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1 etadata further defined 3 of these as highly eosinophilic, 3 as highly neutrophilic, and 2 as highly
2 Grass pollen exposure was associated with eosinophilic airway inflammation 1-2 days after exposure
3 agged 2 single- or double-deficient mice had eosinophilic airway inflammation and a TH2 cell activati
4 rmine whether gammaT supplementation reduces eosinophilic airway inflammation and acute neutrophilic
5 ncy in mice prevented house dust mite-driven eosinophilic airway inflammation and significantly reduc
9 merican subjects were more likely to exhibit eosinophilic airway inflammation than white subjects in
10 3-deficient cDC1s did not develop Th2-driven eosinophilic airway inflammation upon HDM exposure, but
11 required in two different models to amplify eosinophilic airway inflammation via induced expression
12 d OVA induced airway hyperresponsiveness and eosinophilic airway inflammation were both completely di
13 d OVA-induced airway hyperresponsiveness and eosinophilic airway inflammation were both significantly
14 CD11c-Cre mice have a phenotype of increased eosinophilic airway inflammation, allergic sensitization
15 hma phenotype, usually with a severe course, eosinophilic airway inflammation, and increased producti
18 African American subjects exhibit greater eosinophilic airway inflammation, which might explain th
19 derate asthma and were also characterized by eosinophilic airway inflammation, yet increased producti
27 three clinically relevant asthma phenotypes: eosinophilic allergic asthma, eosinophilic nonallergic a
28 wenty-six hospitalized asthma patients (nine eosinophilic allergic; EA, nine noneosinophilic allergic
30 ions and that gammaT supplementation reduces eosinophilic and endotoxin (LPS)-induced neutrophilic ai
31 Clca1 (Gob5) and Muc5ac were upregulated in eosinophilic and even more in neutrophilic phenotype.
33 e dust extracts as adjuvants developed mixed eosinophilic and neutrophilic airway inflammation and ai
34 NP and CRSwNP displayed variable degrees of eosinophilic and neutrophilic inflammation, with a profo
37 bacterial markers that discriminate T2-high (eosinophilic) and T2-low (neutrophilic/mixed-inflammatio
38 L-HCCs: large polygonal cells with granular, eosinophilic, and mitochondria-rich cytoplasm, prominent
40 ils, and VOCs gave a very good prediction of eosinophilic asthma (area under the receiver operating c
41 sed sputum ANCAs compared with patients with eosinophilic asthma (P = 0.002) and healthy controls (P
42 PA (n = 10, serum ANCA(+)), 19 patients with eosinophilic asthma (prednisone dependent), and 13 healt
44 patients aged 12 years or older with severe eosinophilic asthma and a history of at least two exacer
47 t basophils may be particularly important in eosinophilic asthma and that sputum basophil assessment
49 r assess mepolizumab in patients with severe eosinophilic asthma by examining its effect on health-re
50 polizumab, patients with uncontrolled severe eosinophilic asthma experienced clinically significant i
51 blood myeloid DC subsets from patients with eosinophilic asthma have lower LRP-1 expression than cel
56 ncy room visit rates in patients with severe eosinophilic asthma treated with mepolizumab or placebo
57 with sputum IL-1beta protein levels, whereas eosinophilic asthma was associated with an IL-13-induced
58 will allow selection of patients with severe eosinophilic asthma who are most likely to achieve clini
59 research into therapeutics for patients with eosinophilic asthma who do not respond to anti-IL-5 ther
60 th the highest classification performance in eosinophilic asthma with accuracy comparable to that of
61 The proposed prediction model identifies eosinophilic asthma without the need for sputum inductio
62 the majority of these publications relate to eosinophilic asthma, a growing proportion of them focus
63 remodeled asthma, (3) late-onset nonallergic eosinophilic asthma, and (4) late-onset nonallergic none
64 mprovements in HRQOL in patients with severe eosinophilic asthma, and had a safety profile similar to
65 e pathophysiology in stable and exacerbating eosinophilic asthma, and therefore treatment is focused
66 can be classified into 4 unique phenotypes: eosinophilic asthma, neutrophilic asthma, mixed granuloc
84 sal polyp tissues at Week 16 vs baseline for eosinophilic cationic protein (P = 0.008), eotaxin-2 (P
85 ophil degranulation increased, and levels of eosinophilic cationic protein were higher in duodenal fl
89 EG), eosinophilic gastroenteritis (EGE), and eosinophilic colitis (EC), yet these diseases are barely
90 gation, we asked whether esophagitis with an eosinophilic component is observed in young pigs rendere
96 high-grade morphology with abundant granular eosinophilic cytoplasm, resembling mitochondria-rich apo
99 d eosin and Masson trichrome staining showed eosinophilic deposits in subepithelial corneal stroma th
100 lic esophagitis (EoE) is an antigen-mediated eosinophilic disease of the esophagus that involves fibr
103 ces in our understanding of eosinophilia and eosinophilic disorders (excluding asthma) published in t
104 the basis for the use of glucocorticoids in eosinophilic disorders, and it has intrigued clinicians
105 gnosis, treatment, and pathogenesis of other eosinophilic disorders, most notably eosinophilic esopha
106 ar and persist in tissues from patients with eosinophilic disorders, such as asthma, allergic reactio
107 he mechanism of action of glucocorticoids in eosinophilic disorders, with implications for the study
110 sSiglec-8) levels in normal donors (NDs) and eosinophilic donors (EOs) and assess the efficacy of ant
111 who had symptomatic eosinophilic gastritis, eosinophilic duodenitis, or both conditions in a 1:1:1 r
113 ely mimic the Th2 and inflammatory milieu of eosinophilic esophagitis (EoE) and assessed alterations
141 ACKGROUND & AIMS: Pharmacologic treatment of eosinophilic esophagitis (EoE) is limited to off-label u
142 g studies have observed an increased risk of eosinophilic esophagitis (EoE) mostly among first-degree
144 ng eosinophilic tissue inflammation, such as eosinophilic esophagitis (EoE), a chronic inflammatory d
145 ve been recognized as a primary treatment of eosinophilic esophagitis (EoE), an allergic inflammatory
146 L-22, and IL-23) of patients with achalasia, eosinophilic esophagitis (EoE), and gastroesophageal ref
147 advances in the pathologic understanding of eosinophilic esophagitis (EoE), as of yet, no single age
148 orrelate with tissue pathology during active eosinophilic esophagitis (EoE), providing additional evi
157 e of type 2 cytokines in the pathogenesis of eosinophilic esophagitis (EoE); however, heterogeneity i
159 herapy) and 20 controls, stored in the Swiss Eosinophilic Esophagitis Database (SEED) and Biobank, we
160 s recapitulated the majority of the clinical Eosinophilic Esophagitis Diagnostic Profile (EDP) on flu
169 bservational study was continued, a study of eosinophilic esophagitis was initiated, and new therapeu
170 patients with eosinophilic skin diseases or eosinophilic esophagitis were used for in vivo analyses.
171 ergic rhinitis, allergic conjunctivitis, and eosinophilic esophagitis), suggesting both cutaneous and
172 n an allergic inflammatory tissue focused on eosinophilic esophagitis, a prototypic, chronic, allergi
173 elial dysregulation in asthma, food allergy, eosinophilic esophagitis, and allergic rhinosinusitis.
174 in asthma, rhinitis, chronic rhinosinusitis, eosinophilic esophagitis, food allergy, and atopic derma
181 ts of the gastrointestinal tract and include eosinophilic gastritis (EG), eosinophilic gastroenteriti
185 randomly assigned adults who had symptomatic eosinophilic gastritis, eosinophilic duodenitis, or both
186 y (OIT), but there are only a few reports of eosinophilic gastroenteritis (EGE) occurring after OIT.
187 act and include eosinophilic gastritis (EG), eosinophilic gastroenteritis (EGE), and eosinophilic col
188 hout EG were enrolled across 9 Consortium of Eosinophilic Gastrointestinal Disease Researchers-associ
190 mmation due to inflammatory bowel disease or eosinophilic gastrointestinal disease showed the least b
193 angiitis (GPA), microscopic polyangiitis and eosinophilic GPA (EGPA), are defined according to clinic
194 inflamed human tissues, we often find intact eosinophilic granules, but not eosinophils themselves.
195 versus 19% of placebo-treated patients with eosinophilic granulomatosis with polyangiitis (EGPA) ach
199 multiple mononeuritis (MM) in patients with eosinophilic granulomatosis with polyangiitis (EGPA).
201 sculitis, Crohn's disease, Behcet's disease, eosinophilic granulomatosis with polyangiitis, and immun
203 associated with EM were hypersensitivity and eosinophilic granulomatosis with polyangiitis, which acc
204 cut point to define subjects with either an eosinophilic (>/=2%) or noneosinophilic (<2%) inflammato
205 s revealed significant levels of oesophageal eosinophilic infiltration (P < .05) in 4/6 of these anim
206 a, histologic features of disease (including eosinophilic infiltration and a marker of type 2 inflamm
207 their small intestine villi and had reduced eosinophilic infiltration as compared to the untreated b
210 gested that Hsp70 is critically required for eosinophilic infiltration, collagen accumulation, and Th
214 ce ICS treatment response in the presence of eosinophilic inflammation (ie, high pretreatment eosinop
216 n the lung that is accompanied by diminished eosinophilic inflammation and airway hyperresponsiveness
217 ce generated a similar phenotype of enhanced eosinophilic inflammation and allergic sensitization.
218 L-6, TNF-alpha, and IL-17 in contrast to the eosinophilic inflammation and IL-4 production observed i
221 MCs and their products in driving the severe eosinophilic inflammation and respiratory dysfunction th
224 tics had a lower FEV1 and Pc20 and increased eosinophilic inflammation compared to healthy subjects.
226 as a therapeutic strategy for management of eosinophilic inflammation in allergic airway disease, in
227 such, biomarkers currently used to delineate eosinophilic inflammation in asthmatic subjects should b
230 c inflammation in CRSwNP and its relation to eosinophilic inflammation in severe type 2 immune reacti
231 dy levels, but type 2 cytokine responses and eosinophilic inflammation in the airways remained unaffe
232 nd specific signaling pathways that regulate eosinophilic inflammation is critical for development of
233 oids, confirming the importance of measuring eosinophilic inflammation to guide corticosteroid use.
236 attenuates airway hyperresponsiveness (AHR), eosinophilic inflammation, and mucus-production response
237 males with severe airflow limitation, little eosinophilic inflammation, and the least CS responsivene
238 signaling in asthma has been associated with eosinophilic inflammation, but little is known about the
239 in blocking antibodies reduced IL-33-induced eosinophilic inflammation, mucus metaplasia, and type 2
240 tes to lung ILC2 accumulation and downstream eosinophilic inflammation, mucus metaplasia, and type 2
248 )-mediated potentiation of ovalbumin-induced eosinophilic inflammation; recruitment of platelet-adher
250 g neurodegenerative disease characterized by eosinophilic intranuclear inclusions in the nervous syst
254 mation after allergen exposure, with massive eosinophilic lung infiltrates and increased Th2 cytokine
255 6 receptors before sensitization exacerbated eosinophilic lung inflammation and type 2 cytokine produ
256 pates in the progression of allergen-induced eosinophilic lung inflammation to corticosteroid-refract
257 e lacking PTX3 have exaggerated neutrophilic/eosinophilic lung inflammation, mucus production, and ai
259 t phenotypes of allergic airway inflammation-eosinophilic, mixed, and neutrophilic asthma via differe
260 (60.0-85.5) vs 80.5 (69.7-95.0), P=.009] for eosinophilic, mixed, neutrophilic and paucigranulocytic
262 in hypereosinophilic IL-5Tg mice resulted in eosinophilic myocarditis with severe ventricular and atr
263 s had moderate performance in distinguishing eosinophilic N-ERD (for blood eosinophils, AUC = 0.72; f
264 in and CCL26 were significantly increased in eosinophilic N-ERD and correlated with T2 signature in B
265 rmined in 167 participants and classified as eosinophilic (n = 84), neutrophilic (n = 14), paucigranu
268 cerbating inflammatory end points, including eosinophilic, neutrophilic, and ST2(+)CD4(+) T-cell infi
269 ma phenotypes: eosinophilic allergic asthma, eosinophilic nonallergic asthma and noneosinophilic nona
270 (CRSsNP, n = 86), and CRS with nasal polyps (eosinophilic NP: ENP, n = 81; non-eosinophilic NP: NENP,
271 al polyps (eosinophilic NP: ENP, n = 81; non-eosinophilic NP: NENP, n = 113) were enrolled in this st
275 d protein-induced allergic proctocolitis and eosinophilic oesophagitis, is not well understood, leadi
276 lung (asthma), skin (eczema) or oesophagus (eosinophilic oesophagitis; EoE) and cancer at the organ
281 dified intention-to-treat population with an eosinophilic phenotype were stratified according to bloo
282 ted in the recognition of an allergic and an eosinophilic phenotype, which are not mutually exclusive
284 common forms of lung injury, including acute eosinophilic pneumonia and diffuse alveolar hemorrhage,
285 rances include organizing pneumonia or acute eosinophilic pneumonia patterns, the latter consisting o
287 ults suggest that T1 (CXCL9 and CXCL10), T2 (eosinophilic proteins and CCL26), and T3 (CSF3) endotypi
288 d Ccr5, which together control monocytic and eosinophilic recruitment to resting and inflamed sites.
289 -33, group 2 innate lymphoid cell (ILC2) and eosinophilic responses to Alternaria allergen administra
290 aria allergen administration, and diminished eosinophilic responses to Nippostrongylus brasiliensis,
291 IL1RL1 gene expression is associated with eosinophilic SA, whereas NLRP3 inflammasome expression i
292 apies such as severe allergic and refractory eosinophilic severe asthma, while in other inflammatory
296 rogrammed to skew allergic inflammation from eosinophilic T helper cell 2 (TH2) to neutrophilic TH17
297 processes, notably for this review involving eosinophilic tissue inflammation, such as eosinophilic e
298 rophilic inflammation associated with severe eosinophilic type 2 inflammatory CRSwNP, the role of whi