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1 CNS disease were 563.9 (vs 149.3 in isolated lung infection).
2 id 4 (TRPV4), alters the in vivo response to lung infection.
3 disease using a murine model of cryptococcal lung infection.
4 requency of hospitalization due to bacterial lung infection.
5 ng were increased in this model of bacterial lung infection.
6 educe oropharyngeal colonization and prevent lung infection.
7 uginosa virulence in a murine model of acute lung infection.
8 li growth, adhesion to epithelial cells, and lung infection.
9 lic IL-1beta production in response to viral lung infection.
10 ltatfpO mutant was found to be attenuated in lung infection.
11 le protecting against active influenza virus lung infection.
12 cally contribute to immunity to Pneumocystis lung infection.
13 dvantage to Histoplasma yeasts during murine lung infection.
14 and that this is key in the establishment of lung infection.
15 against early clearance in a mouse model of lung infection.
16 cal for defense against C. psittaci in mouse lung infection.
17 ecular mechanisms of the recovery after MRSA lung infection.
18 virulence of Streptococcus pneumoniae during lung infection.
19 ice demonstrated susceptibility to P. murina lung infection.
20 uate P. aeruginosa in a rat model of chronic lung infection.
21 te late events during the recovery from MRSA lung infection.
22 ion profiling between days 1 and 3 post MRSA lung infection.
23 aeruginosa pathogenicity in a mouse model of lung infection.
24 ential role in the innate immune response to lung infection.
25 developed a murine model of S. mucilaginosus lung infection.
26 on the early innate immune responses to MRSA lung infection.
27 mmation in septicemia following pneumococcal lung infection.
28 B-resistant mice highly susceptible to acute lung infection.
29 pathway and protect mice against pseudomonal lung infection.
30 ations in the BM in response to Pneumocystis lung infection.
31 reased in vivo during Pseudomonas aeruginosa lung infection.
32 an increased propensity to later nosocomial lung infection.
33 ors after systemic responses to Pneumocystis lung infection.
34 s susceptibility to Streptococcus pneumoniae lung infection.
35 sm for host defense against pathogens during lung infection.
36 mice and corresponded with reduction of the lung infection.
37 es a siderophore (legiobactin) that promotes lung infection.
38 ed with bacterial growth arrest during mouse lung infection.
39 he context of a chronic cystic fibrosis (CF) lung infection.
40 . tuberculosis in the chronic stage of mouse lung infection.
41 in enhanced protection against P. aeruginosa lung infection.
42 sed to exert important effects in preventing lung infection.
43 taT lymphocytes in response to S. pneumoniae lung infection.
44 to mediate innate immunity to P. aeruginosa lung infection.
45 atory deficit and death, despite progressive lung infection.
46 ve bacteria, both in vitro and after in vivo lung infection.
47 orse pro-inflammatory responses in bacterial lung infection.
48 s not activated during Staphylococcus aureus lung infection.
49 tm1(-/-) mice were more susceptible to viral lung infection.
50 s, and had a history of chronic P aeruginosa lung infection.
51 e MyD88 response in facilitating the primary lung infection.
52 inued, only two subsequently showed signs of lung infection.
53 robial and steroid therapies and the risk of lung infection.
54 ticles for application to an animal model of lung infection.
55 ow distinct evolutionary trajectories during lung infection.
56 on against subsequent active influenza virus lung infection.
57 ed that the prrF locus is required for acute lung infection.
58 its are accompanied by spontaneous bacterial lung infection.
59 nhanced bacterial clearance during sublethal lung infection.
60 e to decreased bacterial burden during acute lung infection.
61 k of bacteremia and meningitis without prior lung infection.
62 reened the mutants in a rat model of chronic lung infection.
63 ung DC and Mvarphi in mice with cryptococcal lung infection.
64 a significant fraction of hospital-acquired lung infections.
65 HIV-negative patients with persistent fungal lung infections.
66 facilitate airway colonization in nosocomial lung infections.
67 of IL-10 blockade in the treatment of fungal lung infections.
68 aving females at greater risk of contracting lung infections.
69 es 1, 5, and 14 in were implicated in 90% of lung infections.
70 originating in the oral microbiome can cause lung infections.
71 was important for Burkholderia mallei mouse lung infections.
72 h and bacteremia infections and pneumococcal lung infections.
73 and transplant outcome and aid in assessing lung infections.
74 ns associated with wound and cystic fibrosis lung infections.
75 ucial in nosocomial pneumonia and in chronic lung infections.
76 oxygen-dependent regulation as paramount in lung infections.
77 nse to antimicrobial treatment of chronic CF lung infections.
78 eased incidence of infections, in particular lung infections.
79 prevalent and chronic Pseudomonas aeruginosa lung infections.
80 ctorial protective immunity to P. aeruginosa lung infections.
81 e function and are especially susceptible to lung infections.
82 ndition that predisposes patients to chronic lung infections.
83 lagella expression was observed during acute lung infections.
84 acterized by chronic airway inflammation and lung infections.
85 isrupts resolution pathways during bacterial lung infections.
86 opathology but also contributes to recurrent lung infections.
87 ripts are stable in chronic CF P. aeruginosa lung infections.
88 ents developed proven or probable IA (5 with lung infection, 1 with mediastinitis, and 1 with lung in
90 ciated infections, including cystic fibrosis lung infection(4), as well as medical device infection a
92 RT-PCR) tests indicated early and persistent lung infection and delayed occurrence of brain infection
93 in C3a receptor (C3aR) in Chlamydia psittaci lung infection and elucidated C3a-dependent adaptive imm
94 defenses in vitro, CatB was dispensable for lung infection and extrapulmonary dissemination in vivo.
95 an established murine model of cryptococcal lung infection and flow cytometric analysis to identify
96 1 signaling promotes persistent cryptococcal lung infection and identifies this pathway as a potentia
97 In cystic fibrosis (CF) patients, chronic lung infection and inflammation due to Pseudomonas aerug
99 preclinical murine model of cystic fibrosis lung infection and inflammation to investigate the role
101 A) of mice i) ensures complete recovery from lung infection and near absolute clearance of bacteria w
102 to trebananib, paclitaxel, and carboplatin (lung infection and neutropenic colitis); two were consid
103 was also effective in protecting against the lung infection and severe lung pathology associated with
104 nsparent juvenile zebrafish to model mucosal lung infection and show that C. albicans and P. aerugino
105 Il22ra2 inhibits IL-22 during S. pneumoniae lung infection and that Il22ra2 deficiency favors downre
107 anges in neutrophil elastase activity during lung infection and to assess the efficacy of a protease
108 e multi-organ disease, the chronic bacterial lung infections and associated inflammation are the prim
109 Bacterial pathogens are a leading cause of lung infections and contribute to acute exacerbations in
110 use disorders are associated with increased lung infections and exacerbations of chronic lung diseas
111 Patients with hypercapnia often develop lung infections and have an increased risk of death foll
112 e of the multiple roles of TLRs in bacterial lung infections and highlights the mechanisms used by pa
115 Cu]DOTA-JF5 distinguished IPA from bacterial lung infections and, in contrast to [(18)F]FDG-PET, disc
116 stent Pseudomonas aeruginosa (P. aeruginosa) lung infection, and presence of meconium ileus (MI), has
117 vels are dynamically varied during bacterial lung infection, and the fluctuation is critical in deter
118 s tropism to cell types that are relevant to lung infection, and therefore may be significant determi
119 s, grade 4 myelodysplastic syndrome, grade 3 lung infection, and two episodes of grade 3 bacteraemia)
120 are more susceptible than wild-type mice to lung infections, and bacterial killing is enhanced in tr
121 dvanced disease frequently develop bacterial lung infections, and hypercapnia is a risk factor for mo
122 th bronchiectasis and Pseudomonas aeruginosa lung infection, antibody can protect the bacterium from
127 ed the diagnostic potential of L-ficolin for lung infection (area under the curve, 0.842; P < .0001).
128 he GI manifestations of CF have left chronic lung infections as the primary cause of morbidity and mo
129 -resistant organisms associated with chronic lung infections as well as with cystic fibrosis patients
130 or that can eradicate chronic P. aeruginosa lung infections associated with cystic fibrosis (CF) wil
132 be for noninvasive detection of A. fumigatus lung infection based on antibody-guided positron emissio
133 ACE2 is not only a consequence of bacterial lung infection but also a critical component of host def
134 ently and repeatedly arise during chronic CF lung infection, but the evolutionary forces governing th
136 ia and reperfusion, as well as in a model of lung infection by Klebsiella pneumoniae Transferring ser
137 sRNAs, but not PrrH, are required for acute lung infection by P. aeruginosa Moreover, we show that t
138 oprotein inhibited inflammation during acute lung infection by Pseudomonas aeruginosa, we asked wheth
140 cant defects in the early innate response to lung infection by the major human pathogen Klebsiella pn
142 ew respiratory viruses (e.g., SARS-CoV), and lung infections caused by antibiotic-resistant "ESKAPE p
145 low as 10 to 100 CFU/mouse produced a fatal lung infection, compared with 10(7) to >10(8) CFU for no
147 n an acute model of Streptococcus pneumoniae lung infection, deficiency in matrix metalloproteinase (
148 y ACE2 restitution in the model of bacterial lung infection delays the recovery process from neutroph
149 improve or worsen the outcome of subsequent lung infections, depending on the immunological history
150 increased mortality following P. aeruginosa lung infection despite enhanced neutrophil recruitment a
151 ce of PMNs, mice cannot resist P. aeruginosa lung infection from extremely small bacterial doses.
153 he mechanisms of protective immunity against lung infection has been largely derived from murine mode
154 stem (T2SS) of Pseudomonas aeruginosa during lung infection has been uncertain despite decades of res
156 The rising incidence of antibiotic-resistant lung infections has instigated a much-needed search for
158 s COPD and asthma, and that of opportunistic lung infections have become more common among this popul
159 ic obstructive pulmonary disease (COPD), and lung infections have critical consequences on mortality
163 in mouse lungs, exemplified by more frequent lung infection in CF with TfpO-expressing P. aeruginosa
166 phenotypes may have particular relevance to lung infection in cystic fibrosis patients since the alt
167 Serious adverse events included grade 3 lung infection in five (14%) of 37 patients in the phase
171 tunistic pathogen that establishes a chronic lung infection in individuals afflicted with cystic fibr
172 train was markedly defective in establishing lung infection in mice, with no detectable lung patholog
179 The agar bead model of chronic P. aeruginosa lung infection in sheep is a relevant platform to invest
180 g that the mice were capable of clearing the lung infection in the absence of a functional T3SS1.
182 ased susceptibility to Aspergillus fumigatus lung infection in the presence of lower interleukin 23 (
184 infection.Respiratory syncytial virus causes lung infections in children, immunocompromised adults, a
189 urkholderia cenocepacia causes opportunistic lung infections in immunocompromised individuals, partic
190 group of closely related bacteria that cause lung infections in immunocompromised patients as well as
191 istic pathogen often associated with chronic lung infections in individuals with the genetic disease
193 Low NF-kappaB activators cause more severe lung infections in mice, and they drive macrophages towa
194 deria cepacia complex (BCC) can cause severe lung infections in patients with cystic fibrosis (CF) or
196 hat Pseudomonas aeruginosa bacteria, causing lung infections in patients with cystic fibrosis, lose c
198 n opportunistic pathogen that causes chronic lung infections in the airways of cystic fibrosis (CF) p
199 re reported in the HF-HD group, including 14 lung infections in the HCO-HD group and three lung infec
201 cile in vitro organoid model of human distal lung infections, including COVID-19-associated pneumonia
202 perate phages active in cystic fibrosis (CF) lung infections, including the transposable phage, 4, wh
203 -gamma neutralization prevented Pneumocystis lung infection-induced BM depression in type I IFN recep
206 diated immune responses and protects against lung infection, inflammation, and pathology but does not
210 munity during early Streptococcus pneumoniae lung infection is well established, the contribution and
213 Their function influences the outcome of lung infections, lung cancer, and chronic inflammatory d
214 of type I IFN signaling during Pneumocystis lung infection may result in deregulation of inflammasom
217 gocytosis of gram-negative bacteria and in a lung infection model the Lum(-/-) mice showed poor survi
229 ompound demonstrated oral efficacy in rodent lung infection models that was comparable to marketed an
232 (CF) patients suffer from chronic bacterial lung infections, most notably by Pseudomonas aeruginosa,
234 to be operative in a Pseudomonas aeruginosa lung infection murine model, and was NE-dependent, becau
235 pneumonitis (n=1 [2%]), headache (n=1 [2%]), lung infection (n=1 [2%]), skin infection (n=1 [2%]), pl
236 intact type I IFN system during Pneumocystis lung infection not only causes BMF in lymphocyte-deficie
240 f disease progression, BLI showed noticeable lung infection on day 2 after inoculation and significan
241 e patients (13%) had grade 3 infections (two lung infections, one upper respiratory tract infection,
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(+))
249 animals had irreversible atelectasis, higher lung infection rates (P<0.0001) and BAL neutrophil perce
251 ation and CFTR loss of function in bacterial lung infections relevant to CF and to other chronic infl
256 tion, after a high-dose inoculum, successful lung infection required rapid bacterial replication, wit
257 We conclude that clearance of cryptococcal lung infection requires the CCR2-mediated massive accumu
258 osis bronchiectasis and chronic P aeruginosa lung infection requiring antibiotic therapy in the prece
259 all molecules against neutrophil damage from lung infections such as Pseudomonas aeruginosa in cystic
260 dulatory role of B cells during Pneumocystis lung infection that complement the modulatory role of ty
261 te a key role for PAR-1 during S. pneumoniae lung infection that is mediated, at least in part, by in
262 re also believed to be more prone to serious lung infections that result in bronchitis and pneumonia.
263 ave proved beneficial against such bacterial lung infection, the design of several multivalent glycos
264 associated epidemiologically with increased lung infections, the identity of the lung cell types tar
265 myocardial infarction (three [1%] vs none), lung infection (three [1%] patients vs none), cardiac fa
269 ents, and included diarrhoea (two patients), lung infection (two patients), disease progression (two
272 state and found that, following Pneumocystis lung infection, type I IFNs act not only in the lung to
273 Populations of P. aeruginosa in chronic CF lung infections typically exhibit high phenotypic divers
276 ting from hematogenous spread from a primary lung infection, was more common than pulmonary disease a
277 rine model of opiate abuse and S. pneumoniae lung infection, we explored the influence of morphine tr
278 01-dependent gene expression during a murine lung infection, we used nanoString profiling of lung tis
279 tly regulated epithelial permeability during lung infections, we examined whether mast cells influenc
281 bone marrow (BM) failure after Pneumocystis lung infection, whereas lymphocyte-deficient mice with i
282 velop bone marrow failure after Pneumocystis lung infection, whereas lymphocyte-deficient, IFN alpha/
283 immune responses fail to adequately control lung infection, will be essential for the development of
284 rapulmonary instillation of corisin or after lung infection with corisin-harboring S. nepalensis comp
285 l fibrillation, grade 4 febrile neutropenia, lung infection with grade 4 absolute neutrophil count, c
286 bit extracellular residence in tissue, early lung infection with infectious spores reveals its unappr
290 tic activity was used for treatment of acute lung infection with Pseudomonas aeruginosa in a mouse mo
292 nts with non-cystic fibrosis bronchiectasis, lung infection with Pseudomonas aeruginosa is associated
294 eath of alveolar macrophages observed during lung infection with Streptococcus pneumoniae is thought
295 or contradict the hypothesis that postnatal lung infection with Ureaplasma parvum is causally relate
296 e used a murine model of S. pneumoniae early lung infection with wild-type, unencapsulated, and para-
297 ia pestis CO92, guinea pigs developed lethal lung infections with hemorrhagic necrosis, massive bacte
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