/bronchiolar spores for A. fumigatus than L. corymbifera.

234 tive contributions of progenitor (Clara) and bronchiolar stem cells to epithelial maintenance and rep

235 We hypothesized that a reduced potential for bronchiolar stem-cell (Clara cell)-related repair in the

236 ed 10-fold in the lung tissue and 22-fold in bronchiolar tissue as compared with their controls.

237 nhibited asbestos-induced AP-1 activation in bronchiolar tissue.

238 The mechanisms controlling this bronchiolar-to-alveolar developmental transition remain

239 PD-L1 expression was increased in the bronchiolar wall, parenchyma, and vascular wall from mil

240 ells, lymphocytes, and eosinophils, into the bronchiolar wall.

241 ng TGF-beta 1 protein that were localized in bronchiolar walls at 10, 14, and 30 d after inoculation.

242 gnificantly decreased compared with those in bronchiolar walls of normal controls.

243 A human bronchiolar xenograft model was employed to investigate

244 Inoculation of human bronchiolar xenografts revealed a significant reduction