ライフサイエンスコーパス: lower airway

1 identical to samples taken directly from the lower airway.

2 d, in particular their ability to infect the lower airway.

3 ubgroup of patients with eosinophilia in the lower airway.

4 recold specimens from either the nose or the lower airway.

5 fference in NO. concentration present in the lower airway.

6 tween bacteria and the host occurring in the lower airway.

7 oaspiration and pneumococcal presence in the lower airways.

8 ex microbial communities (microbiome) in the lower airways.

9 ration may contribute to colonization of the lower airways.

10 nation for CF lung disease in the gland-free lower airways.

11 urable humoral and cellular responses in the lower airways.

12 diatric respiratory disease in the upper and lower airways.

13 lia and, consequently, autonomic tone in the lower airways.

14 uring allergic inflammation in the upper and lower airways.

15 l children with a bacterial infection of the lower airways.

16 ant changes in the measured functions of the lower airways.

17 n both the patency and responsiveness of the lower airways.

18 airway constriction and inflammation of the lower airways.

19 ion by intramuscular mRNA was limited to the lower airways.

20 onella, were more functionally active in the lower airways.

21 ng to downregulation of SP in both upper and lower airways.

22 responses over 1 year in blood and upper and lower airways.

23 ate different regions and tissues within the lower airways.

24 n of viral replication in both the upper and lower airways.

25 observed differential response of upper and lower airways.

26 t of ferrets rather than from trachea or the lower airways.

27 ir respiratory tract deposited dose in their lower airways.

28 es may be informative about processes in the lower airways.

29 th shared and distinct between the upper and lower airways.

30 ief among these are infections involving the lower airways.

31 esis and the interaction with both upper and lower airways.

32 caused materials to accumulate in upper and lower airways.

33 (40% and 36%, respectively), the skin (27%), lower airways (14%) and the gut (8%).

34 ppresses virus replication in both upper and lower airways, a phenomenon not previously observed with

35 recent concept, bringing together upper- and lower-airway allergic diseases with skin, gut, and neuro

36 tic approach of the links between upper- and lower-airway allergic diseases.

37 nse is proportional to that occurring in the lower airway and greater in the presence of a bacterial

38 atory viruses and bacteria, which infect the lower airway and increase airway inflammation.

39 CD8(+) resident memory T (Trm) cells in the lower airway and infer the molecular pathways associated

40 Gas exchange was achieved at lower airway and intrathoracic pressures than those that

41 te molecular phenotypes within the asthmatic lower airway and provide a simple, noninvasive test for

42 Also, the involvement of the lower airway and the potential role of IgE in the bronch

43 e induction may prevent dissemination to the lower airway and thus minimize pathogenesis.

44 in sheep but in the epithelial cells of the lower airways and alveoli.

45 y nebulizing 1 mg ml(-1) bradykinin into the lower airways and by microinjecting 0.5 nmol capsaicin i

46 the transcriptomic profiles of the upper and lower airways and determine their level of similarity ir

47 an important risk factor for HAdV(+) of the lower airways and influences the likelihood of bacterial

48 to chart the cellular landscape of upper and lower airways and lung parenchyma in healthy lungs, and

49 e is evidence that rhinovirus can infect the lower airways and may be associated with bronchiolitis a

50 rentiation of gammadelta T cells in both the lower airways and peripheral blood, with accumulation of

51 Alveolar macrophages (AMs) reside in the lower airways and play a crucial role in lung health and

52 ve in reducing S. aureus colonization in the lower airways and preventing VAT or VAP.

53 bjects underwent evaluation of the upper and lower airways and serologic analysis to determine the pr

54 ings suggest that RV can infect cells of the lower airway, and raise the possibility that such an eff

55 e severe viral respiratory infections of the lower airway, and thus increase the risk of exacerbation

56 Bronchoscopy sampled the upper airways, lower airways, and environmental background.

57 uch as lymph nodes, that drain the upper and lower airways, and further B-cell expansion takes place

58 activity, rapid protection in the upper and lower airways, and no pathologic changes in the lung.

59 markedly reduced viral load in the upper and lower airways, and protected animals against disease in

60 sal-associated lymphoid tissue (d-NALT), the lower airways, and the lung.

61 iruses trigger inflammatory responses in the lower airway are poorly understood, in particular their

62 Most vagal sensory afferents innervating the lower airways are activated by noxious stimuli including

63 Pneumococci that try to invade the lower airways are recognized by innate immune cells thro

64 We show that the upper and lower airways are significantly conserved in their trans

65 zed by recurrent infections of the upper and lower airways, as well as by progressive lung failure an

66 The lower airway bacterial burden in subjects with CHP was h

67 ower lobe bronchiectasis was associated with lower airway bacterial colonization (p = 0.004), higher

68 ociated with more severe COPD exacerbations, lower airway bacterial colonization, and increased sputu

69 Lower airway bacterial community composition was assesse

70 smoking status, exacerbation frequency, and lower airway bacterial load.

71 uffer from recurrent infections of upper and lower airways because of highly reduced numbers of multi

72 on between RV DNA/RNA detection in the upper/lower airways before HCT and the occurrence of allo-LSs.

73 = 0.02), whereas PEEPPL was characterized by lower airway-but not transpulmonary-driving pressure (p

74 A, DB1 reduced viral titers in the upper and lower airways by 3.8 log10 total PFU and 2.7 log10 PFU/g

75 ere colonized with S. mucilaginosus in their lower airways by culture growth from bronchoalveolar lav

76 Colonization of lower airways by Staphylococcus aureus is a risk factor

77 Antigen exposure in the upper or lower airways can also drive expansion of B-lineage cell

78 Lower airways can be also involved.

79 yet the characteristics of RV replication in lower airway cells are incompletely understood.

80 us RNA was detected in both nasal lavage and lower airway cells from all eight subjects 2 to 4 d afte

81 R) and Southern blotting to detect RV RNA in lower airway cells from eight allergic volunteers experi

82 acity of pneumococci to adhere to and infect lower airway cells is mediated by host-expressed platele

83 Combining cytopathology of lower airway cells obtained at bronchoscopy with the bio

84 ) are due, in part, to secreted signals from lower airway cells that modify the immune response and t

85 be associated with the presence of virus in lower airway cells, we used the techniques of reverse tr

86 ndent pneumococcal adhesion and infection of lower airway cells.

87 ll responses were assessed before upper- and lower-airway challenge with SARS-CoV-2.

88 and the host mucosal barrier function of the lower airways, combined with both innate and adaptive im

89 ion of plasmacytoid dendritic cells into the lower airway, commensurate with IFNA production, natural

90 e therapeutic strategies targeting upper and lower airways concomitantly and improving the health of

91 play a role in diverse pathologies including lower airway conditions, but the exact mechanism of acti

92 XCL1) in FABP4(-/-) alveolar macrophages and lower airway CXCL1 levels in FABP4(-/-) mice.

93 namic diameter within the suitable range for lower airway deposition.

94 us exercise in cold environments can lead to lower airway disease and suggest that racing sled dogs m

95 us are major etiological agents of upper and lower airway disease in horses.

96 ial virus (RSV) is the major cause of severe lower airway disease in infants and young children, but

97 tion may inhibit the development of allergic lower airway disease in mice.

98 ntry skiers, have an increased prevalence of lower airway disease that is hypothesized to result from

99 activity questionnaire, and their upper and lower airway disease was managed for 12 months with ever

100 with BPEx was sufficient to inhibit allergic lower airway disease with minimal collateral lung inflam

101 to elicit protection against murine allergic lower airway disease.

102 with asthma, and its activity tracks that of lower airway disease.

103 iscuss the role of TGF-beta in the upper and lower airway diseases.

104 ich are key effector cells in many upper and lower airway diseases.

105 "fingerprinted", using paired EBC, upper and lower airway donor sample sets.

106 ude that inflammatory responses of upper and lower airways during RV-16 colds are similar in asthmati

107 conclude that MIP-1-alpha is present in the lower airways during severe RSV disease.

108 ate inflammatory immune dysregulation in the lower airways during severe viral pneumonia that is dist

109 Conclusions: Lower airway dysbiosis in the setting of smoke exposure

110 Objectives: We investigated whether lower airway dysbiosis occurs in mild-to-moderate COPD a

111 cal murine model exposed to cigarette smoke, lower airway dysbiosis with common oral commensals augme

112 the lower airway, these results suggest that lower airway dysfunction occurs through this mechanism i

113 nce of allergy is a risk factor for enhanced lower airway effects during RV infection, we experimenta

114 at these factors contribute to the increased lower airway effects of RV infection in subjects with as

115 Poor clinical outcome was associated with lower airway enrichment with an oral commensal (Mycoplas

116 ubjects who never developed ACR demonstrated lower airway enrichment with several oral commensals (e.

117 Lower airway eosinophilia was more frequent in N-ERD (54

118 bility of rhinovirus to infect a transformed lower airway epithelial cell line (A549) and to induce I

119 erns of chemokine expression in RSV-infected lower airway epithelial cells (A549 and SAE).

120 We performed RNA sequencing on upper and lower airway epithelial cells from 63 children with or w

121 ls in upper airway tissues and indicate that lower airway epithelial cells have a similar susceptibil

122 mporal changes in expression by RSV-infected lower airway epithelial cells of chemokines, chemotactic

123 sms occurring in the upper airway may mirror lower airway events.

124 nd P. aeruginosa are commonly present in the lower airways from infancy.

125 Parental tobacco smoking is associated with lower airway function and an increased incidence of whee

126 y hyperreactivity, which could contribute to lower airway function and the increased wheezy illnesses

127 osure to parental smoking is associated with lower airway function but not increased airway reactivit

128 on did not produce detectable alterations in lower airway function in health AR and non-AR subjects.

129 ratio of wall to lumen area correlated with lower airway function.

130 rotracheal intubation (thereby isolating the lower airway gas from ambient air contamination or gas c

131 Lower airway gas, sampled through the bronchoscope durin

132 al vascular density was increased at mid- to lower airway generations, which was independent of chang

133 plice variant was significantly increased at lower airway generations.

134 idia, TLR9(-/-) mice exhibited significantly lower airway hyper-responsiveness compared to the TLR9(+

135 eficient (CD8-/-) mice develop significantly lower airway hyperresponsiveness (AHR), eosinophilic inf

136 bumin showed less pulmonary inflammation and lower airway hyperresponsiveness than genetically matche

137 the thickened basement membrane of asthmatic lower airways, (ii) around smooth muscle cells of the as

138 Lower airway immune profiles show considerable heterogen

139 ay imply that clinical insight regarding the lower airway in health and disease can be gained from st

140 ); however, it has also been detected in the lower airway in the stable state, but the consequences o

141 Remodelling has been long identified in the lower airways in asthma and is characterized by epitheli

142 ys and lung parenchyma in healthy lungs, and lower airways in asthmatic lungs.

143 d standard for detection of pathogens in the lower airways in cystic fibrosis (CF).

144 mics, and epigenomics-performed on upper and lower airways in patients with N-ERD.

145 educed inflammatory cell accumulation to the lower airways in response to inhaled LPS.

146 HP.Conclusions: The microbial profile of the lower airways in subjects with CHP is distinct from that

147 sts that differences exist between upper and lower airways in the polarity of available receptors for

148 approach we confirmed the involvement of the lower airways in the response to aerosolized methacholin

149 Cytokine levels in nasal and lower airways in young cystic fibrosis (CF) patients wer

150 idence of bloodstream infection was 20.1 and lower airway infection 9.1 episodes per 1,000 patient da

151 Lower airway infection prevalence was described.

152 ained impaired exercise tolerance; recurrent lower airways infection; and therapy-resistant, irrevers

153 Here, we use cystic fibrosis (CF) lower airway infections as a model system to examine how

154 prevalence and change in prevalence of early lower airway infections in a modern cohort of children w

155 the sampling method for the investigation of lower airway infections.

156 Of the different lower airway-infiltrating immune cells that participate

157 y inflammation correlated with the degree of lower airway inflammation (e.g., nasal wash/sputum myelo

158 c inflammation correlated with the degree of lower airway inflammation (e.g., serum IL-6/sputum IL-8;

159 eveloped significant airflow obstruction and lower airway inflammation after CDE inhalation.

160 poorly understood.Objectives: To investigate lower airway inflammation and infection in preschool chi

161 ons can cause asthma exacerbations and alter lower airway inflammation and physiology, it is unclear

162 ficant determinant of airflow obstruction or lower airway inflammation following CDE inhalation.

163 n bronchial hyperreactivity and eosinophilic lower airway inflammation in asthmatic compared with nor

164 cal recovery, we note surprisingly extensive lower airway inflammation with persistent viral antigen

165 To determine the role of bacterial DNA in lower airway inflammation, we intratracheally instilled

166 tly related to neutrophilic and eosinophilic lower airway inflammation.

167 treatments to attempt to attenuate asthmatic lower airway inflammation.

168 d air may represent a noninvasive measure of lower airway inflammation.

169 samples is the principal method of assessing lower airway inflammation.

170 pect to clinical problems and the pattern of lower airway inflammation.

171 sought to determine the relationship between lower airway inflammatory biomarkers, specifically inter

172 ibutions of cigarette smoke and dysbiosis on lower airway inflammatory injury.

173 These findings have implications for lower airway innate immunity, delivery of airway therape

174 n genetic disease with progressive upper and lower airway involvement.

175 ocess, the observed S. aureus fitness in the lower airways is due to its intrinsic resistance to resi

176 Repeated monthly administration to mouse lower airways is feasible without loss of gene expressio

177 cines on viral replication in both upper and lower airways is important to evaluate in nonhuman prima

178 basis for its restricted replication in the lower airways is poorly understood.

179 Most sensory innervation of the lower airways is provided by vagal afferents, which are

180 r an obstructive inflammatory disease in the lower airways manifesting with symptoms including breath

181 esting that the bacterial communities of the lower airways may act as persistent stimuli for repetiti

182 Rapid and sustained protection in upper and lower airways may eventually require a boost.

183 haracterize the bacterial communities in the lower airways.Measurements and Main Results: Distinct di

184 Lower airway metagenomics has the potential to detect ho

185 In this Review, we provide an overview of lower airway microbial dynamics in health and disease an

186 whether the composition and structure of the lower airway microbiome correlated with clinical charact

187 Targeting the lower airway microbiome in combination with smoking cess

188 are associated with changes of the upper and lower airway microbiome, and that specific microbial sig

189 at compositionally and structurally distinct lower airway microbiomes are associated with discrete lo

190 roat swabs were collected as a surrogate for lower airway microbiota (median 35 days between study vi

191 Conclusions: Dynamic changes in the lower airway microbiota are associated with the developm

192 ublished single-cell gene expression data in lower airway mucosal cells after allergen challenge were

193 sing sensitization, peripheral eosinophilia, lower airway neutrophilia, and bacteriology.

194 Just as in the lower airways, objective and subjective evaluation gives

195 dren, Rint was increased in the patient with lower airway obstruction and five of six patients withou

196 unction tests revealed air trapping and mild lower airway obstruction in the ECMO group, compared wit

197 six with parenchymal lung disease; one with lower airway obstruction) and six without primary lung d

198 Parasympathetic ganglia neurons in the lower airway of laboratory animals have membrane propert

199 Pseudomonas aeruginosa (Pa) density from the lower airway of young children with cystic fibrosis.

200 pithelial cells as a means to persist in the lower airways of adults with COPD.

201 , we show viral replication in the upper and lower airways of AG129 mice (double IFNalpha/beta and IF

202 al replication was achieved in the upper and lower airways of animals after high-dose SARS-CoV-2 resp

203 terferons, were significantly reduced in the lower airways of asthma patients compared to healthy con

204 different inflammatory changes in upper and lower airways of asthmatic and healthy subjects, we inoc

205 nin, and the B2 receptor agonist, BK, in the lower airways of asthmatics and in the upper airways of

206 -2 MA was able to replicate in the upper and lower airways of both young adult and aged BALB/c mice.

207 ormed molecular sequencing of HAdVs from the lower airways of children with chronic endobronchial sup

208 -C is the major HAdV species detected in the lower airways of children with PBB and BE.

209 The lower airways of children with severe asthma display a d

210 M. pneumoniae was present in the lower airways of chronic, stable asthmatics with greater

211 a link between bacterial colonization of the lower airways of COPD sufferers and an increase in exace

212 y despite heavy attenuation in the upper and lower airways of cotton rats.

213 airway epithelial cells and in the upper and lower airways of cotton rats.

214 he cellular immune responses observed in the lower airways of humans with pneumotypeSPT indicate a ro

215 demonstrates significant inoculation of the lower airways of immunocompromised children with diverse

216 kine concentrations were not elevated in the lower airways of moderate influenza patients compared wi

217 ly abundant in secretions from the upper and lower airways of N-ERD patients.

218 y, assessment of host gene expression in the lower airways of patients reveals distinct immunological

219 In the lower airways of patients with asthma, mucous cell hyper

220 investigate immune mediator profiles in the lower airways of patients with N-ERD.

221 pathologies, IFNs are overrepresented in the lower airways of patients with severe COVID-19 that exhi

222 in virus titers recovered from the upper or lower airways of SARS-CoV-2-infected wild-type mice comp

223 demonstrate the frequent colonization of the lower airways of stable CB patients with multiple strain

224 gnificant proportion of T lymphocytes in the lower airways of subjects with asthma expressed high lev

225 n the microbial profiles were evident in the lower airways of subjects with CHP and IPF.

226 ubjects, microbiome analyses showed that the lower airways of subjects with COPD were enriched with c

227 limited spread of the Omicron strain in the lower airways of the virus-infected hamsters.

228 e and effective for significant reduction of lower airway Pa density in young children with cystic fi

229 ties, ensuring alleviation of both upper and lower airway pathology by systemic biological therapy.

230 Rhinovirus (RV) infections can alter lower airway physiology and inflammation, yet the charac

231 , and baseline PD20 influence the changes in lower airway physiology caused by RV infection and raise

232 IgE receptor expression on lower airway plasmacytoid dendritic cells was significan

233 Sputum samples containing lower airway plugs were obtained from 10 healthy childre

234 airway cross-sectional area was decreased by lowering airway pressure.

235 ective ventilation, a strategy that achieves lower airway pressures and Vt than the current standard.

236 Surprisingly, these IL-5 TG mice showed lower airway reactivity to methacholine.

237 oprost therapy, 36% stopped iloprost, due to lower airway reactivity, clinical deterioration, or deat

238 tribute to inflammation, adversely effecting lower airway remodeling and asthma severity.

239 s and IL-8 level in the BAL fluid, inhibited lower airway remodeling and fibrosis, and nearly abolish

240 cells is a key determinant in the control of lower airway remodeling posttransplantation.

241 Here, we examine how, in the lower airways, resident cell populations contribute to t

242 predicted TLC 134.8% vs 109.6%; P < .05) and lower airway resistance (mean %of predicted Raw 101.9% v

243 Upper airway resistance (Rua), lower airway resistance (RIa), and lung volume did not c

244 Upper and lower airway resistance can increase the risk for sleep-

245 (reflective of temperatures in the upper and lower airway, respectively) revealed that replication of

246 '-NT and NS AP mRNA dominating in higher and lower airways, respectively.

247 severe viral pneumonia that is distinct from lower airway responses seen in human patients with sympt

248 induce clinical, physiologic, and pathologic lower airway responses typical of an asthma exacerbation

249 mice, CD8(-/-) mice developed significantly lower airway responsiveness to inhaled methacholine and

250 mice, BLT1 -/- mice developed significantly lower airway responsiveness to inhaled methacholine, low

251 lenge, fB-/- mice demonstrated significantly lower airway responsiveness to methacholine and less air

252 treated C57BL/6 mice injected with OC-20 had lower airways responsiveness than HDM-treated mice injec

253 sults derived from lung transplant recipient lower airway samples collected at multiple time points.

254 in RSV-infected WD-PBECs reflected those in lower airway samples from RSV-hospitalized infants.

255 Blood, upper airway, and (in a subgroup) lower airway samples were obtained throughout infection.

256 il secretory ribonucleases, were detected in lower airway secretions from RSV-infected patients; ECP

257 alpha, RANTES, and IL-8 were also present in lower airway secretions obtained from patients with RSV

258 serve as a useful model for the analysis of lower-airway secretions and their role in host defense a

259 as a determinant for infection spread to the lower airways, severity of accompanying inflammatory sym

260 id prevalence of infections of the upper and lower airway, skin/soft tissue, and urinary tract (all P

261 ed to the upper airway, yet can cause severe lower airway symptoms in children and adults with asthma

262 mAb targeting IL-4Ralpha, improves upper and lower airway symptoms in patients with aspirin-exacerbat

263 n origin and in which sinus, pharyngeal, and lower airway symptoms, although frequently present, are

264 lel with 18 cytokines in the nose, upper and lower airway symptoms, and lung function.

265 upper airway disease is also associated with lower airway symptoms.

266 ffline in 391 children aged 3-47 months with lower airway symptoms.

267 lloimmune responses and inhibits BOS through lowering airway TGF-beta bioavailability without alterin

268 ed for reduction of viral replication in the lower airway than in the upper airway.

269 actor expressed during infection of the COPD lower airways that contributes to invasion of host respi

270 s characterized by an acute infection of the lower airways that may progress rapidly to organ failure

271 known local gene expression footprint in the lower airways that on one hand appears to be a result of

272 ve been shown to reflect colonization of the lower airways, the actual site of inflammation in asthma

273 driven chronic inflammation of the upper and lower airways, the estimated contribution of these novel

274 In the lower airways, the Na+ concentrations were 80-85 meq/lit

275 o deliver WKS13 to both the nasal cavity and lower airways, the two critical sites of infection cause

276 Allergic diseases of the (upper and lower) airways, the skin and the gastrointestinal tract,

277 ecrease of the bacterial colonization of the lower airways, there was pervasive trachea-bronchial-lun

278 n confirming that RV can infect cells in the lower airway, these results suggest that lower airway dy

279 of resident memory CD4+ T (Trm) cells in the lower airway; these Trm cells displayed progressive diff

280 xpression changes were more prominent in the lower airway, they were reflected in nasal epithelium an

281 location, and frequency of RV appearance in lower airway tissues during an acute infection, immunohi

282 These results confirm that infection of lower airway tissues is a frequent finding during a cold

283 nvestigate the protease repertoire of murine lower airway tissues, primary type II alveolar epithelia

284 Sampling various compartments within the lower airways to examine human bronchial epithelial cell

285 measured the effects on the response of the lower airways to histamine.

286 tinent to allergic diseases of the upper and lower airways, to function as professional APCs, those s

287 NTHi causes upper and lower airway tract infections in individuals with compro

288 was significantly associated with COPD, with lower airway tree caliber relative to lung size associat

289 D gene expression signature in the upper and lower airways.Trial registration: ClinicalTrials.gov reg

290 markably reduced viral load in the upper and lower airways upon SARS-CoV-2 challenge even at 108 days

291 Similar measurements made on the lower airway via the bronchoscope have been successful i

292 of strong relationships between virus load, lower airway virus-induced inflammation and asthma exace

293 The reduced concentration of cells in the lower airways was associated with enhanced apoptosis of

294 Equivalent control of virus replication in lower airways was observed following Omicron challenge 1

295 CD4+ T cells in blood and the lower airway were analyzed by flow cytometry and immunoh

296 er airway isolated from and connected to the lower airway were performed before and following bilater

297 a distinct host transcriptome profile of the lower airways were most predictive of mortality.

298 d genes associated with atopic wheeze in the lower airway, which could equally distinguish atopic and

299 e review demonstrates that several upper and lower airway work-related diseases may present with chro

300 Its pathogenesis involves both upper and lower airways, yet most studies to date have examined th