ライフサイエンスコーパス: pneumocyte

1 syndrome caused by prematurity of the type I pneumocyte.

2 ure, bronchial epithelial cells, and type II pneumocytes.

3 is expressed in bronchial cells and type II pneumocytes.

4 on, did we detect any engraftment as type II pneumocytes.

5 C lines, as compared to normal human type-II pneumocytes.

6 under the control of doxycycline in type II pneumocytes.

7 l epithelium and appears in type II alveolar pneumocytes.

8 seen associated with the mycobacteria on the pneumocytes.

9 ocytes (19%) but not in endothelial cells or pneumocytes.

10 characteristics of their cell of origin, AT2 pneumocytes.

11 t in both rat lung and isolated rat granular pneumocytes.

12 of both IAV and IBV in primary human type II pneumocytes.

13 en conidia and A549 cells, a line of type II pneumocytes.

14 and is associated with apoptosis of type II pneumocytes.

15 factor (KGF) is a growth factor for type II pneumocytes.

16 ells) and predominantly localized in type II pneumocytes.

17 caused by the fusion of SARS-CoV-2-infected pneumocytes.

18 c decrease of the TG2 expression in the lung pneumocytes.

19 F327S), specifically in lung alveolar type 2 pneumocytes.

20 rus replication occurring mainly in alveolar pneumocytes.

21 thelial cells expressing markers of alveolar pneumocytes.

22 tiation to alveolar type I- and type II-like pneumocytes.

23 ESAT6 causes cytolysis of type 1 and type 2 pneumocytes.

24 ng cells, middle ear cells, and A549 type II pneumocytes.

25 ific gene expression by fusing with diseased pneumocytes.

26 s, and accounted for 0% to 0.553% of type II pneumocytes.

27 evaluate for Y-chromosome-containing type II pneumocytes.

28 ferentiated, with some maturation of type II pneumocytes.

29 Marked apoptosis of CD68-negative type II pneumocytes (30 to 80%) was detected in four of the seve

30 eltaRD1 mutants failed to cause cytolysis of pneumocytes, a phenotype that had been previously used t

31 l incorporates human lung epithelial type II pneumocyte (A549) (upper chamber) and endothelial cell (

32 n in cultured human hepatocytes (Huh7.5) and pneumocytes (A549) to generate conditioned culture mediu

33 Following germination of pneumocyte-adherent conidia for 12 h, direct penetration

34 growth mechanics of fetal lungs and type II pneumocytes after tracheal ligation (TL).

35 brotic conditions, indicating that pulmonary pneumocyte and not pleural expression of mesothelin may

36 ral RNA was detected in approximately 20% of pneumocytes and alveolar endothelial cells as determined

37 ining Langerhans' cells, hyperplastic type 2 pneumocytes and alveolar macrophages within and surround

38 IAV in human airway cells and IBV in type II pneumocytes and as a potential target for the developmen

39 munohistology revealed abundant PVM-positive pneumocytes and bronchial and bronchiolar epithelial cel

40 ly active in cell lines derived from type II pneumocytes and Clara cells (MLE-15 and mtCC1-2 mouse ce

41 ung cancer of sheep that arises from type II pneumocytes and Clara cells of the lung epithelium.

42 ng cancer of sheep, originating from type II pneumocytes and Clara cells.

43 y, mice without lung Klf2 lack mature type I pneumocytes and die shortly after birth, closely recapit

44 ry for cytokeratin and surfactant identified pneumocytes and epithelial syncytial cells as important

45 CXCR3 was expressed by type II pneumocytes and fibroblasts in fibrotic areas in close p

46 ema, hyaline membranes, and proliferation of pneumocytes and fibroblasts.

47 ive lipid deposition in both macrophages and pneumocytes and increased levels of surfactant.

48 mice, S. aureus alpha-toxin directly injures pneumocytes and increases mortality, whereas alpha-toxin

49 BAX expression was markedly increased in pneumocytes and interstitial cells in DAD compared with

50 in determining the susceptibility of type II pneumocytes and interstitial cells to apoptosis.

51 The percentage of positively staining pneumocytes and interstitial cells was estimated in each

52 increased cholesterol biosynthesis in type-2 pneumocytes and lipofibroblasts and altered relative fre

53 virus was mainly found in SPC(+) and LDLR(+) pneumocytes and macrophages in the lungs.

54 NA-78 demonstrated that hyperplastic Type II pneumocytes and macrophages were the predominant cellula

55 used loss of the cytolytic phenotype in both pneumocytes and macrophages.

56 ective localization of the viral RNA in many pneumocytes and pulmonary endothelial cells using a high

57 Virus-positive pneumocytes and renal tubular epithelial cells also were

58 ordinated differentiation of alveolar type 1 pneumocytes and specialized alveolar capillary endotheli

59 ptidase 4 showed colocalization in scattered pneumocytes and syncytial cells.

60 fficient infection of human alveolar type II pneumocytes and thus more-severe lung damage.

61 apacity to productively replicate in type II pneumocytes and to cope with the induced cytokine respon

62 lity of self-renewal and differentiated into pneumocytes and tracheal epithelial cells.

63 e alveolar damage, with virus located in the pneumocytes and tracheal epithelium.

64 mbers of bacteria attached to and within the pneumocytes and we determined by viable-cell counting th

65 d THP-1 cells as models of type 1 and type 2 pneumocytes, and alveolar macrophages, respectively.

66 of SARS-CoV-2 antigen-positive macrophages, pneumocytes, and bronchial epithelial cells in TLR7(-/-)

67 asolateral laminin-expressing surface of the pneumocytes, and damage the cells and the basement membr

68 f CYP1A1 in airway epithelial cells, type II pneumocytes, and endothelial cells.

69 were defective for adherence to macrophages, pneumocytes, and hepatocytes.

70 irway smooth muscle cells, cardiac myocytes, pneumocytes, and infiltrated inflammatory cells, but was

71 mycobacterial DNA was found in endothelium, pneumocytes, and macrophages from the lung and in Bowman

72 us antigen was observed in airway epithelia, pneumocytes, and macrophages.

73 Type II pneumocyte apoptosis was confirmed by electron microscop

74 ift in polyamine metabolism may occur as new pneumocytes are produced.

75 Alveolar type II (ATII) pneumocytes as defenders of the alveolus are critical to

76 nd life-threatening respiratory illness with pneumocytes as its main target.

77 ruginosa invasion of rat primary type I-like pneumocytes as well as a murine lung epithelial cell lin

78 edigrees differentiate to type I and type II pneumocytes as well as bronchiolar secretory cells follo

79 munoreactivity was present in normal type II pneumocytes as well as in a range of atypical lesions de

80 and transdifferentiate into type I alveolar pneumocytes (AT1 cells).

81 This process occurs when type II alveolar pneumocytes (AT2 cells) proliferate and transdifferentia

82 ean 0.95+/-1.18 Sp-C+ cells per 1000 type II pneumocytes by confocal microscopy).

83 binding of ESAT6 to laminin and the lysis of pneumocytes by free and bacterium-associated ESAT6 toget

84 to infected alveolar macrophages and type-1 pneumocytes by immunohistochemistry.

85 to monitor gene expression in the A549 lung pneumocyte cell line during exposure to P. aeruginosa.

86 UC1 is a powerful new marker for the type II pneumocyte cell lineage that allows us to follow the typ

87 ar epithelial cells, macrophages and type II pneumocytes; cell types involved in adaptive immunity an

88 ation of M. tuberculosis with human alveolar pneumocyte cells (2%) was less than that observed with f

89 erculosis replicated in association with the pneumocyte cells by more than 55-fold by day 7 postinfec

90 ata, SARS-CoV-2-infected ciliated and type 2 pneumocyte cells in airway and alveolar regions, respect

91 cytosed and degraded by cultured pre-type II pneumocyte cells, and both processes could be blocked by

92 , which are expressed exclusively in type II pneumocytes, cells that proliferate in ventilator associ

93 lar type-II pneumocytes that is dependent on pneumocyte Clr-g expression.

94 icate the NKR-P1B:Clr-g signaling axis in AM-pneumocyte communication as being important for maintain

95 an and bovine lung tissue containing primary pneumocytes could be used as a more accurate and relevan

96 CXCL12 was expressed in type II pneumocytes covering LAM nodules and caused AML cell gro

97 ining differentiation of human fetal type II pneumocyte culture.

98 MIS-C does not result in pneumocyte damage but is associated with vascular endoth

99 othelial cells, and primary alveolar type II pneumocytes, demonstrating a much broader tissue tropism

100 fferentiation of human alveolar type 2 cells/pneumocytes derived from primary lung tissue.

101 mediated PCR was performed in murine type II pneumocyte-derived MLE-15 cells infected with a chimeric

102 in mid-gestation HFL explants during type II pneumocyte differentiation in culture, we performed miRN

103 We show that TR and SMRT control type I pneumocyte differentiation through Klf2, which, in turn,

104 ved in lung development, specifically type I pneumocyte differentiation, and suggest a possible new t

105 ow significant distal airspace formation and pneumocyte differentiation.

106 Cells expressing ET-1 (pneumocytes, endothelial cells, airway epithelial cells,

107 These model systems include a human alveolar pneumocyte epithelial cell line, a murine macrophage cel

108 Both types of pneumocytes express membrane laminin, and ESAT6 exhibits

109 Cultured pneumocytes express the severe acute respiratory syndrom

110 migatus conidia may be binding of conidia to pneumocytes, followed by hyphal penetration of the epith

111 GSH) is essential for adequate protection of pneumocytes from potential toxicity mediated by extracel

112 d by discoveries of the complexity of type 1 pneumocyte function and characterization of mesenchymal

113 turn, seems to directly activate the type I pneumocyte gene program.

114 ssion of neuroendocrine genes and of type II pneumocyte genes, respectively.

115 fluent monolayers of alveolar type II (ATII) pneumocytes has been decreased by NO.

116 Apoptosis of type II pneumocytes has been identified in diffuse alveolar dama

117 Proliferation of type II pneumocytes has been linked to a repair process during t

118 myomatosis (LAM) and multifocal micronodular pneumocyte hyperplasia (MMPH) produce cystic and nodular

119 Histopathology showed abundant type II pneumocyte hyperplasia in the lungs of animals pretreate

120 KGF pretreatment and the resultant pneumocyte hyperplasia reduce fluid flux in models of lu

121 In conclusion, KGF, through type II alveolar pneumocyte hyperplasia with increased sodium-potassium-a

122 Type II pneumocyte hyperplasia, a common reaction to lung injury

123 his protection are likely related to type II pneumocyte hyperplasia, but remain to be specifically el

124 g growth factor that causes alveolar type II pneumocyte hyperplasia.

125 iated with death on a ventilator and type II pneumocyte hyperplasia.

126 r septal thickening and intermittent type II pneumocyte hyperplasia.

127 g pathology including lung inflammation, and pneumocyte hypertrophy in the lungs.

128 novel role for PGC1alpha in maintaining AT2 pneumocyte identity.

129 Pneumocyte II population kinetics were analyzed using a

130 RSS2 co-expressing cells within lung type II pneumocytes, ileal absorptive enterocytes, and nasal gob

131 ceptor inactivation also resulted in type II pneumocyte immaturity, which was apparent from their inc

132 istry studies localized MMP-1 to the Type II pneumocyte in patients with emphysema and not normal con

133 hat up-regulation of p53 and WAF1 in type II pneumocytes in DAD is associated with underlying DNA dam

134 ruses preferentially infect alveolar type II pneumocytes in human lung.

135 acts and a cellular tropism for type 1 and 2 pneumocytes in lung but is generally a mild infection un

136 al pulmonary surfactant production by type 2 pneumocytes in lung.

137 l types, including distal type I and type II pneumocytes in the late term.

138 The authors investigated whether type II pneumocytes in the lungs of cross-gender lung transplant

139 Our data suggest a mechanism by which fused pneumocytes in the lungs of patients with COVID-19 may e

140 ation of lipid-laden macrophages and type II pneumocytes in the lungs.

141 idence suggesting the involvement of type II pneumocytes in the replication of PRRSV.

142 role of the epithelium, particularly type II pneumocytes, in the initiation and perpetuation of fibro

143 lar bacterial CFU obtained from the infected pneumocytes increased by fourfold by day 7 after the add

144 lung injury, extensive apoptosis of type II pneumocytes is largely responsible for the disappearance

145 was observed in endothelial cells, alveolar pneumocytes, kidney glomeruli, mammary myoepithelial cel

146 ion of BRAF(V600E) and PIK3CA(H1047R) in AT2 pneumocytes leads to rapid cell de-differentiation, with

147 und to antagonize viral replication in human pneumocyte-like cells derived from induced pluripotent s

148 lineage that allows us to follow the type II pneumocyte lineage during the process of lung carcinogen

149 s for the peripheral lung, i.e., the type II pneumocyte lineage markers MUC1 and surfactant protein-A

150 ic interstitial pneumonia, only rare type II pneumocytes (< 5%) exhibited apoptosis, and they showed

151 alized in ciliated cells, endothelial cells, pneumocytes, macrophages, and smooth muscle cells; fibro

152 of bone marrow cells can express the type I pneumocyte markers, T1alpha and aquaporin-5.

153 pithelial cells expressed type I and type II pneumocyte markers.

154 ression of these marker genes during type II pneumocyte maturation.

155 gand have long been known to promote type II pneumocyte maturation; prenatal administration of glucoc

156 in Mycobacterium tuberculosis replicating in pneumocytes may utilize surface ESAT6 to anchor onto the

157 We conclude that proliferation of type II pneumocytes occurs during the early phase of acute lung

158 The number of type II pneumocytes of male karyotype showed a statistically sig

159 phological and molecular phenotype of type I pneumocytes of the alveolar epithelium.

160 Signals transmitted between AM and pneumocytes of the pulmonary niche coordinate these spec

161 TGF-beta1 within either hyperplastic type 2 pneumocytes or alveolar macrophages.

162 SPARKY exhibited a Type II pneumocyte phenotype characterized by surfactant and thy

163 In chronic interstitial pneumonia, type II pneumocytes proliferate continuously, although to a much

164 has been shown to play an important role in pneumocyte proliferation and lung development.

165 ng a protective role for KGF-induced type II pneumocyte proliferation in lung injury.

166 se cells contribute minimally to the type II pneumocyte proliferation that is often present in these

167 enhanced bronchiolar epithelial and type II pneumocyte proliferation.

168 nute discrete foci of cytologically atypical pneumocyte proliferations designated as atypical adenoma

169 , BAX was identified on an average of 10% of pneumocytes (range 0 to 20%) but not in interstitial cel

170 identified on an average of 80% of alveolar pneumocytes (range 30 to 100%) and 70% of interstitial c

171 transplant recipients develop low levels of pneumocyte repopulation by bone marrow-derived stem cell

172 Type II pneumocytes respond to influenza A infection by activati

173 The decreased number of type II alveolar pneumocytes results in absent or reduced surfactant prod

174 s altered in emphysema such that the Type II pneumocyte secretes MMP-1 and suggests that MMP-1 may be

175 the setting of post-transplant inflammation, pneumocyte-specific reprogramming of transplanted BMDCs

176 n of a proteolytic enzyme within the Type II pneumocyte suggests that the cells within the lung itsel

177 Gene expression analysis of isolated type II pneumocytes suggests potential explanations for the obse

178 nally, differentiated type II but not type I pneumocytes supported the replication of influenza virus

179 ble conidia subsequently became clustered on pneumocyte surfaces.

180 g carcinoma (BAC), a neoplasm of the Type II pneumocyte that affects humans, sheep, and small animals

181 uman lung epithelial cells, including type-2 pneumocytes that are present in alveoli and ciliated air

182 imilar reduction in DNMT activity in type II pneumocytes that give rise to the tumors.

183 ysical relay between AM and alveolar type-II pneumocytes that is dependent on pneumocyte Clr-g expres

184 pathway controlling the formation of type I pneumocytes, the cells that mediate gas exchange, is poo

185 esat6 transcripts in bacteria replicating in pneumocytes, the specific association of ESAT6 with the

186 Notably, the H5N1 virus targeted type II pneumocytes throughout the 7-day infection, and induced

187 Because this time frame is similar to pneumocyte turnover time, the shift in polyamine metabol

188 s and KS tumor cells, as well as epithelioid pneumocytes (two of two).

189 eural cellular accumulation, macrophage, and pneumocyte type 2 hypertrophy, massive lipid deposition

190 We found that it was the macrophage, and not pneumocyte type II cells or other nonhematopoietic cells

191 Studies with A-549 cells, a model for pneumocytes type 2, demonstrate that overexpression of A

192 or the L858R mutant (EGFR(L858R)) in type II pneumocytes under the control of doxycycline.

193 we showed that P. aeruginosa invades type I pneumocytes via a lipid raft-mediated mechanism.

194 ase of acute lung injury, PCNA positivity in pneumocytes was extremely rare.

195 a marker of terminally differentiated type I pneumocytes, was also induced.

196 ear epithelial cells (HMEE), as well as A549 pneumocytes, was measured.

197 b-family A member 3 (ABCA3) positive type II pneumocytes, was observed in the histological assessment

198 Y-chromosome-containing type II pneumocytes were found in 9 of 25 biopsy specimens from

199 Rat type II pneumocytes were incubated with [3H]choline, purified gp

200 lls, or hiPSC-derived alveolar type II (AT2) pneumocytes were infected with SARS-CoV-2 to create in v

201 Alveolar epithelial type II pneumocytes were isolated and purified from adult rat lu

202 way epithelium, and only occasional alveolar pneumocytes were labeled.

203 al proliferative lesions of alveolar type II pneumocytes were observed as early as seven days after i

204 acute/proliferative phase, apoptotic type II pneumocytes were rare whereas PCNA expression was quite

205 r lining cells, including type I and type II pneumocytes, were the primary infected cells.

206 y concentrated at the basolateral surface of pneumocytes where they rest on the basement membrane, wh

207 helium, airway submucosal glands, and type 1 pneumocytes, where it can participate in respiratory tra

208 fic proteins synthesized in alveolar type II pneumocytes, where it is assembled and stored intracellu

209 rus in the lungs appeared to occur mainly in pneumocytes, whereas macrophages drove the inflammatory

210 uman lung tissue, including alveolar type II pneumocytes, which express avian-type receptors.

211 calization of LCAD to human alveolar type II pneumocytes, which synthesize and secrete pulmonary surf

212 s of patients with COVID-19 contain infected pneumocytes with abnormal morphology and frequent multin

213 were detected almost exclusively in type II pneumocytes, with a minor involvement of alveolar macrop