ライフサイエンスコーパス: pulmonary infection

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

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

3 timately confers increased susceptibility to pulmonary infection.

4 ological consequences of acute P. aeruginosa pulmonary infection.

5 ndependent inflammation during P. aeruginosa pulmonary infection.

6 were secondarily subjected to P. aeruginosa pulmonary infection.

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

8 nderwent CLP were resistant to the secondary pulmonary infection.

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

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

11 iation during the granulopoietic response to pulmonary infection.

12 irulence of Francisella tularensis following pulmonary infection.

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

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

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

16 reased bacteremia but no difference in local pulmonary infection.

17 ntaminated aerosols, resulting in an initial pulmonary infection.

18 pathogens during the very earliest stages of pulmonary infection.

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

20 emic infection concurrent with the localized pulmonary infection.

21 cking PCho for clearance from mice following pulmonary infection.

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

23 scontinued prophylaxis experienced recurrent pulmonary infection.

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

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

26 sent a central innate protective response to pulmonary infection.

27 induced by Mycobacterium tuberculosis during pulmonary infection.

28 ims and to ameliorate inflammation following pulmonary infection.

29 rod from a transplant recipient with a fatal pulmonary infection.

30 clinical or radiographic evidence of active pulmonary infection.

31 (beta h/c) in a neonatal-rabbit model of GBS pulmonary infection.

32 ause of a number of complications, including pulmonary infection.

33 in virulence in models of both systemic and pulmonary infection.

34 licited significant protection against focal pulmonary infection.

35 emic infection concurrent with the localized pulmonary infection.

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

37 that develop perinatally and protect against pulmonary infection.

38 , chronic obstructive pulmonary disease, and pulmonary infection.

39 rlier findings of the protective response to pulmonary infection.

40 organ dysfunction syndrome (MODS) following pulmonary infection.

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

42 2(+) monocytes to clearance of K. pneumoniae pulmonary infection.

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

44 Aspergillus most commonly caused pulmonary infection.

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

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

47 organ injury in animals with an established pulmonary infection.

48 mmune response against L. pneumophila during pulmonary infection.

49 tial utility as an early intervention during pulmonary infections.

50 nd nonmalignant conditions is complicated by pulmonary infections.

51 ionella pneumophila, Pseudomonas aeruginosa) pulmonary infections.

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

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

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

55 augment innate immune defenses in refractory pulmonary infections.

56 icularly, alcoholics are more susceptible to pulmonary infections.

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

58 ed lifelong risk of developing mycobacterial pulmonary infections.

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

60 be particularly susceptible to Pneumocystis pulmonary infections.

61 le for Pseudomonas aeruginosa during chronic pulmonary infections.

62 eased susceptibility of premature infants to pulmonary infections.

63 that may permit a more effective response to pulmonary infections.

64 Increased resistance was also seen during pulmonary infections.

65 mune system is effective at controlling most pulmonary infections.

66 drive development of new strategies against pulmonary infections.

67 ecognizing and responding to microbes during pulmonary infections.

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

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

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

71 During pulmonary infections, a careful balance between activati

72 lmonary hemorrhage secondary to a cavitating pulmonary infection after aspiration pneumonia 6 weeks a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

90 el) Slc11a1(s)(B10 x C2D) are susceptible to pulmonary infections and develop pneumonia when naturall

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

92 Pulmonary infections and pneumonitis occur frequently af

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

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

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

96 1b augments pro-inflammatory response during pulmonary infection, and caffeine suppresses the effect

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

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

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

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

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

102 nt recipients are particularly vulnerable to pulmonary infections; and (5) chronic allograft dysfunct

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

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

105 Chronic pulmonary infections are responsible for the morbidity a

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

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

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

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

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

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

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

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

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

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

118 Pulmonary infection by Streptococcus pneumoniae is chara

119 Acute pulmonary infection by Streptococcus pneumoniae is chara

120 dase has a key role in the initial stages of pulmonary infection by targeting bacterial glycoconjugat

121 vaccine is presently available, results from pulmonary infection by the bacterium Yersinia pestis.

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

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

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

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

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

127 Pulmonary infection by Yersinia pestis causes pneumonic

128 Pulmonary infection by Yersinia pestis causes pneumonic

129 Secondary pulmonary infections by encapsulated bacteria including

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

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

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

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

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

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

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

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

138 Many pulmonary infections elicit lymphocyte responses that le

139 Murine cryptocococcal pulmonary infection elicited serum immunoglobulin M (IgM

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

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

142 lar macrophages (AM) in host defense against pulmonary infection has been difficult to establish usin

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

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

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

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

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

148 determine if differences in the severity of pulmonary infection in cystic fibrosis seen with late is

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

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

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

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

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

154 a durable protective immune response against pulmonary infection in mice.

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

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

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

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

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

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

161 n macrophages and during the early phases of pulmonary infection in vivo.

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

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

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

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

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

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

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

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

170 nd their enhanced maturation/migration after pulmonary infection/inflammation.

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

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

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

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

175 During pulmonary infection, locally produced cytokines enter th

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

177 Using a pulmonary infection model that reflects human infection,

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

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

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

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

182 Bacillus anthracis interactions in a murine pulmonary-infection model.

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

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

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

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

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

188 Pulmonary infection of mice with Aspergillus fumigatus i

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

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

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

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

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

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

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

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

197 rulence within murine models of systemic and pulmonary infection regardless of the inoculation route

198 by which hematopoietic tissues respond to a pulmonary infection remains poorly understood.

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

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

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

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

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

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

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

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

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

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

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

210 5%) to (11/14; 78.6%), reduction in clinical pulmonary infection score, lower white blood cell count

211 Recurrent sino-pulmonary infections secondary to immunodeficiency and h

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

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

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

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

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

217 nts with respiratory failure associated with pulmonary infection, there were no survivors among those

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

219 With accumulating evidence of pulmonary infection via aerosolized nontuberculous mycob

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

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

222 Pulmonary infection was cleared even in the absence of b

223 A concomitant pulmonary infection was identified more frequently among

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

225 ys in the host defense against P. aeruginosa pulmonary infection, we challenged C3-, C4-, and factor

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

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

228 Pulmonary infections were the most common source of seps

229 vivors quickly succumbed (100% mortality) to pulmonary infection when intratracheally challenged, at

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

248 l aspartyl proteases, protected mice against pulmonary infection with Coccidioides posadasii.

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

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

251 Persistent pulmonary infection with Cryptococcus neoformans in C57B

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

253 Upon pulmonary infection with Cryptococcus, Treg cells accumu

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

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

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

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

258 appears to actually increase the severity of pulmonary infection with F. tularensis.

259 Following pulmonary infection with Francisella tularensis, we obse

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

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

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

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

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

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

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

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

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

269 The effects of IL-23 on the outcome of pulmonary infection with M. tuberculosis have not been d

270 valuate the impact of alcohol consumption on pulmonary infection with M. tuberculosis in a murine mod

271 e CD4(+)- and CD8(+)-lymphocyte responses to pulmonary infection with M. tuberculosis were blunted in

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

273 tion is associated with decreased control of pulmonary infection with M. tuberculosis, which is accom

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

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

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

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

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

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

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

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

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

283 Pulmonary infection with P. murina, combined with cigare

284 Chronic pulmonary infection with Pseudomonas aeruginosa is a fea

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

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

287 14 were not more susceptible or resistant to pulmonary infection with SchuS4.

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

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

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

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

292 Pulmonary infection with the bacterium Yersinia pestis c

293 Clearance of pulmonary infection with the fungal pathogen Cryptococcu

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

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

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

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

298 A significant clinical complication of pulmonary infections with Klebsiella pneumoniae is perip

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

300 duced resistance against experimental fungal pulmonary infections with two agents, Blastomyces dermat