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1 neumoniae to induce either lung infection or lung inflammation.
2 d with IRF4 and NFAT1 expression in allergic lung inflammation.
3 luding increased mortality, weight loss, and lung inflammation.
4 ection, but they also contribute to allergic lung inflammation.
5 ultiple adverse clinical sequelae, including lung inflammation.
6 lonella, bacteria previously associated with lung inflammation.
7 aB inhibitor) markedly mitigated mouse acute lung inflammation.
8 only attenuated RV-induced CXCL-10, but also lung inflammation.
9 are resistant to the development of allergic lung inflammation.
10 - and Alternaria-induced ILC2 activation and lung inflammation.
11 h HMPV displayed less airway dysfunction and lung inflammation.
12 mproved histologic lung injury, and dampened lung inflammation.
13 nto nascent alveoli at sites of interstitial lung inflammation.
14 role for autophagy as negative regulator of lung inflammation.
15 nous pathways that help to control excessive lung inflammation.
16 tion between platelets and AECs during acute lung inflammation.
17 irrespective of aggregation during skin and lung inflammation.
18 d interaction in human ILC2s reduced AHR and lung inflammation.
19 oimmunity in systemic lupus erythematosus or lung inflammation.
20 denosine aggravated ragweed-induced allergic lung inflammation.
21 mast cell accumulation in models of allergic lung inflammation.
22 ms also operated during HDM-induced allergic lung inflammation.
23 own Norway rat acute OVA model of Th2-driven lung inflammation.
24 al pathology and IL-9 production in allergic lung inflammation.
25 blood and pleural fluid of a mouse model of lung inflammation.
26 /beta-catenin signaling in AECs during acute lung inflammation.
27 duced lung injury and HDM-triggered allergic lung inflammation.
28 erminants of susceptibility to ozone-induced lung inflammation.
29 ase-1 activity was associated with increased lung inflammation.
30 ls may lead to new insights into controlling lung inflammation.
31 okine secretion in myeloid leukocytes during lung inflammation.
32 il interactions that regulates the extent of lung inflammation.
33 iming, could accelerate resolution of severe lung inflammation.
34 r infiltration in a murine model of allergic lung inflammation.
35 ine, a signaling molecule known to attenuate lung inflammation.
36 a key suppressor of neutrophil migration and lung inflammation.
37 monocytes promote, early events in allergic lung inflammation.
38 in regulating neutrophil recruitment during lung inflammation.
39 tin-2, respectively, to promote TH2-mediated lung inflammation.
40 requirement for ILC2s in inducing TH2-driven lung inflammation.
41 burst of promyelocytes and in vivo to image lung inflammation.
42 transfusion and HMGB1 release on LPS-induced lung inflammation.
43 pressive signals to reduce endotoxin-induced lung inflammation.
44 scular injury and plays an important role in lung inflammation.
45 novel target for therapies aimed at reducing lung inflammation.
46 ed and was associated with an attenuation of lung inflammation.
47 ed attenuation of Th2 cytokines and allergic lung inflammation.
48 athogenesis and therapy of fungus-associated lung inflammation.
49 Nippostrongylus brasiliensis or induction of lung inflammation.
50 gregation, stronger and prolonged anemia and lung inflammation.
51 ILC2 development and restores IL-33-mediated lung inflammation.
52 no signs of hemorrhage in models of skin or lung inflammation.
53 the effects of IL-33 on ILC2 activation and lung inflammation.
54 C2-mediated airway hyperreactivity (AHR) and lung inflammation.
55 mately 92 cluster in ILC2s displayed reduced lung inflammation.
56 e recruitment and ultimately contributing to lung inflammation.
57 act (HDE), to test their role in maintaining lung inflammation.
58 es isolated from aged blood into mice caused lung inflammation.
59 ultiple adverse clinical sequelae, including lung inflammation.
60 rentiating K. pneumoniae lung infection from lung inflammation.
61 les were unaffected by the presence of acute lung inflammation.
62 el in mice, and blocked papain-induced acute lung inflammation.
63 this can lead to susceptibility to asthmatic lung inflammation.
64 crease in metabolic activity associated with lung inflammation.
65 t and activation of specific immune cells in lung inflammation.
66 nd IL-1RI upregulation on the development of lung inflammation.
67 rden and histopathologic evidence of chronic lung inflammation.
68 ncy attenuates atherosclerosis but not acute lung inflammation.
69 -/-) mice, including increased mortality and lung inflammation.
70 es isolated from aged blood into mice caused lung inflammation.
71 urther showed that AM pyroptosis exaggerates lung inflammation.
72 PEG-PTX conjugates induced lung inflammation.
73 ring influenza infection to limit widespread lung inflammation.
74 e end of the imaging period was unaltered by lung inflammation.
75 ammations, and (c) bearing ovalbumin-induced lung inflammations.
77 in both a house dust mouse model of allergic lung inflammation (40 mg/kg qd) as well as a guinea pig
78 sculin significantly suppressed neutrophilic lung inflammation, a hallmark of acute lung injury (ALI)
79 mpaired chloride permeability and persistent lung inflammation, a multidrug approach is required for
83 n the nanomaterial HIC index value and acute lung inflammation after pulmonary administration to mice
88 ome activation may also be involved in acute lung inflammation after viral infection and during progr
90 infection, ovalbumin (OVA)-induced allergic lung inflammation (ALI) was induced in mice followed by
91 olog) in lung epithelial cells and lungs and lung inflammation, all of which were reduced by Compound
92 Influenza induced persistent parenchymal lung inflammation, alveolar epithelial metaplasia, and e
93 to ozone, a source of oxidative stress, had lung inflammation and AHR associated with mitochondrial
94 and sufficient for B. cenocepacia-triggered lung inflammation and also protects mice from lethal B.
96 f the RAGE ligand, and the impact of RAGE on lung inflammation and antimicrobial resistance in fungal
98 une mechanisms have evolved that can lead to lung inflammation and asthma, which is the focus of this
99 oxP/loxP) SPC Cre(+) mice confirmed elevated lung inflammation and attenuated alveolar fluid clearanc
101 gnaling via this receptor results in reduced lung inflammation and cellular recruitment as well as re
102 activates the NLRP3 inflammasome and induces lung inflammation and cellular recruitment that is NLRP3
103 posed to cigarette smoke developed increased lung inflammation and compromised adaptive immunity rela
104 ulated ILC2s and Th2 cells, causing allergic lung inflammation and elevated immunoglobulin E titers.
105 Cre Pparg(flox/flox) mice led to spontaneous lung inflammation and emphysema that resembled the pheno
106 ction faster than controls and had decreased lung inflammation and endoplasmic reticulum stress.
107 s in BeO-exposed HLA-DP2 Tg mice exacerbated lung inflammation and enhanced granuloma formation.
108 te respiratory distress syndrome by reducing lung inflammation and enhancing alveolar fluid clearance
111 ts that mesenchymal stem cells may attenuate lung inflammation and fibrosis in acute lung injury.
112 ntrol of the CD2 promoter/enhancer augmented lung inflammation and IgE levels in the setting of exper
114 n IP(-/-) mice restored both the HDM-induced lung inflammation and ILC2 numbers, whereas transfer of
115 in human and murine CF, the impact of IDO on lung inflammation and immunity in murine CF, and the pot
116 Despite the different accumulation, the lung inflammation and inflammatory T cell responses were
118 f NADPH oxidase and Nrf2 in modulating acute lung inflammation and injury in clinically relevant mode
119 Mechanical ventilation caused significant lung inflammation and injury that was prevented in the p
120 sgene overexpression reduced E. coli-induced lung inflammation and injury, decreased nuclear factor-k
121 s of CALCA, procalcitonin, and NPCT; reduced lung inflammation and injury, neutrophil infiltration, a
122 Chronic asthma is associated with persistent lung inflammation and long-term remodelling of the airwa
125 icient mice developed exuberant neutrophilic lung inflammation and proinflammatory cytokine responses
128 Bronchiectasis is a disorder of persistent lung inflammation and recurrent infection, defined by a
129 ciated with higher viral loads and increased lung inflammation and reduced influenza A virus-specific
130 ghly compacted DNA nanoparticles may prevent lung inflammation and remodeling in a mouse model of all
133 ct of immunological priming on resolution of lung inflammation and significantly reduced alveolar mac
134 laying a role in dampening LPS-induced acute lung inflammation and suggest that C1P could be a valuab
135 PPP1R11 in mouse lungs significantly affects lung inflammation and the clearance of Staphylococcus au
136 e sought to address the role of autophagy in lung inflammation and the pathogenesis of corticosteroid
137 igen-specific Th17 responses during allergic lung inflammation and the size of Foxp3(+) regulatory T
138 so infected with rhinovirus 1B to exacerbate lung inflammation and therapeutically administered salme
139 ght control the extent of IFN-gamma-mediated lung inflammation and therefore play a tissue-restricted
140 ognized role for MMP-28 in promoting chronic lung inflammation and tissue remodeling induced by cigar
141 was to assess the variation in AgNP-induced lung inflammation and toxicity across multiple inbred mo
142 rodent studies indicate that AgNPs can cause lung inflammation and toxicity in a strain- and particle
143 d infiltration of neutrophils during sterile lung inflammation and were less sensitive to bacterial s
144 ne innate immune cellular and cytokine-based lung inflammation and were resistant to lethal influenza
145 neutrophil accumulation in a model of acute lung inflammation and, at 0.001 mg/kg, alleviates pulmon
146 rosis patients because it causes accelerated lung inflammation and, in some cases, a lethal necrotizi
149 system by beta2AR signaling with metabolism, lung inflammation, and an enhanced susceptibility to thr
151 induced airway hyperresponsiveness (AHR) and lung inflammation, and bleomycin-induced lung fibrosis;
152 ls decreased goblet cell metaplasia, reduced lung inflammation, and decreased airway resistance in re
153 ft from Th1 to Th2 cytokine bias, pronounced lung inflammation, and defective classical macrophage ac
154 and emerging PET techniques for quantifying lung inflammation, and discuss potential clinical applic
156 th increased airway and tissue eosinophilia, lung inflammation, and IL-4, IL-5, IL-13, and IgE produc
157 T mice, sensitized PHIL mice maintained AHR, lung inflammation, and increased levels of IL-4, IL-5, a
159 mediating airway hyperresponsiveness (AHR), lung inflammation, and mucus metaplasia in a dual Th2/Th
163 (COPD), some reports have suggested enhanced lung inflammation as a factor in ZZ-AT homozygotes.
164 duction also decreased viral replication and lung inflammation, as evidenced by a reduced neutrophil
165 mice exhibited exacerbated protease-induced lung inflammation associated with reduced numbers of reg
166 reus pneumonia is characterized by extensive lung inflammation associated with severe morbidity and m
167 d pulmonary pathology in a model of allergic lung inflammation but also reduced ability to combat inf
168 not essential for the development of AHR and lung inflammation but contributed to the resolution of A
170 lating basal airway function and LPS-induced lung inflammation, but does not play a role in bleomycin
171 virus, a mouse pathogen that causes chronic lung inflammation, but its role in the development of po
172 type 2 T helper cell-mediated (Th2-mediated) lung inflammation, but the molecular mechanisms by which
173 ne response and serve to prevent exacerbated lung inflammation by promoting the rapid control of resp
174 MDA5 modulates the development of chronic lung inflammation by regulating the early inflammatory r
175 of mouse ILC-intrinsic Arg1 abrogated type 2 lung inflammation by restraining ILC2 proliferation and
178 and LTalphabeta contribute to development of lung inflammation characteristic of asthma and idiopathi
179 inhalation of SplD without adjuvant induced lung inflammation characterized by TH2 cytokines and eos
180 ge to subtilisin induces prototypic allergic lung inflammation, characterized by airway eosinophilia,
182 hese mice presented with spontaneous sterile lung inflammation, characterized by marked recruitment o
184 rticles carrying thymulin plasmids prevented lung inflammation, collagen deposition and smooth muscle
186 thetic CpG-oligonucleotides elicited minimal lung inflammation compared with low-dose LPS but nonethe
188 ental allergens and less severe IL-33-driven lung inflammation, correlating with an impaired expansio
189 ycolate-induced peritonitis, and LPS-induced lung inflammation, CSF-1 neutralization lowered inflamma
190 ) on CD4 T cells is required for OVA-induced lung inflammation, DCs have also been shown to be target
191 ocomotor activity in parallel with increased lung inflammation, disrupted rhythms of pulmonary functi
192 th Haemophilus influenzae resulted in lethal lung inflammation due to massive production of proinflam
193 respiration, and concomitant attenuation of lung inflammation during ALI were specific for alveolar-
194 A5-deficient mice led to an enhanced chronic lung inflammation, epithelial cell hyperplasia, airway h
195 and that mice and humans with NEC-associated lung inflammation express higher levels of pulmonary TLR
196 entity, characterized by noninfectious acute lung inflammation following allogeneic stem cell transpl
198 ited exacerbation of cardiac dysfunction and lung inflammation, greater increases in levels of plasma
199 MCP-6(-/-)/H-2bc mice had strikingly reduced lung inflammation, IgE responses, and Th2 cell responses
201 ET) radiotracer for noninvasive detection of lung inflammation in a mouse model of lung injury and in
203 have emerged as major mediators of allergic lung inflammation in animal models as well as humans.
204 ndritic cells (DC) are critical mediators of lung inflammation in asthma, but the characteristics of
206 Intranasal bleomycin challenge exacerbated lung inflammation in autophagy-deficient mice and produc
207 auma and atelectrauma on the distribution of lung inflammation in experimental acute respiratory dist
208 that chemical epigenetic modifiers can limit lung inflammation in experimental ALI models, studies to
210 can be used to image iNOS activity in acute lung inflammation in humans and may be a useful PET trac
212 B cells, dramatically ameliorates kidney and lung inflammation in lupus-prone MRL.Fas(lpr) mice.
213 nted the exaggerated airway eosinophilia and lung inflammation in mice given HDM-pulsed Map3k8(-/-) D
214 PLA2 isoform cPLA2alpha dramatically reduced lung inflammation in mice upon high-dose pulmonary chall
218 ision-cut lung slice (PCLS) contraction, and lung inflammation in naive and Aspergillus fumigatus-cha
219 ver, FPS-ZM1 treatment significantly reduced lung inflammation in Nrf2(+/+) , but not in Nrf2(-/-) mi
220 S-1 showed lower IL-33 levels and attenuated lung inflammation in response to repetitive Alternaria i
225 ed the severity of OVA/alum-induced allergic lung inflammation in WT BALB/c mice to mice that lack ex
226 y properties in a model of DEP-induced acute lung inflammation, in contrast to anti-inflammatory effe
227 unable to induce the development of allergic lung inflammation, including recruitment of CD4(+) T cel
228 roduction of IL-10 and enhance resolution of lung inflammation induced by a lethal dose of LPS or by
233 y is characterized by rapid alveolar injury, lung inflammation, induced cytokine production, neutroph
234 mmation, p52 overexpression caused increased lung inflammation, injury, and mortality following intra
235 me arginase-1 (Arg1) during acute or chronic lung inflammation is a conserved trait of mouse and huma
239 onsequence house dust mite- and IL-33-driven lung inflammation, late phase cutaneous anaphylaxis, and
242 rophils recovered from skin, peritoneal, and lung inflammation lesions but not on those in bone marro
243 macrophages are the key cells that initiate lung inflammation, less is known about lung macrophage p
244 anscript activity was highly correlated with lung inflammation (lung [(18)F]fluorodeoxyglucose [FDG]
245 d to image cellular metabolism, which during lung inflammation mainly reflects neutrophil activity, a
247 nflammatory agent in the carrageenan-induced lung inflammation model, suggesting that this compound m
250 -phosphorylated in vivo in acute and chronic lung inflammation models and this response is required t
251 3 have exaggerated neutrophilic/eosinophilic lung inflammation, mucus production, and airway hyperres
253 Disease severity was assessed by measuring lung inflammation, pathology, cytokine responses, and se
254 ammatory biomarkers to delineate the type of lung inflammation present in asthmatic subjects is incre
255 investigated the effects of human MSC MVs on lung inflammation, protein permeability, bacterial clear
256 review the clinical techniques used to image lung inflammation, provide an overview of clinical and e
259 tion of this normal homeostatic dampening of lung inflammation results in increased resistance to inf
260 ietic deletion of Ship1 leads to spontaneous lung inflammation, selective deletion of Ship1 in T cell
261 deregulation of host erythropoiesis, and the lung inflammation signature was linked to increased neut
263 nd augmented the histopathologic evidence of lung inflammation, suggesting a suppressive role for rAM
264 targets Tregs and ILC2s to restrain allergic lung inflammation, suggesting MaR1 as the basis for a ne
265 ith asthma, and in animal models of allergic lung inflammation suggests that platelets may also contr
266 istress syndrome, volutrauma promoted higher lung inflammation than atelectrauma at comparable low ti
267 ovel mouse model of spontaneous IL-17-driven lung inflammation that exhibits many similarities to ast
268 didate susceptibility genes for AgNP-induced lung inflammation that warrant additional exploration in
269 dontis and Altenaria alternata induced acute lung inflammation, that inflammation of the pleural cavi
270 staining exhibited goblet cell hyperplasia, lung inflammation, thickening of smooth muscle layer on
271 atopoietic AR expression limits IL-33-driven lung inflammation through a cell-intrinsic inhibition of
272 rgens and parasites, initiates innate type 2 lung inflammation through incompletely defined pathways.
273 RBC transfusion enhances susceptibility to lung inflammation through release of HMGB1 and induces n
274 C transfusion sensitized mice to LPS-induced lung inflammation through release of the danger signal H
276 progression of allergen-induced eosinophilic lung inflammation to corticosteroid-refractory neutrophi
278 to develop an experimental model of allergic lung inflammation to subtilisin and to determine the imm
279 hese results suggested that the reduction in lung inflammation together with a more robust antiviral
281 ulted in increased morbidity and exacerbated lung inflammation upon subsequent infection with influen
282 inflammatory responses in poly(I:C)-induced lung inflammation using a tamoxifen-inducible versican-d
283 hese issues in the context of acute allergic lung inflammation using house dust mite and OVA murine m
284 was to assess the location and magnitude of lung inflammation using PET imaging of [(18)F]fluoro-2-d
286 ions after 4 weeks of high-fat diet, whereas lung inflammation was assessed after inhalation of lipop
291 om acid sphingomyelinase-deficient mice, and lung inflammation was studied in mice receiving transfus
292 om acid sphingomyelinase-deficient mice, and lung inflammation was studied in mice receiving transfus
294 n of inflammatory cells into the airway, and lung inflammation were enhanced in AT2CC(-/-) mice relat
296 ell trafficking in animal models of allergic lung inflammation, which are known to be platelet depend
297 PP2A activity in AAD and rhinovirus-induced lung inflammation, which might potentially account for s
299 bone marrow-derived dendritic cells augments lung inflammation with increased IL-17A levels in the lu
300 Zc3h12a(-/-) mice have spontaneous severe lung inflammation, with an increase in mainly IL-5- and
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