ライフサイエンスコーパス: pulmonary infection

1 spiratory syndrome (MERS) is a highly lethal pulmonary infection.

2 Aspergillus most commonly caused pulmonary infection.

3 IL-1 receptor (IL-1R) signaling during early pulmonary infection.

4 attenuated in a neutropenic, murine model of pulmonary infection.

5 organ injury in animals with an established pulmonary infection.

6 mmune response against L. pneumophila during pulmonary infection.

7 d their effector cytokines in the context of pulmonary infection.

8 35 immuno-compromised patients suspected of pulmonary infection.

9 timately confers increased susceptibility to pulmonary infection.

10 ological consequences of acute P. aeruginosa pulmonary infection.

11 ndependent inflammation during P. aeruginosa pulmonary infection.

12 were secondarily subjected to P. aeruginosa pulmonary infection.

13 omplement strains in a BALB/c mouse model of pulmonary infection.

14 nderwent CLP were resistant to the secondary pulmonary infection.

15 tant role in the pathogenesis of severe MRSA pulmonary infection.

16 iation during the granulopoietic response to pulmonary infection.

17 irulence of Francisella tularensis following pulmonary infection.

18 quired via inhalation, leading to an initial pulmonary infection.

19 of C. neoformans cells or spores results in pulmonary infection.

20 ions are encountered by H. influenzae during pulmonary infection.

21 reased bacteremia but no difference in local pulmonary infection.

22 pathogens during the very earliest stages of pulmonary infection.

23 ctivity of memory CD4+ T cells responding to pulmonary infection.

24 emic infection concurrent with the localized pulmonary infection.

25 cking PCho for clearance from mice following pulmonary infection.

26 f TLR2 in the control of P. gingivalis acute pulmonary infection.

27 scontinued prophylaxis experienced recurrent pulmonary infection.

28 10), two MMPs induced by acute P. aeruginosa pulmonary infection.

29 ctive airway disease, were also present with pulmonary infection.

30 sent a central innate protective response to pulmonary infection.

31 induced by Mycobacterium tuberculosis during pulmonary infection.

32 ells for intracellular growth during natural pulmonary infection.

33 forded complete protection against Y. pestis pulmonary infection.

34 nnate protective function of SAP in an acute pulmonary infection.

35 c model of the human bronchiole for studying pulmonary infection.

36 a dual role for Pla in the initial stages of pulmonary infection.

37 Mo-DCs) in the lungs after F. tularensis LVS pulmonary infection.

38 most upregulated IVE-TB genes during in-vivo pulmonary infection.

39 ntaminated aerosols, resulting in an initial pulmonary infection.

40 that develop perinatally and protect against pulmonary infection.

41 , chronic obstructive pulmonary disease, and pulmonary infection.

42 rlier findings of the protective response to pulmonary infection.

43 organ dysfunction syndrome (MODS) following pulmonary infection.

44 ant role in host defense against C. burnetii pulmonary infection.

45 2(+) monocytes to clearance of K. pneumoniae pulmonary infection.

46 ecognizing and responding to microbes during pulmonary infections.

47 rotection against K. pneumoniae (ATCC 43816) pulmonary infections.

48 nd nonmalignant conditions is complicated by pulmonary infections.

49 ionella pneumophila, Pseudomonas aeruginosa) pulmonary infections.

50 ich continues to be a major cause of serious pulmonary infections.

51 c stem cell transplant therapy is limited by pulmonary infections.

52 augment innate immune defenses in refractory pulmonary infections.

53 icularly, alcoholics are more susceptible to pulmonary infections.

54 ed lifelong risk of developing mycobacterial pulmonary infections.

55 t the target site of action in patients with pulmonary infections.

56 be particularly susceptible to Pneumocystis pulmonary infections.

57 creased incidence of disease severity during pulmonary infections.

58 tial utility as an early intervention during pulmonary infections.

59 d by early structural lung disease caused by pulmonary infections.

60 antibiotic resistance, is a common cause of pulmonary infections.

61 drive development of new strategies against pulmonary infections.

62 tions (107 [74%] vs 101 [62%]; p=0.0174) and pulmonary infections (20 [14%] vs 10 [6%]; p=0.0214) wer

63 respectively; serious AEs included bacterial pulmonary infections (8%), respiratory failure (7%), sep

64 nit transfer (10 [20%] vs 9 [19%]; P = .80), pulmonary infection (9 [18%] vs 6 [13%]; P = .10), and m

65 During pulmonary infections, a careful balance between activati

66 mic lung injury further enhances the risk of pulmonary infection after lung transplantation.

67 administered to mice before M. tuberculosis pulmonary infection, an accelerated local inflammatory r

68 ccus neoformans is a fungal pathogen causing pulmonary infection and a life-threatening meningoenceph

69 m disease characterized primarily by chronic pulmonary infection and bronchiectasis, pancreatic exocr

70 sis, including initiation and persistence of pulmonary infection and dissemination to the central ner

71 lating macrophage function in the context of pulmonary infection and fibrosis.

72 fluenza A virus (IAV) results in a localized pulmonary infection and inflammation and elicits an IAV-

73 he roles of CCR7 in the host defense against pulmonary infection and innate immunity are not well und

74 Severe ENT form is associated with pulmonary infection and is easily detected by nasal fibe

75 y infective deaths and 3 further deaths from pulmonary infection and lung allograft rejection.

76 re significant only in randomized trials for pulmonary infection and only in nonrandomized trials for

77 ial proliferation and sustained M. abscessus pulmonary infection and permits evaluation of efficacies

78 s that promotes establishment of the initial pulmonary infection and plays a key role in disease prog

79 The relationship of SARS-CoV-2 pulmonary infection and severity of disease is not fully

80 ression is highly induced in the lung during pulmonary infection and that Klebsiella-induced mortalit

81 owledge that smokers are more susceptible to pulmonary infection and that the airway epithelium of sm

82 ferentially influence fungal survival during pulmonary infection and the onset of meningoencephalitis

83 Key proportions of patients with findings of pulmonary infection and those requiring further inpatien

84 ression was elevated in patients with active pulmonary infection and was highly correlated with IFN l

85 cohort studies (the Infant Susceptibility to Pulmonary Infections and Asthma Following RSV Exposure [

86 The incidence of pulmonary infections and CMV reactivation were also moni

87 inflammation as well as on the incidence of pulmonary infections and cytomegalovirus (CMV) reactivat

88 xoU-secreting P. aeruginosa with more severe pulmonary infections and for the tendency of hospital-ac

89 quencing on isolates from early pediatric CF pulmonary infections and from comparator groups in the s

90 e and is partially responsible for recurrent pulmonary infections and inflammation events that ultima

91 Pulmonary infections and pneumonitis occur frequently af

92 aryotic hosts, to allow real-time imaging of pulmonary infections and rapid quantification of bacteri

93 seudomonas aeruginosa during cystic fibrosis pulmonary infections and that the presence of these oral

94 pression are linked to reduced resistance to pulmonary infections and to the development of emphysema

95 1b augments pro-inflammatory response during pulmonary infection, and caffeine suppresses the effect

96 cosal lesions, intensive care unit transfer, pulmonary infection, and mortality.

97 One patient died postoperatively because of pulmonary infection, and one patient died 6 months after

98 refractory CLL (due to progressive disease, pulmonary infection, and pneumonia; none thought to be t

99 tients with advanced lung disease and severe pulmonary infections, and it is associated with high mor

100 ty to sweat, decreased lacrimation, frequent pulmonary infections, and missing and malformed teeth.

101 sms and subsequent effector functions during pulmonary infection are largely unknown.

102 for the treatment of Pseudomonas aeruginosa pulmonary infections are associated with the increase in

103 Mab pulmonary infections are difficult, or sometimes impossi

104 Chronic pulmonary infections are responsible for the morbidity a

105 Complications of pulmonary infections are the most common causes of death

106 This unique case confirms S. intermedius pulmonary infection as the source of metastatic CNS infe

107 me, bronchospasm, new pulmonary infiltrates, pulmonary infection, aspiration pneumonitis, pleural eff

108 eumonia (PCP), the most common opportunistic pulmonary infection associated with HIV infection, is ma

109 aphylococcus aureus causes especially severe pulmonary infection, associated with high morbidity and

110 of patients (four of 1964) with findings of pulmonary infection at chest radiography (all of whom we

111 In the murine model of pulmonary infection, B. anthracis virulence was capsule

112 irway obstruction, ventilation, oxygenation, pulmonary infections, bleeding complications, and surviv

113 s are dispensable for FSTL-1 Hypo control of pulmonary infection but are required for dissemination c

114 neutrophil influx during Chlamydia muridarum pulmonary infection, but its role during C. muridarum ge

115 ygiW, firR, and firS were attenuated during pulmonary infection, but not otitis media.

116 We induced sustained pulmonary infection by a human S. pneumoniae isolate in

117 ent of mucosal innate immune defense against pulmonary infection by a relevant airway pathogen, and p

118 on-cut lung slices as a platform to evaluate pulmonary infection by bacterial pathogens.

119 Factors required for pulmonary infection by NTHI are not well understood.

120 e of airway homeostasis during M. pneumoniae pulmonary infection by preventing an overzealous proinfl

121 Acute pulmonary infection by Streptococcus pneumoniae is chara

122 Pulmonary infection by Streptococcus pneumoniae is chara

123 Pulmonary infection by the respiratory syncytial virus (

124 of PVL but not LukAB resulted in more-severe pulmonary infection by the wild-type strain (with a 30-f

125 in the United States and the first report of pulmonary infection by this pathogen in the literature.

126 to examine the role of GRK5 in monomicrobial pulmonary infection by using an intratracheal Escherichi

127 immunity in vivo, we used a murine model of pulmonary infection by using the live vaccine strain (LV

128 bacterial burden and prolong survival during pulmonary infection by virulent F. tularensis.

129 Pulmonary infection by Yersinia pestis causes pneumonic

130 Pulmonary infection by Yersinia pestis causes pneumonic

131 Secondary pulmonary infections by encapsulated bacteria including

132 A case of symptomatic pulmonary infection caused by M. paraffinicum is describ

133 There is also an increased risk of pulmonary infection caused by Streptococcus pneumoniae,

134 an important role in host protection against pulmonary infection caused by Streptococcus pneumoniae.

135 estinal and other morbidity (cardiovascular, pulmonary, infection, cerebrovascular, thromboembolic);

136 Manifestations include self-limited pulmonary infection, chronic fibrocavitary pulmonary dis

137 in almost all patients with chronic cavitary pulmonary infections, chronic invasive and granulomatous

138 onized by a diverse bacterial community, and pulmonary infections commonly present in lung cancer pat

139 that L-selectin-deficient mice are prone to pulmonary infection compared with wild-type controls.

140 During pulmonary infection, cryptococcal cells form large polyp

141 The primary fate of pulmonary infection demonstrated key differences with pu

142 Successful host defense against numerous pulmonary infections depends on bacterial clearance by p

143 s of chronic lung disease, lung cancers, and pulmonary infections despite antiretroviral therapy (ART

144 their transcriptional profiles during murine pulmonary infection differed both from their in vitro pr

145 se are the first documented cases of primary pulmonary infection due to this organism from a freshwat

146 Many pulmonary infections elicit lymphocyte responses that le

147 In contrast, progressive pulmonary infection, enhanced Th2-type cytokine producti

148 us (HIV)-positive persons are predisposed to pulmonary infections, even after receiving effective hig

149 METH enhances C. neoformans pulmonary infection, facilitating its dissemination and

150 nduction of BMF in response to this strictly pulmonary infection has been unclear.

151 nduction of BMF in response to this strictly pulmonary infection has been unclear.

152 Most notably, after mycobacterial pulmonary infection, heterogeneous subsets of tetramer(+

153 sule was not required for the development of pulmonary infection; however, the capsule seemed to be i

154 respiratory distress syndrome in 84 (6.9%), pulmonary infection in 80 (6.5%), and pulmonary embolism

155 ry Pneumocystis infection is the most common pulmonary infection in early infancy, making it importan

156 tic organism isolated once previously from a pulmonary infection in Japan.

157 f naive mice and humans typically lack BALT, pulmonary infection in mice leads to the development of

158 mary F. tularensis live vaccine strain (LVS) pulmonary infection in mice that are defective in IgA (I

159 However, pulmonary infection in mice with C. neoformans strain H9

160 viously unrecognized defect in resistance to pulmonary infection in patients with advanced lung disea

161 ratory tract bacteria may not only aggravate pulmonary infection in some CF patients but may also eli

162 nd prolonged Mtb containment with unilateral pulmonary infection in some mice.

163 that is capable of causing acute and chronic pulmonary infection in the immunocompromised host.

164 cannot disseminate to other organs following pulmonary infection in the murine inhalation model of cr

165 e description of invasive N. cyriacigeorgica pulmonary infection in the United States identified to t

166 usion, these IVE-TB Ags are expressed during pulmonary infection in vivo, are immunogenic, induce str

167 threat due to its involvement in septic and pulmonary infections in areas of endemicity and is recog

168 mic adverse effects and improve outcomes for pulmonary infections in CF.

169 eria (NTM) have become emergent pathogens of pulmonary infections in cystic fibrosis (CF) patients, w

170 as aeruginosa strains recovered from chronic pulmonary infections in cystic fibrosis patients are fre

171 ing modality of choice for the evaluation of pulmonary infections in immunocompromised patients.

172 ypeable Haemophilus influenzae (NTHi) causes pulmonary infections in patients with chronic obstructiv

173 contributing to increased susceptibility to pulmonary infections in smokers, ex-smokers, and vulnera

174 t targets for mucosal vaccination to prevent pulmonary infections in susceptible hosts.

175 d effectively prevent Pseudomonas aeruginosa pulmonary infections in the settings of cystic fibrosis

176 lity worldwide, with higher risks to develop pulmonary infections, including Aspergillus infections.

177 ransplant (HSCT) patients are susceptible to pulmonary infections, including bacterial pathogens, eve

178 he elderly population is more susceptible to pulmonary infections, including tuberculosis.

179 and (iii) that the efficacy of passive Ab in pulmonary infection is a function of dose and mouse stra

180 among immunocompromised persons, subclinical pulmonary infection is also common among immunocompetent

181 he degree to which IL-22BP controls IL-22 in pulmonary infection is not well defined.

182 or the treatment of diseases like cancer and pulmonary infections is gaining attention.

183 for the treatment of multiple-drug-resistant pulmonary infections is gaining attention.

184 nificant clinical complication of Klebsiella pulmonary infections is peripheral blood dissemination,

185 By inhalation and subsequent pulmonary infection, it may disseminate to the CNS and c

186 In response to pulmonary infection, mice deficient in the surface IL-17

187 of the microbial pathogens in patients with pulmonary infections might lead to targeted antimicrobia

188 Using a pulmonary infection model that reflects human infection,

189 sponse contributed to reduced lethality in a pulmonary infection model with S. pneumoniae.

190 tion in vitro and their virulence in a mouse pulmonary infection model.

191 uired for full Schu S4 virulence in a murine pulmonary infection model.

192 L1, loss of ALL2 attenuated virulence in the pulmonary infection model.

193 d viability assays, and in vivo using murine pulmonary infection models with intranasal PPMO treatmen

194 aeruginosa-laden agarose beads, modeling the pulmonary infection observed in many patients with cysti

195 esponse to Cryptococcus neoformans following pulmonary infection of C57BL/6 wild-type (WT) mice resul

196 Our results demonstrate that pulmonary infection of mice with a C. neoformans strain

197 Experimental pulmonary infection of mice with a C. neoformans strain

198 Pulmonary infection of mice with Aspergillus fumigatus i

199 Our data suggest that, during pulmonary infection of mice with K. pneumoniae, conventi

200 We find that pulmonary infection of mice with type 3 translocation-co

201 tors and harbor viable L. pneumophila during pulmonary infection of mice.

202 children with respiratory compromise due to pulmonary infection, one premature baby with respiratory

203 al number of organisms culminated in chronic pulmonary infection or death over a 90-day period.

204 ry complications (postoperative lung injury, pulmonary infection, or barotrauma).

205 ith increased eosinophil activity, recurrent pulmonary infections, or both, as evident by the concomi

206 characterized by recurrent and often severe pulmonary infections, pneumatoceles, eczema, staphylococ

207 e safe for the lung, but close monitoring of pulmonary infections remains essential.

208 % (1925 of 1964 radiographs) and findings of pulmonary infection represented 2.0% (39 of 1964 radiogr

209 f the asymptomatic patients with findings of pulmonary infection required supplemental oxygenation, a

210 upregulation of Cmt proteins, C. neoformans pulmonary infection results in increased serum Cu concen

211 ung cytokine levels in the context of active pulmonary infection revealed increased expression of int

212 in CD8+ T cell response to HIV-1, increased pulmonary infection risk among cystic fibrosis patients,

213 the study highlights that, in situations of pulmonary infection risk, such as in diabetic subjects,

214 ive ventilation groups, a lower incidence of pulmonary infection (RR, 0.45; 95% CI, 0.22 to 0.92; I2,

215 infection (purulent secretions and Clinical Pulmonary Infection Score >/=6).

216 The corresponding Clinical Pulmonary Infection Score (CPIS) was collected simultane

217 h placebo, AA significantly reduced Clinical Pulmonary Infection Score (mean +/- SEM, 9.3 +/- 2.7 to

218 uspected VAP, defined as a modified Clinical Pulmonary Infection Score of 5 or greater.

219 efore screening; and had a modified Clinical Pulmonary Infection Score of at least 6.

220 of pneumonia (as determined by the Clinical Pulmonary Infection Score) increased from 24% on day 1 t

221 5%) to (11/14; 78.6%), reduction in clinical pulmonary infection score, lower white blood cell count

222 tion during Streptococcus pneumoniae-induced pulmonary infection, suggesting an important role for PA

223 ignificantly more resistant to S. pneumoniae pulmonary infection than their wild-type (Wt) counterpar

224 mmunocompetent patients, producing a primary pulmonary infection that can later disseminate to other

225 gionnaires' Disease (LD), a life-threatening pulmonary infection that can spread systemically.

226 etting of neutropenic leukemia patients with pulmonary infection, the presence of the RHS on CT was a

227 es a spectrum of disease, ranging from local pulmonary infection to disseminated disease.

228 itamin D supplementation in the treatment of pulmonary infections to accelerate resolution of inflamm

229 With accumulating evidence of pulmonary infection via aerosolized nontuberculous mycob

230 ouse model of acute Burkholderia cenocepacia pulmonary infection was assessed.

231 infection model, (ii) that susceptibility to pulmonary infection was associated with macrophage permi

232 A concomitant pulmonary infection was identified more frequently among

233 In multivariable analysis, pulmonary infection was significantly associated with se

234 One death, due to atypical pulmonary infection, was assessed as possibly related to

235 TPA) for detecting angioinvasive patterns of pulmonary infection, we performed a single-center, prosp

236 culosis Using a mouse model of P. aeruginosa pulmonary infection, we show that INP1855 improves survi

237 Pulmonary infections were the most common source of seps

238 al the species or strain of pathogen causing pulmonary infection, which can lead to inappropriate tre

239 These can range from initial pulmonary infection, which eventually resolves whether o

240 neoformans is a fungal pathogen that causes pulmonary infections, which may progress into life-threa

241 factor alpha (TNF-alpha) produced in active pulmonary infection, while low doses induced apoptosis,

242 evasive mechanisms used by pathogens during pulmonary infection will deepen our knowledge of immunop

243 In contrast, pulmonary infection with a C. neoformans strain that sec

244 iated immune (CMI) responses in mice given a pulmonary infection with a Cryptococcus neoformans strai

245 ies have demonstrated an association between pulmonary infection with a herpesvirus and IPF.

246 del provides a means of study of a long-term pulmonary infection with a human pathogen in a rodent sy

247 Mice given a pulmonary infection with an IFN-gamma-producing C. neofo

248 or vaccine-induced protection against lethal pulmonary infection with B. dermatitidis in mice.

249 CCR2(-/-) mice were extremely susceptible to pulmonary infection with B. mallei, compared with wild-t

250 r immune responses in protective immunity to pulmonary infection with B. mallei.

251 B-1 B cells in the innate B cell response to pulmonary infection with C. neoformans and reveal that I

252 Our results demonstrate that pulmonary infection with C. neoformans strain H99gamma r

253 -IL-17A antibodies and given an experimental pulmonary infection with C. neoformans strain H99gamma.

254 the initial innate immune response following pulmonary infection with C. neoformans.

255 We used a murine model of chronic pulmonary infection with CF-related strains of P. aerugi

256 en shown to be essential for defense against pulmonary infection with Coccidioides species.

257 type (WT) mice showed similar outcomes after pulmonary infection with Coccidioides, while vaccinated

258 ype 2 CD4(+) helper T (T(H)2) cell bias upon pulmonary infection with Cryptococcus neoformans and oth

259 Persistent pulmonary infection with Cryptococcus neoformans in C57B

260 B-2 B cell populations in C57BL/6 mice after pulmonary infection with Cryptococcus neoformans.

261 Upon pulmonary infection with Cryptococcus, Treg cells accumu

262 is required for protective immunity against pulmonary infection with F. tularensis live vaccine stra

263 responses, exhibit increased mortality after pulmonary infection with F. tularensis live vaccine stra

264 e between host immunity and pathology during pulmonary infection with F. tularensis live vaccine stra

265 , XID mice displayed increased resistance to pulmonary infection with F. tularensis.

266 Following pulmonary infection with Francisella tularensis, we obse

267 e of interleukin-10 (IL-10) in cutaneous and pulmonary infection with Francisella tularensis.

268 ase (ALT) elevation with fevers, and grade 3 pulmonary infection with grade 3 maculopapular rash.

269 Thus, concurrent pulmonary infection with influenza A virus is associated

270 t respiratory syncytial virus, their role in pulmonary infection with influenza virus has remained un

271 in wild-type and Mincle(-/-) mice undergoing pulmonary infection with K. pneumoniae was compared.

272 component of mucosal immune defense against pulmonary infection with K. pneumoniae.

273 In a murine model of pneumonic sepsis using pulmonary infection with Klebsiella pneumoniae, the expr

274 bs are able to mediate local protection from pulmonary infection with Legionella pneumophila, the cau

275 mice were significantly more susceptible to pulmonary infection with LVS.

276 derstand how BCG extends time to death after pulmonary infection with M. tuberculosis, we examined cy

277 ocytes are important in the host response to pulmonary infection with methicillin-resistant S. aureus

278 stigated the role of SP-A during acute phase pulmonary infection with Mp using mice deficient in SP-A

279 ned the participation of CCR4 in response to pulmonary infection with Mycobacterium bovis Bacille-Cal

280 DCs) to activate naive CD4(+) T cells during pulmonary infection with Mycobacterium bovis bacillus Ca

281 Here we show that pulmonary infection with Mycobacterium tuberculosis (Mtb

282 However, the role of M-CSF in pulmonary infection with Mycobacterium tuberculosis is n

283 No longer mainly a complication after pulmonary infection with Mycobacterium tuberculosis, div

284 We report a case of pulmonary infection with Neoscytalidium dimidiatum in an

285 key element in host defense against chronic pulmonary infection with P. aeruginosa.

286 Pulmonary infection with P. murina, combined with cigare

287 Chronic pulmonary infection with Pseudomonas aeruginosa is a fea

288 le of CCR7 in the host defense against acute pulmonary infection with Pseudomonas aeruginosa.

289 nredundant component of host defense against pulmonary infection with RSV, functioning as a first poi

290 14 were not more susceptible or resistant to pulmonary infection with SchuS4.

291 ith IpaD were fully protected against lethal pulmonary infection with Shigella flexneri and Shigella

292 gene, exhibited greater resistance to acute pulmonary infection with Streptococcus pneumoniae.

293 of B7x-deficient (B7x(-/-)) mice to a lethal pulmonary infection with Streptococcus pneumoniae.

294 We report the first case of mixed pulmonary infection with Strongyloides stercoralis and B

295 Clearance of pulmonary infection with the fungal pathogen Cryptococcu

296 A striking feature of pulmonary infection with the Gram-negative intracellular

297 s (cDCs) are critical for protection against pulmonary infection with the opportunistic fungal pathog

298 , which mediates IL-17A signaling, following pulmonary infection with wild-type C. neoformans strain

299 ditionally, the patient experienced repeated pulmonary infections with Aspergillus, leading to multip

300 trate that CF mice are highly susceptible to pulmonary infections with S. aureus and fail to clear th