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1                                              BALF exosomes from asthmatics might contribute to subcli
2                                              BALF from an IPF patient contained ADP-ribosyl-HNP-ornit
3                                              BALF levels of IL-6 declined similarly during the study
4                                              BALF levels of total protein, neutrophils, and leukotrie
5                                              BALF was also collected and tested from negative control
6                                              BALF was assessed for pepsin, bile salts, interleukin-8
7                                              BALF was collected from ALI/ARDS patients within 48 hrs
8                                              BALF was collected from three groups of patients: BOS (n
9                                              BALF was tested for chitinase activity and YKL-40 (an en
10                                              BALFs were standardized in protein concentration.
11  in BALF (p = 0.016) and plasma (p < 0.001); BALF levels of epithelial neutrophil-activating protein-
12 pients without such deficiency (171 of 2,137 BALF; 8%).
13              Pepsin was detected in 11 of 15 BALF samples signifying aspiration (median: 18 ng/mL; ra
14 ptomatic HCMV disease, proposing that CCL-18 BALF levels could serve as a marker.
15                          Furthermore, CCL-18 BALF levels were significantly higher in 8 LTRs who addi
16  a significant increase of CCL-18 and CCL-20 BALF levels (P < 0.001, Wilcoxon signed-rank test) and a
17               For comparison, we included 34 BALF specimens (2 for each CARV case) that were negative
18  was inhibited > or = 47% by BALF or SP-A-/- BALF (at 290 or 580 microg of protein/ml, P < 0.05 to 0.
19                                   If SP-A-/- BALF was mixed in equal amounts with SP-D-/- BALF, TNF-a
20 ized, there was little effect on the AHR and BALF cellular differential.
21 o AHR, and a selective decrease in blood and BALF eosinophils, lung Il13 levels, collagen, and smooth
22 vage fluid (BALF) lactate dehydrogenase, and BALF neutrophils.
23      We report increased MIF in the lung and BALF of sensitized wild-type mice.
24 al colony counts, BALF total cell number and BALF protein concentration significantly decreased at da
25 n St3gal3 mutants, whereas peribronchial and BALF eosinophil numbers were greater in the mutants, wit
26  CS-exposed mice showed increased plasma and BALF glycerolipids and glycerophospholipids.
27 uced IL-6 and TNF-alpha levels in plasma and BALF.
28 i-DQ mAb significantly reduced pulmonary and BALF eosinophilia in cockroach allergen-sensitized mice.
29 release of nitrites in A549 cells, SAEC, and BALF.
30 , GT is detectable in mouse lungs, serum and BALF during neutropenic IA, suggesting that GT may be us
31 were captured in mice sera, lung tissues and BALF, including purines, pyrimidines, acylcarnitines, fa
32 were observed in mice sera, lung tissues and BALF, indicating the molecular differences between syste
33 stology, AHR, T regulatory cells (Tregs) and BALF cytokines was examined.
34                                    ALI/ ARDS BALF demonstrated potent alphaSMA induction with a mean
35    There was no correlation between ALI/ARDS BALF-induced alphaSMA and procollagen 3 induction (r = -
36                                     ALI/ARDS BALF-induced myofibroblast differentiation is partially
37 receptor inhibitor SB431542 reduced ALI/ARDS BALF-stimulated alphaSMA induction by 52% (p < .005).
38        Furthermore, depletion of IGF in ARDS BALF led to enhanced fibroblast apoptosis.
39 by enzyme-linked immunosorbent assay in ARDS BALF.
40 ty of human MDMs stimulated with LPS or ARDS BALF.
41 resent in complex biological fluids, such as BALF, from which hypotheses can be developed and tested.
42 lopment of AHR in sensitized mice as well as BALF and tissue eosinophilia.
43  observational trial the association between BALF cytokine/chemokine profiles and subsequent infectio
44   No major differences were observed between BALF exosomes from before and after allergen provocation
45 s revealed significant relationships between BALF neutrophil counts and indices of alveolar-capillary
46 esulted in WT-like lung injury severity, but BALF leukocyte levels increased only in WT and A1-KO mic
47 alpha production was inhibited > or = 47% by BALF or SP-A-/- BALF (at 290 or 580 microg of protein/ml
48                                   Concurrent BALF lymphocyte subsets were examined by flow cytometry,
49                                 In contrast, BALF neutrophils and AHR increased, but eosinophils decr
50 y 1 post infection, bacterial colony counts, BALF total cell number and BALF protein concentration si
51 /ml, P < 0.05 to 0.01); in contrast, SP-D-/- BALF did not significantly inhibit TNF-alpha production.
52          Finally, pure SP-D added to SP-D-/- BALF inhibited TNF-alpha production by BAM-B. dermatitid
53 BALF was mixed in equal amounts with SP-D-/- BALF, TNF-alpha production by BAM-B. dermatitidis was in
54 -) BALF, or a mixture of SP-A-/- and SP-D-/- BALF.
55  or surfactant protein D-deficient (SP-D-/-) BALF, or a mixture of SP-A-/- and SP-D-/- BALF.
56  and study days 4 and 7 to obtain BAL fluid (BALF) for measurement of total protein, ceruloplasmin, a
57 beta1 in bronchoalveolar lavage (BAL) fluid (BALF).
58 responsiveness (AHR), bronchoalveolar fluid (BALF) cellular and cytokine profile, antigen-specific Ig
59 uated by using bronchoalveolar lavage fluid (BALF) analysis and pathology.
60                Bronchoalveolar lavage fluid (BALF) analysis demonstrated an approximate 18-fold incre
61 ation in both bronchioalveolar lavage fluid (BALF) and blood of doxycycline-treated CCSP-rtTA/(tetO)7
62  detectable in bronchoalveolar lavage fluid (BALF) and culture medium of lung epithelial cells.
63   Lung tissue, bronchoalveolar lavage fluid (BALF) and draining lymph node cells were analysed for in
64 e cytokines in bronchoalveolar lavage fluid (BALF) and explore predicting factors of severe MPP in ch
65    We examined bronchoalveolar lavage fluid (BALF) and histological lung sections after 1 week, 1 mon
66 atant of mouse bronchoalveolar lavage fluid (BALF) and in nonciliated bronchiolar cells, alveolar typ
67 neumoniae, and bronchoalveolar lavage fluid (BALF) and lung CFU values were determined.
68  to 12 wk, and bronchoalveolar lavage fluid (BALF) and lung tissue collected after the last challenge
69 e (CARDS) toxin in bronchiolar lavage fluid (BALF) and lung.
70 bmGT in serum, bronchoalveolar lavage fluid (BALF) and lungs of A. fumigatus-infected chronic granulo
71 dministration, bronchoalveolar lavage fluid (BALF) and plasma G-CSF concentrations increased, compare
72 tein levels in bronchoalveolar lavage fluid (BALF) and plasma were evaluated.
73 etween matched bronchoalveolar lavage fluid (BALF) and plasma, identifies the degree of congruence be
74 nflammation in bronchoalveolar lavage fluid (BALF) and Th2 responses in lung explants and draining LN
75   BORT reduced bronchoalveolar lavage fluid (BALF) and tissue eosinophils and inflammation, IL-5, IL-
76  infection had bronchoalveolar lavage fluid (BALF) available for analysis.
77 d in lungs and bronchoalveolar lavage fluid (BALF) by multiparametric flow cytometry.
78 s, we analyzed bronchoalveolar lavage fluid (BALF) by shotgun proteomics.
79 erial burdens, bronchoalveolar lavage fluid (BALF) cell counts, cell types, and cytokine levels were
80  by increased broncho-alveolar lavage fluid (BALF) cells and cytokines (IL-6 and TNF-alpha), increase
81                Bronchoalveolar lavage fluid (BALF) cells and eicosanoid mediators were also measured
82 ial clearance, bronchoalveolar lavage fluid (BALF) characterization, lung histology, lung cell prolif
83 ators, and the bronchoalveolar lavage fluid (BALF) contain elevated levels of prostaglandin D2.
84 by 80% in COPD bronchoalveolar lavage fluid (BALF) due to serine protease cleavage, primarily by cath
85 mice developed bronchoalveolar lavage fluid (BALF) eosinophilia and pulmonary eosinophilia.
86 matory role of bronchoalveolar lavage fluid (BALF) exosomes in patients with sarcoidosis and to find
87     We studied bronchoalveolar lavage fluid (BALF) from 36 patients with ARDS (20 survivors, 16 non-s
88 ung tissue and bronchoalveolar lavage fluid (BALF) from a non-lethal mouse model with influenza A vir
89 ermine whether bronchoalveolar lavage fluid (BALF) from ALI/ARDS patients can induce myofibroblast di
90  or = 0.05) in bronchoalveolar lavage fluid (BALF) from asbestos-exposed mice, but to a lesser extent
91 , sputum, and bronchioalveolar lavage fluid (BALF) from asthmatic patients and time/dose-dependent ex
92 re measured in bronchoalveolar lavage fluid (BALF) from children with CF (n = 57; 6.1 +/- 5.9 yr) and
93 ers present in bronchoalveolar lavage fluid (BALF) from chlorine gas exposed mice.
94                Bronchoalveolar lavage fluid (BALF) from LPS-treated MMP-8(-/-) mice had more MIP-1alp
95 -alpha, in the bronchoalveolar lavage fluid (BALF) from lung transplant recipients was associated wit
96 s in blood and bronchoalveolar lavage fluid (BALF) from mechanically ventilated patients with acute r
97    We obtained bronchoalveolar lavage fluid (BALF) from patients with ARDS or ventilated control pati
98 ed with LPS or bronchoalveolar lavage fluid (BALF) from patients with ARDS.
99  identified in bronchoalveolar lavage fluid (BALF) from patients with asthma, idiopathic pulmonary fi
100 was present in bronchoalveolar lavage fluid (BALF) from recipients transplanted for emphysema associa
101             In bronchoalveolar lavage fluid (BALF) from subjects with IPF, we found short-fragment hy
102  (MLE-15) with bronchoalveolar lavage fluid (BALF) harvested from mice infected with S. pneumoniae.
103 arynx (OP) and bronchoalveolar lavage fluid (BALF) in a cohort of 40 CF patients during the first 3 y
104 tokines in the bronchoalveolar lavage fluid (BALF) in a murine model of allergic asthma.
105 tection in the bronchoalveolar lavage fluid (BALF) indicates HCMV replication in the pulmonary compar
106     Culture of bronchoalveolar lavage fluid (BALF) is the gold standard for detection of pathogens in
107 ng wet weight, bronchoalveolar lavage fluid (BALF) lactate dehydrogenase, and BALF neutrophils.
108 ion that local bronchoalveolar lavage fluid (BALF) levels of vitamin D are severely deficient in HIV(
109 ure and in the bronchoalveolar lavage fluid (BALF) obtained from Balb/c mice after RSV infection.
110 T cells in the bronchoalveolar lavage fluid (BALF) of Af5517-aspirated mice displayed decreased gamma
111 lated from the bronchoalveolar lavage fluid (BALF) of M bovis BCG-infected mice contain the mycobacte
112 ntified in the bronchoalveolar lavage fluid (BALF) of patients with acute lung injury.
113  isolated from bronchoalveolar lavage fluid (BALF) of patients with asthma and idiopathic pulmonary f
114 ome profile in bronchoalveolar lavage fluid (BALF) of patients with sarcoidosis, but their role in as
115                Bronchoalveolar lavage fluid (BALF) offers a potential means to diagnose acute rejecti
116 ed proteins in bronchoalveolar lavage fluid (BALF) on the interaction of BAM and Blastomyces dermatit
117 zone increased bronchoalveolar lavage fluid (BALF) protein, a marker of lung permeability, in all gen
118 Neutrophils in bronchoalveolar lavage fluid (BALF) served as markers of inflammation.
119 8% increase in bronchoalveolar lavage fluid (BALF) TK activity.
120                Bronchoalveolar lavage fluid (BALF) was analysed for total protein, lactate dehydrogen
121                Bronchoalveolar lavage fluid (BALF) was collected from children undergoing clinically
122 ng activity of bronchoalveolar lavage fluid (BALF) was observed following secondary CA04 challenge of
123                Bronchoalveolar lavage fluid (BALF) was obtained on the fifth day.
124               Broncho alveolar lavage fluid (BALF) was sampled from donors prior to procurement and i
125 ung tissue and bronchoalveolar lavage fluid (BALF) were analyzed for inflammation, as well as various
126 ctive MCP-1 in human bronchial lavage fluid (BALF) were associated with the continuum from acute to c
127 sine levels in bronchoalveolar lavage fluid (BALF) were increased by approximately 3-fold.
128 7 cytokines in bronchoalveolar lavage fluid (BALF), accompanied by an increment in transcription fact
129                Bronchoalveolar lavage fluid (BALF), airway inflammation and hyperresponsiveness (AHR)
130 leen cells and bronchoalveolar lavage fluid (BALF), and cellular distribution in BALF were then exami
131 nalysis of the bronchoalveolar lavage fluid (BALF), and characterization of ex vivo cytokine response
132 xposure, SpO2, bronchoalveolar lavage fluid (BALF), and histologic analyses were performed.
133 and macrophages in bronchiolar lavage fluid (BALF), as well infiltrating inflammatory cells, and decr
134 r cells in Wsh bronchoalveolar lavage fluid (BALF), despite similar levels of cytokines and chemokine
135 neutrophils in bronchoalveolar lavage fluid (BALF), lung inflammation, and BHR.
136  plasma to the bronchoalveolar lavage fluid (BALF), protein and CINC-1 concentrations in the BALF, an
137 surements, and bronchoalveolar lavage fluid (BALF), serum, and lungs were collected on day 28 for fur
138 heir serum and bronchoalveolar lavage fluid (BALF), significantly reduced inflammatory cytokine level
139 bile salts) in bronchoalveolar lavage fluid (BALF).
140 d cytokines in bronchoalveolar lavage fluid (BALF).
141  biomarkers in bronchoalveolar lavage fluid (BALF).
142 4/CD8 ratio in bronchoalveolar lavage fluid (BALF).
143  levels in the bronchoalveolar lavage fluid (BALF).
144  production in bronchoalveolar lavage fluid (BALF).
145 y cytokines in bronchoalveolar lavage fluid (BALF).
146 tion increased bronchoalveolar lining fluid (BALF) adenosine comparably in WT and A1-KO mice.
147 ound in bronchoalveolar lavage (BAL) fluids (BALF) of LTR at CLAD diagnosis, are elevated and potenti
148 e activity in bronchoalveolar lavage fluids (BALF) and myeloperoxidase immunoreactivity in epithelial
149 al protein in bronchoalveolar lavage fluids (BALF) from patients with sepsis-related acute respirator
150 s detected in bronchoalveolar lavage fluids (BALF) in a macrophage- and neutrophil-dependent manner.
151  9, and 12 in bronchoalveolar lavage fluids (BALF).
152 e assessed in bronchoalveolar lavage fluids (BALFs) after allergen challenge.
153 y secretions, bronchoalveolar lavage fluids (BALFs) were collected from children undergoing clinicall
154 nificant interstrain variation was found for BALF inflammatory cells and protein (heritability estima
155  as compared with ELR(-) CXC chemokines from BALF of patients with ARDS as compared with controls.
156 ms were to investigate whether exosomes from BALF have LT biosynthetic capacity and to explore phenot
157 nce of miRNAs was confirmed in exosomes from BALF of both asthmatic patients and healthy control subj
158 isolated alveolar macrophages harvested from BALF from HA-treated mice.
159                   Native SP-BN isolated from BALF also killed bacteria but only at acidic pH; the bac
160                  Exosomes were isolated from BALF from healthy control subjects (n = 10) and patients
161 n of CXCR1 was decreased on neutrophils from BALF compared with blood (median difference in MFI 1337,
162         Among CARV infected patients, a high BALF concentration of either CXCL10 or CXCL11 was predic
163 ith marked signs of airway remodelling, high BALF eosinophilia, increased BALF pro-inflammatory cytok
164                         Mouse BALF and human BALF had a strong positive correlation with 2040 metabol
165 their presence in in vitro chlorinated human BALF.
166  metabolites present across mouse and human, BALF and plasma.
167              Furthermore, transfer of immune BALF obtained from nonasthmatic, but not asthmatic, dono
168                                           In BALF, the levels of IL-5, IL-13, eotaxin-1 and eotaxin-2
169 rd elevated neutrophil counts (P = 0.002) in BALF and increased mortality (P = 0.046).
170          The finding of ADP-ribosyl-HNP-1 in BALF but not in leukocyte granules suggests that the mod
171 d increases in IL-4, MIP-1beta, and MCP-1 in BALF that were more elevated (p < or = 0.05) in Tg(+) mi
172  in total protein levels, IL-5, and IL-13 in BALF.
173 duced amounts of matrix metalloprotease-9 in BALF and were resistant to epithelial integral membrane
174 cient mice failed to accumulate adenosine in BALF and exhibited significantly less radiation-induced
175 rway tissue eosinophilia preceded changes in BALF.
176 evels of various cytokines and chemokines in BALF were not significantly different among these 3 type
177    Among CF patients, SP-A concentrations in BALF were inversely related to inflammation, bacterial c
178 n the lung increased kinin concentrations in BALF, a result consistent with the PPE-induced increase
179 r hypertrophy index, and total cell count in BALF.
180                               Cell counts in BALF and lung immunohistology demonstrated that eosinoph
181                Our data suggest that SP-D in BALF binds beta-glucan on B. dermatitidis, blocking BAM
182 d with BALF inhibited the binding of SP-D in BALF to B. dermatitidis as demonstrated by IFA.
183 liminary investigation showing a decrease in BALF levels of IL-8 and leukotriene B4 and the associate
184 ut soluble, active MMP-8 was not detected in BALF samples.
185 -alpha, but neither cytokine was detected in BALF.
186 f immunomodulatory cells in vivo detected in BALF.
187                   Significant differences in BALF exosomal miRNA was detected for 24 miRNAs with a su
188 e fluid (BALF), and cellular distribution in BALF were then examined.
189 d CCL-20 levels were quantitated by ELISA in BALF and serum samples from 60 LTRs.
190 erential cell counts revealed eosinophils in BALF that increased (p < or = 0.05) in Tg(+) mice at 9 d
191 S toxin and numbers of mycoplasma genomes in BALF and the degree of histologic pulmonary inflammation
192 IL-13, and IL-5 were significantly higher in BALF of symptomatic as compared with clinically asymptom
193     Moreover, the protein levels of IL17A in BALF were also found greatly decreased in children with
194 P = 0.036) and a trend toward an increase in BALF eosinophils as compared to HDM challenge.
195 uced bronchoconstriction and the increase in BALF TK activity in a dose- dependent and molecular weig
196  consistent with the PPE-induced increase in BALF TK activity.
197 -like antimicrobial properties) increased in BALF (p = 0.016) and plasma (p < 0.001); BALF levels of
198 n concentration was also highly increased in BALF and blood of these models with tumors.
199 Cd39(-/-) mice exhibited marked increases in BALF ATP levels but paradoxically exhibited limited AAI
200 esponse upon HDM exposure, with increases in BALF cytokines IL-17A and KC, and Th17 cytokine producin
201 ficantly attenuated cellular infiltration in BALF and allergic airway hyperresponsiveness.
202 interleukin-5 and interferon-gamma levels in BALF and in OVA-incubated splenocytes.
203 nes significantly reduced IL-1beta levels in BALF during ALI.
204              Thus, decreased IL17A levels in BALF may be a valuable biomarker to identify severe MPP
205 Extracellular histone and IL-1beta levels in BALF were also elevated in C5a-induced and IgG immune co
206 ulation in the BALF; IL-4 and IL-5 levels in BALF were also significantly reduced.
207        Eosinophil peroxidase (EPO) levels in BALF were elevated in OVA-sensitized/challenged mice at
208 nase activity and increased YKL-40 levels in BALF.
209  procollagen I and procollagen III levels in BALF.
210 stone H3 tissue levels and NET-DNA levels in BALF.
211 LI) and reduced cytokine/chemokine levels in BALF.
212 dications for transplant had unopposed NE in BALF.
213 elated with the percentage of neutrophils in BALF (r = 0.41, P < 0.05 and r = 0.46, P < 0.05, respect
214 IL-22(+) TCRbeta(+) cells and neutrophils in BALF.
215 atment-dependent variation in neutrophils in BALF.
216 ar leukocytes, predominately neutrophils, in BALF after 9 days of asbestos inhalation.
217 e by up to 20-fold in lung tissue but not in BALF.
218 utrophils relative to bacteria were noted in BALF from CF compared with non-CF subjects.
219 more than half of the metabolites present in BALF were also present in plasma.
220 nd eosinophil numbers and IL-5 production in BALF.
221 me, we detected vitamin D-binding protein in BALF exosomes, which was more abundant in patients.
222 wer ratio of kallistatin to total protein in BALF showed a significant trend toward elevated neutroph
223 orated pulmonary oedema and total protein in BALF.
224             Furthermore, eosinophil ratio in BALF was 3%, hyperplasia of goblet cell, eosinophilic in
225 s fed EPA+GLA had a significant reduction in BALF ceruloplasmin and IL-8 during the study as compared
226                A trend toward a reduction in BALF tumor necrosis factor-alpha was observed on study d
227 ed serum IL-4 and IL-17 levels and increased BALF % CD4(+) T cells that produce IL-5 and IL-13.
228 ouse lung PAFR mRNA expression and increased BALF and lung pneumococcal CFU values.
229                Repeated DAC caused increased BALF neutrophils, eosinophils, and sulfidopeptide leukot
230 modelling, high BALF eosinophilia, increased BALF pro-inflammatory cytokines, reduced BALF IL-10 leve
231 e over baseline RP), inflammation, increased BALF concentrations of leukotriene (LT) C(4), LTD(4), an
232 d to BALF exosomes from healthy individuals, BALF exosomes from asthmatics displayed higher levels of
233 en challenge, IL-33 is rapidly released into BALFs at levels that do not correlate with other immedia
234                              We investigated BALF enhancement or inhibition of TNF-alpha production b
235                                      Matched BALF and plasma was collected from mice (ambient air or
236 ence of > or = 10(5) colony forming units/ml BALF of aerobic bacteria.
237                                    Moreover, BALF-induced RelA activity was completely abolished foll
238                                        Mouse BALF and human BALF had a strong positive correlation wi
239 ised human cell-based assays, ex vivo murine BALF, in vivo pre-clinical models and human samples to t
240  with B. dermatitidis without or with normal BALF, surfactant protein A-deficient (SP-A-/-) or surfac
241 bmGT, was detected in 71% of sera and 50% of BALF of neutropenic mice; neither was detected in serum/
242 y at acidic pH; the bactericidal activity of BALF at acidic pH was completely blocked by SP-BN Ab.
243 phenotypic and functional characteristics of BALF exosomes in asthma.
244 spectrometric proteomics characterization of BALF exosomes from 15 patients with sarcoidosis and 5 he
245 ysis, to assess the bacterial composition of BALF from children with CF and disease controls (DC).
246 r, and there was decreased immunostaining of BALF cells for SP-D in CF.
247    Hypoxemia, pulmonary edema, and levels of BALF alveolar macrophages, neutrophils, IFN-gamma, and I
248                                    Levels of BALF leukocytes, gamma interferon (IFN-gamma), and inter
249  where plasma may be interrogated in lieu of BALF or lung tissue.
250 t cell degranulator, increased the number of BALF cells and bacterial burden.
251        Significantly greater mean numbers of BALF neutrophils were found in Notch3-/- and Notch4-/- m
252 ukotriene B4 and the associated reduction of BALF neutrophils and alveolar membrane protein permeabil
253   SP-D was detected by anti-SP-D antibody on BALF-treated unwashed B. dermatitidis in an immunofluore
254                  Differential cell counts on BALF revealed decreased proportions of macrophages and i
255 umonia (n=10), CXCR1 and CXCR2 expression on BALF neutrophils was higher than in controls (n=3) (medi
256 d diagnostic bronchoscopies had at least one BALF containing unopposed NE, usually associated with th
257 nd chemokines also were detected in serum or BALF from MIF(-/-) mice.
258                               Likewise, PLTP BALF activity levels decreased by 20 and 40% in smoke-ex
259                                    Pneumonic BALF, but not S. pneumoniae, induced degradation of Ikap
260                           Epithelial and RBC BALF-MV are elevated at CLAD diagnosis, have a potential
261        In MS-WF-exposed mice CV-3988 reduced BALF CFU values.
262 sed BALF pro-inflammatory cytokines, reduced BALF IL-10 levels, reduced blood Tregs, increased expres
263 , inhibited eosinophil infiltration, reduced BALF concentrations of LTC(4), LTD(4), and LTE(4) and PG
264    Cromolyn, a mast cell stabilizer, reduced BALF cells and bacterial burden similar to the levels se
265 tropenic mice; neither was detected in serum/BALF of CGD or steroid-treated mice.
266 ORT had complementary effects and suppressed BALF and tissue eosinophils and inflammation, MSC number
267 ssay experiments demonstrated that Muc5ac-Tg BALF and purified Muc5ac reduced infection, likely via b
268 ted MMP-8(-/-) mice had more MIP-1alpha than BALF from LPS-treated WT mice, but similar levels of oth
269                    Furthermore, we show that BALF exosomes contain enzymes for LT biosynthesis.
270                                          The BALF depleted by a coating of B. dermatitidis lost the a
271                                          The BALF was collected from 37 LTR at time point of CLAD dia
272                                          The BALF-MV levels of epithelial and red blood cell (RBC) or
273 2 is released and biologically active in the BALF and can regulate airway epithelial cell cytokine ex
274 sociated with higher Gal-3 expression in the BALF as well as lung tissue.
275 ese LTRs displayed HCMV DNA detection in the BALF by PCR, whereas other infectious agents were undete
276 rived extracellular histones appeared in the BALF during ALI and directly activated the NLRP3 inflamm
277 ore than 690 proteins were identified in the BALF exosomes, several of which displayed significant up
278                     Most of the HNP-1 in the BALF from individuals with a history of smoking was, in
279 er the curve (AUC) for each biomarker in the BALF of 40 lung transplant patients who had at least fou
280        Chitinase activity was greater in the BALF of asthmatics (mean, 0.85 +/- 1.2 U/mL) compared wi
281 ise YKL-40 concentrations were higher in the BALF of asthmatics and correlated with chitinase activit
282 towards increased fungal-specific IgG in the BALF of asthmatics compared with non-asthmatics and for
283 oformans and A. fumigatus was greater in the BALF of asthmatics compared with non-asthmatics.
284 and IgA reactivity to fungal proteins in the BALF of asthmatics may reflect a local response to funga
285 ntified 1115 high confidence proteins in the BALF out of which 142 were differentially expressed betw
286 dings demonstrating early differences in the BALF protein expression in ARDS survivors vs. non-surviv
287 nally, total inflammatory cell counts in the BALF were markedly reduced 1-5 days after apoptotic cell
288 F), protein and CINC-1 concentrations in the BALF, and the lung histology.
289 phil recruitment, and myeloperoxidase in the BALF.
290 mphocyte, and neutrophil accumulation in the BALF; IL-4 and IL-5 levels in BALF were also significant
291 by small sample size in the mouse study, the BALF metabolome appeared to be more affected by CS than
292 urthermore, when patients with BOS had their BALF analyzed from their last bronchoscopy before the de
293 educed inflammatory cytokine levels in their BALF, and reduced levels of morbidity relative to animal
294                                  Compared to BALF exosomes from healthy individuals, BALF exosomes fr
295                                     A unique BALF lymphocyte profile was associated with rejection an
296                                        Using BALF from three patients, we identified a total of 870 d
297 robial activity, B. dermatitidis may utilize BALF constituents, such as SP-D, to blunt the host defen
298                                Thus, whereas BALF constituents commonly mediate antimicrobial activit
299                           In contrast, while BALF levels of vascular endothelial growth factor were e
300               B. dermatitidis incubated with BALF and washed, plus BAM, stimulated 63% less productio
301                   beta-Glucan incubated with BALF inhibited the binding of SP-D in BALF to B. dermati

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