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1 helium and stroma (e.g., edema and extensive eosinophil infiltration).
2 ting C. neoformans-driven pulmonary IL-5 and eosinophil infiltration.
3 ry end point was the reduction in esophageal eosinophil infiltration.
4 tion of NMO-IgG and complement showed marked eosinophil infiltration.
5 lammation characterized by TH2 cytokines and eosinophil infiltration.
6 and numbers were negatively correlated with eosinophil infiltration.
7 tly impaired, whereas there was no effect on eosinophil infiltration.
8 n in ear edema, inflammation, mast cell, and eosinophil infiltration.
9 in the reduction of cytokine production and eosinophil infiltration.
10 release from basophil/mast cells and induce eosinophil infiltration.
11 matory reactions and to look for evidence of eosinophil infiltration.
12 symptoms accompanied by a massive pulmonary eosinophil infiltration.
13 emokine genes expressed at stages of massive eosinophil infiltration.
14 lergic airway inflammation, increased airway eosinophil infiltration (24-fold) correlated with secret
17 tion between Th2 cytokine production, tissue eosinophil infiltration and activation, and, importantly
18 e PPD response to a type 2-like pattern with eosinophil infiltration and decreased TNF and RANTES, bu
19 At day 21, 16/16 test mice developed intense eosinophil infiltration and degranulation of the human m
21 athological changes, including inhibition of eosinophil infiltration and excess mucus production in t
23 ivo adduct-sensitized mice exhibited reduced eosinophil infiltration and IL-13 expression in the airw
24 piratory failure, and death, associated with eosinophil infiltration and increased expression of eota
25 ostinfection, mice lacking SP-D have reduced eosinophil infiltration and interleukin-5 (IL-5) in lung
27 es of asthma, including airway inflammation, eosinophil infiltration and non-specific bronchial respo
28 during airway allergen challenge, inhibited eosinophil infiltration and prevented the development of
29 ter treatment, preceding the onset of dermal eosinophil infiltration and the development of clinicall
30 mmatory disorder of the esophagus defined by eosinophil infiltration and tissue remodeling with resul
31 vity, T(H)2 responses, mucus hypersecretion, eosinophil infiltration, and collagen deposition were no
32 cell, macrophage-like mononuclear cell, and eosinophil infiltration, and elevation of total serum Ig
33 ons exhibit epidermal and dermal thickening, eosinophil infiltration, and increased levels of the cys
34 markedly reduced epidermal thickening, lower eosinophil infiltration, and lower serum IgE levels comp
35 the gut microbiome induced IL-33, subsequent eosinophil infiltration, and mounting of Th2 immune resp
36 have drastically reduced lung inflammation, eosinophil infiltration, and mucous production following
37 ity to aerosolized methacholine, lung tissue eosinophil infiltration, and numbers of proliferating ce
38 sed allergen-induced airway hyperreactivity, eosinophil infiltration, and production of pro-inflammat
39 eosinophil-associated chemokines, eotaxins, eosinophil infiltration, and subsequent HILI were unclea
40 onist decreases significantly lymphocyte and eosinophil infiltration as well as mRNA expression of eo
41 ng on the underlying disease and mechanisms, eosinophil infiltration can lead to organ dysfunction, c
42 hibited increased lung ILC counts and tissue eosinophil infiltration compared with values in lean mic
44 tures of asthma such as airway constriction, eosinophil infiltration, edema, and mucus accumulation.
45 n-challenged null mice showed increased lung eosinophil infiltration, enhanced bone marrow and blood
46 Such metabolic improvements are mediated by eosinophil infiltration, enhanced type 2 cytokine signal
47 cytokine-associated disease characterized by eosinophil infiltration, epithelial cell hyperplasia, an
48 ced pulmonary inflammation, characterized by eosinophil infiltration, goblet cell hyperplasia with mu
50 F and lung immunohistology demonstrated that eosinophil infiltration in OVA-challenged Gal-3 KO mice
51 verall clinical findings appear to implicate eosinophil infiltration in proximal and distal dysmotili
53 ever, only perforin-sufficient CTL inhibited eosinophil infiltration in the airway, mucus production,
56 IgE, increased Th2 cytokine production, and eosinophil infiltration in the stomach-draining lymph no
57 tures of allergic disease, including AHR and eosinophil infiltration, in uninfected OVA-sensitized/ch
58 irway damage in asthmatic mice by decreasing eosinophil infiltration, inhibiting chemokines/cytokines
59 i-T1/ST2 monoclonal antibody (mAb) inhibited eosinophil infiltration, interleukin 5 secretion, and Ig
60 antibody treatment can effectively decrease eosinophil infiltration into hamster cutaneous healing w
61 ngly, DRD3 deficiency results in exacerbated eosinophil infiltration into the airways of mice undergo
62 and challenge increased ocular symptoms and eosinophil infiltration into the conjunctiva over PBS co
67 ,696 correlated with up to a 97% decrease in eosinophil infiltration into the lower spinal cord as de
68 as shown by a clear inhibition of T cell and eosinophil infiltration into the lung tissue and airways
69 of 5 mg/kg Sephadex caused a time-dependent eosinophil infiltration into the lung, reaching a peak a
75 h included a significant reduction in airway eosinophil infiltration, mucus hypersecretion, and airwa
76 itor, PNRI-299, significantly reduced airway eosinophil infiltration, mucus hypersecretion, edema, an
77 montelukast significantly reduced the airway eosinophil infiltration, mucus plugging, smooth muscle h
78 pithelium were intensely immunoreactive, and eosinophil infiltration occurred at sites of eotaxin upr
80 ly, Th2 responses including, IgE production, eosinophil infiltration of the airway, subepithelial fib
81 on of a T helper 2-type cytokine response or eosinophil infiltration of the airways after allergic se
82 Airway sensitization was associated with eosinophil infiltration of the airways and increased pro
83 is an inflammatory disease characterized by eosinophil infiltration of the airways, actions of beta-
84 nable to develop airway hyperresponsiveness, eosinophil infiltration of the lung parenchyma, or IL-5
86 obstruction by approximately 50%, inhibited eosinophil infiltration, reduced BALF concentrations of
87 a mechanism involving eotaxin to explain the eosinophil infiltration seen in a variety of human disea
88 racterized by increased CCL11 production and eosinophil infiltration such as Hodgkin's lymphoma, nasa
89 ls of airway hyperreactivity and lung tissue eosinophil infiltration that were similar to those of th
90 CR1 deficiency did not inhibit neutrophil or eosinophil infiltration to the cornea or development of
91 hase pulmonary inflammation, blocking airway eosinophil infiltration, VCAM-1 expression, and mucus hy
93 nocyte, lymphocyte, and, to a lesser degree, eosinophil infiltration was observed, peaking at 10-24 h
94 ic asthma is characterized mainly by massive eosinophil infiltration, which induces airway injury and
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