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1 CNS disease were 563.9 (vs 149.3 in isolated lung infection).
2 dvantage to Histoplasma yeasts during murine lung infection.
3 and that this is key in the establishment of lung infection.
4  against early clearance in a mouse model of lung infection.
5 cal for defense against C. psittaci in mouse lung infection.
6 ecular mechanisms of the recovery after MRSA lung infection.
7 virulence of Streptococcus pneumoniae during lung infection.
8 ice demonstrated susceptibility to P. murina lung infection.
9 uate P. aeruginosa in a rat model of chronic lung infection.
10 te late events during the recovery from MRSA lung infection.
11 ion profiling between days 1 and 3 post MRSA lung infection.
12 ow distinct evolutionary trajectories during lung infection.
13 aeruginosa pathogenicity in a mouse model of lung infection.
14 ential role in the innate immune response to lung infection.
15 developed a murine model of S. mucilaginosus lung infection.
16 on the early innate immune responses to MRSA lung infection.
17 mmation in septicemia following pneumococcal lung infection.
18 B-resistant mice highly susceptible to acute lung infection.
19 pathway and protect mice against pseudomonal lung infection.
20 ations in the BM in response to Pneumocystis lung infection.
21 reased in vivo during Pseudomonas aeruginosa lung infection.
22 ed that the prrF locus is required for acute lung infection.
23  an increased propensity to later nosocomial lung infection.
24 its are accompanied by spontaneous bacterial lung infection.
25 ors after systemic responses to Pneumocystis lung infection.
26 s susceptibility to Streptococcus pneumoniae lung infection.
27 sm for host defense against pathogens during lung infection.
28  mice and corresponded with reduction of the lung infection.
29 es a siderophore (legiobactin) that promotes lung infection.
30 ed with bacterial growth arrest during mouse lung infection.
31 he context of a chronic cystic fibrosis (CF) lung infection.
32 . tuberculosis in the chronic stage of mouse lung infection.
33 in enhanced protection against P. aeruginosa lung infection.
34 sed to exert important effects in preventing lung infection.
35 taT lymphocytes in response to S. pneumoniae lung infection.
36  to mediate innate immunity to P. aeruginosa lung infection.
37 atory deficit and death, despite progressive lung infection.
38 nhanced bacterial clearance during sublethal lung infection.
39 rs protection against P. gingivalis in acute lung infection.
40  in non-CF patients suffering from bacterial lung infection.
41 e to decreased bacterial burden during acute lung infection.
42 to significantly increased susceptibility to lung infection.
43  lung disease is characterized by persistent lung infection.
44 controls in the face of mucoid P. aeruginosa lung infection.
45 est-studied prognostic indicators of chronic lung infection.
46 k of bacteremia and meningitis without prior lung infection.
47 n vivo and protect mice against experimental lung infection.
48                    Death often occurred from lung infection.
49 inued, only two subsequently showed signs of lung infection.
50 reened the mutants in a rat model of chronic lung infection.
51 ung DC and Mvarphi in mice with cryptococcal lung infection.
52 disease using a murine model of cryptococcal lung infection.
53 requency of hospitalization due to bacterial lung infection.
54 ng were increased in this model of bacterial lung infection.
55 robial and steroid therapies and the risk of lung infection.
56 educe oropharyngeal colonization and prevent lung infection.
57 uginosa virulence in a murine model of acute lung infection.
58 li growth, adhesion to epithelial cells, and lung infection.
59 lic IL-1beta production in response to viral lung infection.
60 ltatfpO mutant was found to be attenuated in lung infection.
61 ticles for application to an animal model of lung infection.
62 cally contribute to immunity to Pneumocystis lung infection.
63 HIV-negative patients with persistent fungal lung infections.
64 facilitate airway colonization in nosocomial lung infections.
65 acterized by chronic airway inflammation and lung infections.
66 of IL-10 blockade in the treatment of fungal lung infections.
67 aving females at greater risk of contracting lung infections.
68 es 1, 5, and 14 in were implicated in 90% of lung infections.
69 originating in the oral microbiome can cause lung infections.
70  was important for Burkholderia mallei mouse lung infections.
71 h and bacteremia infections and pneumococcal lung infections.
72  and transplant outcome and aid in assessing lung infections.
73 ucial in nosocomial pneumonia and in chronic lung infections.
74 isrupts resolution pathways during bacterial lung infections.
75  oxygen-dependent regulation as paramount in lung infections.
76 eased incidence of infections, in particular lung infections.
77 prevalent and chronic Pseudomonas aeruginosa lung infections.
78 ctorial protective immunity to P. aeruginosa lung infections.
79 e function and are especially susceptible to lung infections.
80 ions in CFTR and is characterized by chronic lung infections.
81 ions, particularly from cystic fibrosis (CF) lung infections.
82 ation mitigates early secondary pneumococcal lung infections.
83  associated with cystic fibrosis and chronic lung infections.
84 ular bacteria that cause aerosol-transmitted lung infections.
85 mportant to improve outcome in P. aeruginosa lung infections.
86 opathology but also contributes to recurrent lung infections.
87 ripts are stable in chronic CF P. aeruginosa lung infections.
88  a significant fraction of hospital-acquired lung infections.
89 ents developed proven or probable IA (5 with lung infection, 1 with mediastinitis, and 1 with lung in
90  is understudied in Streptococcus pneumoniae lung infection, a prevalent pathogen of pneumonia.
91 RT-PCR) tests indicated early and persistent lung infection and delayed occurrence of brain infection
92 in C3a receptor (C3aR) in Chlamydia psittaci lung infection and elucidated C3a-dependent adaptive imm
93  defenses in vitro, CatB was dispensable for lung infection and extrapulmonary dissemination in vivo.
94  an established murine model of cryptococcal lung infection and flow cytometric analysis to identify
95 1 signaling promotes persistent cryptococcal lung infection and identifies this pathway as a potentia
96    In cystic fibrosis (CF) patients, chronic lung infection and inflammation due to Pseudomonas aerug
97                                Opportunistic lung infection and inflammation is a hallmark of chronic
98  preclinical murine model of cystic fibrosis lung infection and inflammation to investigate the role
99 way in modulating neutrophil function during lung infection and inflammation, but they also establish
100  infection, 1 with mediastinitis, and 1 with lung infection and mediastinitis).
101 A) of mice i) ensures complete recovery from lung infection and near absolute clearance of bacteria w
102 was also effective in protecting against the lung infection and severe lung pathology associated with
103 nsparent juvenile zebrafish to model mucosal lung infection and show that C. albicans and P. aerugino
104 hosphate-limited conditions during mammalian lung infection and that expression of the phosphate star
105                           Although bacterial lung infection and the resulting inflammation cause most
106 e multi-organ disease, the chronic bacterial lung infections and associated inflammation are the prim
107   Bacterial pathogens are a leading cause of lung infections and contribute to acute exacerbations in
108  use disorders are associated with increased lung infections and exacerbations of chronic lung diseas
109      Patients with hypercapnia often develop lung infections and have an increased risk of death foll
110 e of the multiple roles of TLRs in bacterial lung infections and highlights the mechanisms used by pa
111 of cell-based therapeutic protocols to treat lung infections and related complications.
112 Cu]DOTA-JF5 distinguished IPA from bacterial lung infections and, in contrast to [(18)F]FDG-PET, disc
113 stent Pseudomonas aeruginosa (P. aeruginosa) lung infection, and presence of meconium ileus (MI), has
114 s tropism to cell types that are relevant to lung infection, and therefore may be significant determi
115  are more susceptible than wild-type mice to lung infections, and bacterial killing is enhanced in tr
116 dvanced disease frequently develop bacterial lung infections, and hypercapnia is a risk factor for mo
117 th bronchiectasis and Pseudomonas aeruginosa lung infection, antibody can protect the bacterium from
118 pattern and mechanisms of recovery from MRSA lung infection are largely unknown.
119                       Pseudomonas aeruginosa lung infections are a major cause of death in cystic fib
120 ed the diagnostic potential of L-ficolin for lung infection (area under the curve, 0.842; P < .0001).
121 he GI manifestations of CF have left chronic lung infections as the primary cause of morbidity and mo
122 -resistant organisms associated with chronic lung infections as well as with cystic fibrosis patients
123  or that can eradicate chronic P. aeruginosa lung infections associated with cystic fibrosis (CF) wil
124                  We show that in response to lung infection, B1a B cells migrate from the pleural spa
125 be for noninvasive detection of A. fumigatus lung infection based on antibody-guided positron emissio
126 ently and repeatedly arise during chronic CF lung infection, but the evolutionary forces governing th
127                                              Lung infection by Burkholderia species, in particular Bu
128 ia and reperfusion, as well as in a model of lung infection by Klebsiella pneumoniae Transferring ser
129 e responses to repeated Chlamydia pneumoniae lung infection by multivariate modeling with four dichot
130  sRNAs, but not PrrH, are required for acute lung infection by P. aeruginosa Moreover, we show that t
131                                      Chronic lung infection by Pseudomonas aeruginosa causes signific
132 oprotein inhibited inflammation during acute lung infection by Pseudomonas aeruginosa, we asked wheth
133 cant defects in the early innate response to lung infection by the major human pathogen Klebsiella pn
134  both activating and inhibitory roles during lung infections by different bacteria and fungi.
135 of cross-reactive T and B cell epitopes, one lung infection can modify immunity and pathology to the
136 fied immune responses, as exemplified during lung infection, can cause extensive tissue damage.
137 ew respiratory viruses (e.g., SARS-CoV), and lung infections caused by antibiotic-resistant "ESKAPE p
138 eclinical development as a new drug to treat lung infections caused by Gram-negative bacteria.
139                                              Lung infections caused by opportunistic or virulent path
140  low as 10 to 100 CFU/mouse produced a fatal lung infection, compared with 10(7) to >10(8) CFU for no
141                        In the United States, lung infections consistently rank in the top 10 leading
142                                      Chronic lung infections could not be established with mucoid P.
143 n an acute model of Streptococcus pneumoniae lung infection, deficiency in matrix metalloproteinase (
144  improve or worsen the outcome of subsequent lung infections, depending on the immunological history
145  increased mortality following P. aeruginosa lung infection despite enhanced neutrophil recruitment a
146 usceptibility of mice to P. aeruginosa acute lung infection does not go through TLR2 or TLR4, implyin
147 tion, emphasizing the requirement for active lung infection during initial exposure.
148 ce of PMNs, mice cannot resist P. aeruginosa lung infection from extremely small bacterial doses.
149 n (18)F-FDG in differentiating K. pneumoniae lung infection from lung inflammation.
150 he mechanisms of protective immunity against lung infection has been largely derived from murine mode
151 stem (T2SS) of Pseudomonas aeruginosa during lung infection has been uncertain despite decades of res
152 g, key effector mediating innate immunity to lung infection has not been utilized.
153 hanisms of APP induction in the liver during lung infection have yet to be defined.
154 ic obstructive pulmonary disease (COPD), and lung infections have critical consequences on mortality
155 was observed for both tracheal infection and lung infection; (iii) was observed during the early and
156 ay epithelial integrity during P. aeruginosa lung infection in a mouse model.
157  in virulence in human macrophages or during lung infection in a murine model of histoplasmosis.
158 one treatment-related fatal adverse event: a lung infection in a patient given cetuximab.
159 er the pathological response to pneumococcal lung infection in BALB/c mice with serotype 8 pneumonia
160 the propensity of S. aureus to cause chronic lung infection in CF patients.
161 in mouse lungs, exemplified by more frequent lung infection in CF with TfpO-expressing P. aeruginosa
162 nt role in the pathogenesis of P. aeruginosa lung infection in cystic fibrosis (CF).
163  phenotypes may have particular relevance to lung infection in cystic fibrosis patients since the alt
164      Serious adverse events included grade 3 lung infection in five (14%) of 37 patients in the phase
165                            We found that RSV lung infection in HIS mice results in an RSV-specific pa
166 y and bone marrow failure after Pneumocystis lung infection in IFrag(-/-) mice.
167 ons, as evidenced by studies of cryptococcal lung infection in IL-10-deficient mice.
168 tunistic pathogen that establishes a chronic lung infection in individuals afflicted with cystic fibr
169 derophore production during the course of CF lung infection in nearly all strains tested.
170 ed protection against Pseudomonas aeruginosa lung infection in neonate mice.
171                     The causes of death were lung infection in one patient, intestinal perforation an
172 -demand hematopoiesis following Pneumocystis lung infection in our model.
173 thogen Pseudomonas aeruginosa causes chronic lung infection in patients with cystic fibrosis.
174        We used antibiotic therapy of chronic lung infection in persons with cystic fibrosis as a mode
175 The agar bead model of chronic P. aeruginosa lung infection in sheep is a relevant platform to invest
176 CFU of Y. pseudotuberculosis caused a lethal lung infection in some mice.
177 g that the mice were capable of clearing the lung infection in the absence of a functional T3SS1.
178 as deferens disease; and a predisposition to lung infection in the early postnatal period.
179 tenuated for nasopharyngeal colonization and lung infection in the mouse, establishing its role in fi
180 ased susceptibility to Aspergillus fumigatus lung infection in the presence of lower interleukin 23 (
181                     Our comparison of fungal lung infection in wild-type mice and IL-17A-deficient mi
182 infection.Respiratory syncytial virus causes lung infections in children, immunocompromised adults, a
183  mutant Pseudomonas aeruginosa cause chronic lung infections in cystic fibrosis (CF) patients and are
184 thogen Pseudomonas aeruginosa causes chronic lung infections in cystic fibrosis (CF) patients.
185 known as mucoidy, is associated with chronic lung infections in cystic fibrosis (CF).
186 al pathogen commonly associated with chronic lung infections in cystic fibrosis (CF).
187 n opportunistic pathogen that causes chronic lung infections in cystic fibrosis patients and is a maj
188 iously ill, and the primary agent of chronic lung infections in cystic fibrosis patients.
189 ated in nosocomial infections and in chronic lung infections in cystic fibrosis patients.
190 onas aeruginosa is a poor prognosticator for lung infections in cystic fibrosis.
191 ses a spectrum of diseases, including lethal lung infections in immunocompromised humans and allergic
192 urkholderia cenocepacia causes opportunistic lung infections in immunocompromised individuals, partic
193 group of closely related bacteria that cause lung infections in immunocompromised patients as well as
194 istic pathogen often associated with chronic lung infections in individuals with the genetic disease
195   Low NF-kappaB activators cause more severe lung infections in mice, and they drive macrophages towa
196 at causes otitis media in young children and lung infections in patients with chronic obstructive pul
197                 Pseudomonasaeruginosa causes lung infections in patients with cystic fibrosis (CF).
198 hat Pseudomonas aeruginosa bacteria, causing lung infections in patients with cystic fibrosis, lose c
199 n opportunistic pathogen that causes chronic lung infections in people suffering from cystic fibrosis
200 n opportunistic pathogen that causes chronic lung infections in the airways of cystic fibrosis (CF) p
201 perate phages active in cystic fibrosis (CF) lung infections, including the transposable phage, 4, wh
202 -gamma neutralization prevented Pneumocystis lung infection-induced BM depression in type I IFN recep
203 epresent a novel target for the treatment of lung infection/inflammation.
204             In summary, the impact of T2S on lung infection is a combination of at least three factor
205                                              Lung infection is caused by respiratory bacterial and fu
206 munity during early Streptococcus pneumoniae lung infection is well established, the contribution and
207              CF is characterized by repeated lung infections leading to respiratory failure.
208                    In Psuedomonas aeruginosa lung infections, lumican-deficient (Lum(-/-)) mice faile
209  of type I IFN signaling during Pneumocystis lung infection may result in deregulation of inflammasom
210                          During Pneumocystis lung infection, mice deficient in both lymphocytes and t
211 cpE mutant using two animal models; an acute lung infection model and a skin infection model.
212 gocytosis of gram-negative bacteria and in a lung infection model the Lum(-/-) mice showed poor survi
213                            Furthermore, this lung infection model with Y. pseudotuberculosis can be u
214                       In an Escherichia coli lung infection model, CD45E613R mice displayed a decreas
215 A. fumigatus in Olfm4-deficient mice using a lung infection model.
216 ainst both types of this organism in a mouse lung infection model.
217 ryngeal colonization and was attenuated in a lung infection model.
218  of phage therapy in an acute B. cenocepacia lung infection model.
219 d shows excellent activity in the TB aerosol lung infection model.
220 ility of the bacterium to cause disease in a lung infection model.
221  immunization reduced acute lung injury in a lung infection model.
222 -resistant Staphylococcus aureus in an acute lung infection model.
223 r in vivo efficacy than telithromycin in rat lung infection models against Streptococcus pneumoniae a
224 ompound demonstrated oral efficacy in rodent lung infection models that was comparable to marketed an
225 e also show that Ga is effective in 2 murine lung infection models.
226 nasal colonization and virulence in skin and lung infection models.
227  (CF) patients suffer from chronic bacterial lung infections, most notably by Pseudomonas aeruginosa,
228                          After M. pneumoniae lung infection, Muc18(-/-) mice exhibited lower levels o
229  to be operative in a Pseudomonas aeruginosa lung infection murine model, and was NE-dependent, becau
230                                       During lung infection, Mycobacterium tuberculosis resides in ma
231 intact type I IFN system during Pneumocystis lung infection not only causes BMF in lymphocyte-deficie
232                                              Lung infection occurred in 87% of patients, whereas live
233 he exopolysaccharide alginate during chronic lung infection of cystic fibrosis (CF) patients.
234 ytoid dendritic cells, and type I IFN during lung infection of mice.
235 uce surface bound capsule during early acute lung infection of mice.
236                     Moreover, treatment of a lung infection of P. aeruginosa results in a large reduc
237 f disease progression, BLI showed noticeable lung infection on day 2 after inoculation and significan
238 e patients (13%) had grade 3 infections (two lung infections, one upper respiratory tract infection,
239  7909) was found to protect BALB/c mice from lung infection or death after aerosol challenge with Bur
240  dead Klebsiella pneumoniae to induce either lung infection or lung inflammation.
241                                       During lung infection, our analysis indicated that 79 M. hyopne
242                         To form a chronic CF lung infection, P. aeruginosa must grow and proliferate
243 scessus has emerged as an important cause of lung infection, particularly in patients with bronchiect
244 s, and Cre-Lox virus marking showed nose and lung infections passing through LysM-positive (LysM(+))
245           In this study, we show that fungal lung infection promoted an increase in Th17 T cells that
246                    An in vivo mouse model of lung infection provided an almost complete protection ag
247 animals had irreversible atelectasis, higher lung infection rates (P<0.0001) and BAL neutrophil perce
248                    Seven of 10 patients with lung infection received amphotericin B (AMB) induction t
249 ation and CFTR loss of function in bacterial lung infections relevant to CF and to other chronic infl
250 lved in the immune response to P. aeruginosa lung infection remain incompletely defined.
251 by which aging impacts immunity to influenza lung infection remain unclear.
252 nd activation of pulmonary DC populations in lung infection remain widely elusive.
253 to nutrition, airway clearance, treatment of lung infection) remain today.
254                                              Lung infections represent a tremendous disease burden an
255 tion, after a high-dose inoculum, successful lung infection required rapid bacterial replication, wit
256   We conclude that clearance of cryptococcal lung infection requires the CCR2-mediated massive accumu
257 all molecules against neutrophil damage from lung infections such as Pseudomonas aeruginosa in cystic
258 dulatory role of B cells during Pneumocystis lung infection that complement the modulatory role of ty
259 te a key role for PAR-1 during S. pneumoniae lung infection that is mediated, at least in part, by in
260 re also believed to be more prone to serious lung infections that result in bronchitis and pneumonia.
261 ave proved beneficial against such bacterial lung infection, the design of several multivalent glycos
262  associated epidemiologically with increased lung infections, the identity of the lung cell types tar
263  myocardial infarction (three [1%] vs none), lung infection (three [1%] patients vs none), cardiac fa
264 stridium orbiscindens) promote resistance to lung infection through Nod2 and GM-CSF.
265                   In a murine model of early lung infection, trappin-2-treated PA01 was cleared more
266 ents, and included diarrhoea (two patients), lung infection (two patients), disease progression (two
267 ents), chest pain (four [15%] patients), and lung infections (two [7%]).
268                    We propose that during PC lung infection type-I IFNs induce SOCS1-associated regul
269 state and found that, following Pneumocystis lung infection, type I IFNs act not only in the lung to
270   Populations of P. aeruginosa in chronic CF lung infections typically exhibit high phenotypic divers
271                                     Isolated lung infection was present in 105 (69.1%) patients; 47 (
272         A small-animal model of Ad14-induced lung infection was used to test the translational releva
273 rculosis factors important for growth during lung infection, we developed an intranasal model of infe
274 rine model of opiate abuse and S. pneumoniae lung infection, we explored the influence of morphine tr
275 01-dependent gene expression during a murine lung infection, we used nanoString profiling of lung tis
276 tly regulated epithelial permeability during lung infections, we examined whether mast cells influenc
277  (Mtb) infection by curing them of a primary lung infection were compared with naive mice in terms of
278 fected mice allowed specific localization of lung infection when combined with PET.
279  cell surface during chronic cystic fibrosis lung infection, where it is associated with an increased
280  bone marrow (BM) failure after Pneumocystis lung infection, whereas lymphocyte-deficient mice with i
281 velop bone marrow failure after Pneumocystis lung infection, whereas lymphocyte-deficient, IFN alpha/
282  immune responses fail to adequately control lung infection, will be essential for the development of
283 , we have characterized the progression of a lung infection with an enteric Yersinia pathogen and sho
284 l fibrillation, grade 4 febrile neutropenia, lung infection with grade 4 absolute neutrophil count, c
285 bit extracellular residence in tissue, early lung infection with infectious spores reveals its unappr
286 n sensitization and challenge prior to acute lung infection with K. pneumoniae.
287 luding the loss of GPL, occur during chronic lung infection with M. abscessus.
288                                 In models of lung infection with Pseudomonas aeruginosa and Staphyloc
289                                      Chronic lung infection with Pseudomonas aeruginosa is a major co
290  chloride channel in inflammation induced by lung infection with Pseudomonas aeruginosa remains to be
291 neumonia using the mouse model of intranasal lung infection with S. aureus strain 8325-4 (hla(+) S. a
292 ndependent clearance mechanisms during early lung infection with S. pneumoniae.
293 eath of alveolar macrophages observed during lung infection with Streptococcus pneumoniae is thought
294  or contradict the hypothesis that postnatal lung infection with Ureaplasma parvum is causally relate
295 e used a murine model of S. pneumoniae early lung infection with wild-type, unencapsulated, and para-
296 ia pestis CO92, guinea pigs developed lethal lung infections with hemorrhagic necrosis, massive bacte
297                                              Lung infections with Mycobacterium abscessus, a species
298 de and is characterized by chronic bacterial lung infections with the opportunistic pathogen Pseudomo
299 re highly susceptible to fatal P. aeruginosa lung infection, with bacterial doses of <120 CFU being l
300  efficacy in a murine model of P. aeruginosa lung infection, with the concentration of pyocin S5 requ

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