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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
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
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
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
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
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
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
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
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
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
135 of cross-reactive T and B cell epitopes, one lung infection can modify immunity and pathology to the
137 ew respiratory viruses (e.g., SARS-CoV), and lung infections caused by antibiotic-resistant "ESKAPE p
140 low as 10 to 100 CFU/mouse produced a fatal lung infection, compared with 10(7) to >10(8) CFU for no
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
148 ce of PMNs, mice cannot resist P. aeruginosa lung infection from extremely small bacterial doses.
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
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
159 er the pathological response to pneumococcal lung infection in BALB/c mice with serotype 8 pneumonia
161 in mouse lungs, exemplified by more frequent lung infection in CF with TfpO-expressing P. aeruginosa
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
168 tunistic pathogen that establishes a chronic lung infection in individuals afflicted with cystic fibr
175 The agar bead model of chronic P. aeruginosa lung infection in sheep is a relevant platform to invest
177 g that the mice were capable of clearing the lung infection in the absence of a functional T3SS1.
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 (
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
187 n opportunistic pathogen that causes chronic lung infections in cystic fibrosis patients and is a maj
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
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
206 munity during early Streptococcus pneumoniae lung infection is well established, the contribution and
209 of type I IFN signaling during Pneumocystis lung infection may result in deregulation of inflammasom
212 gocytosis of gram-negative bacteria and in a lung infection model the Lum(-/-) mice showed poor survi
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
227 (CF) patients suffer from chronic bacterial lung infections, most notably by Pseudomonas aeruginosa,
229 to be operative in a Pseudomonas aeruginosa lung infection murine model, and was NE-dependent, becau
231 intact type I IFN system during Pneumocystis lung infection not only causes BMF in lymphocyte-deficie
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
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(+))
247 animals had irreversible atelectasis, higher lung infection rates (P<0.0001) and BAL neutrophil perce
249 ation and CFTR loss of function in bacterial lung infections relevant to CF and to other chronic infl
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
266 ents, and included diarrhoea (two patients), lung infection (two patients), disease progression (two
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
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
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
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
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
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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