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1 t cell hyperplasia, collagen deposition, and peribronchial accumulation of contractile tissue.
2 veloping lung, this process is stimulated by peribronchial accumulation of laminin (LN)-2.
3  and migration, in turn resulting in chronic peribronchial airway inflammation and goblet cell metapl
4  associated with airway hyperresponsiveness, peribronchial allergic inflammation, and goblet cell hyp
5                         A major reduction in peribronchial and airway eosinophilia was observed in CC
6 ungs but less so in St3gal3 mutants, whereas peribronchial and BALF eosinophil numbers were greater i
7                                              Peribronchial and bronchoalveolar lavage eosinophils, ke
8 irway eosinophilia, histological evidence of peribronchial and perivascular airway inflammation, clus
9 C10-IL-18-transgenic mice, accumulate mostly peribronchial and perivascular CD274-expressing eosinoph
10               Histological analysis revealed peribronchial and perivascular eosinophilic inflammation
11 issues with dense, B cell (B220(+))-enriched peribronchial and perivascular infiltrates with germinal
12 pulmonary disease (COPD) is characterized by peribronchial and perivascular inflammation and largely
13                                              Peribronchial and perivascular inflammation and mucus pr
14 ory response to the recall Ag, inhibition of peribronchial and perivascular lung inflammation, and in
15                            The proliferative peribronchial and perivascular mesenchymal cells appear
16 ted abnormal histopathology characterized by peribronchial and perivascular mononuclear infiltrates.
17 organized accumulation of eosinophils in the peribronchial and perivascular regions of allergen-chall
18 for 3 days causes a slightly more pronounced peribronchial and perivascular spindle cell proliferatio
19 heal injection in rats causes an increase in peribronchial and perivascular stromal cells on days 2 a
20 olidations and ground-glass opacities in the peribronchial and subpleural areas of both lungs.
21  was associated histologically with enhanced peribronchial and/or perivascular cellularity (score of
22 ere pneumonia characterized by perivascular, peribronchial, and interstitial infiltrates of lymphocyt
23 the role of HIF-1alpha in the development of peribronchial angiogenesis and inflammation in a murine
24            During the development of asthma, peribronchial angiogenesis is induced in response to aer
25 othelial progenitor cells and a reduction of peribronchial angiogenesis.
26 elial fibrosis, smooth muscle thickness, and peribronchial angiogenesis.
27 influx of eosinophils and lymphocytes in the peribronchial area, and severe airway hyperreactivity th
28 n cells extracted from the lungs, and in the peribronchial areas of BALB/c mice passively sensitized
29                 Broncholithiasis occurs when peribronchial calcific nodes produce bronchial obstructi
30 ation-regulated chemokine and the numbers of peribronchial CD4(+) lymphocytes that drive the ongoing
31 egulated chemokine, as well as the number of peribronchial CD4(+) lymphocytes that express Th2 cytoki
32 els of airway mucus, airway eosinophils, and peribronchial CD4+ cells in ovalbumin-challenged mice we
33 aminin alpha1 chain exhibited alterations in peribronchial cell shape and decreased smooth muscle dev
34 resolution of lung eosinophilia, and reduced peribronchial-cell apoptosis.
35                                The number of peribronchial cells expressing TGF-beta1, as well as TGF
36 eosinophils, as well as increased numbers of peribronchial cells expressing TGF-beta1.
37 had a significant reduction in the number of peribronchial cells staining positive for major basic pr
38  had a significant increase in the number of peribronchial cells staining positive for major basic pr
39 with increased airway smooth muscle mass and peribronchial collagen deposition.
40 chial fibrosis (total lung collagen content, peribronchial collagens III and V) and significantly les
41 e in (64)Cu-LLP2A uptake, predominantly in a peribronchial distribution.
42 n = 1) or nodules following perivascular and peribronchial distributions (n = 5).
43 /-) T cells, particularly those derived from peribronchial draining lymph nodes, revealed a dramatic
44 oblet cell hyperplasia, mucus secretion, and peribronchial edema and also inhibited the release of IL
45 -18 was instilled, a significant increase in peribronchial eosinophil accumulation was observed in al
46 cantly attenuated airway hyperreactivity and peribronchial eosinophil accumulation, and significantly
47 , or leukotriene levels at 24 hours although peribronchial eosinophilia was significantly reduced.
48        Furthermore, chemokine production and peribronchial eosinophilia were not restored during the
49 ignificantly reduced airway hyperreactivity, peribronchial eosinophilia, and the overall inflammatory
50 Experimental ABPA was associated with severe peribronchial eosinophilia, bronchial hyperresponsivenes
51 y hyperresponsiveness (AHR) to methacholine, peribronchial eosinophilic and lymphocytic inflammation,
52 thacholine (MCh), and histologic evidence of peribronchial eosinophilic infiltration and mucoid cell
53 lec-F Ab had significantly reduced levels of peribronchial eosinophilic inflammation and significantl
54  allergen-induced airway hyperreactivity and peribronchial eosinophilic inflammation in a murine mode
55 okine resulted in a dramatic accumulation of peribronchial eosinophils and striking pathologic change
56 ecreases in airway hyperreactivity (AHR) and peribronchial eosinophils compared with wild-type contro
57  number of CD274-expressing perivascular and peribronchial eosinophils with induced collagen, goblet
58 ich was associated with increased numbers of peribronchial eosinophils, as well as increased numbers
59                    We identify and implicate peribronchial fibroblasts in lung disease.
60 e challenged with OVA had significantly less peribronchial fibrosis (total lung collagen content and
61   IL-5-deficient mice had significantly less peribronchial fibrosis (total lung collagen content, per
62                                              Peribronchial fibrosis and goblet cell hyperplasia were
63 , established by the presence of pleural and peribronchial fibrosis and impaired lung mechanics deter
64 llergen-induced airway remodeling, including peribronchial fibrosis and mucus production.
65 yperreactivity, goblet cell hyperplasia, and peribronchial fibrosis at day 28 after conidia.
66 ed airway hyperreactivity, eosinophilia, and peribronchial fibrosis compared with nonsensitized mice
67 After 11 challenges, airway eosinophilia and peribronchial fibrosis further declined and the cytokine
68 lial cells, resulting in significantly lower peribronchial fibrosis in CC10-Cre(tg)/Ikkbeta(delta/del
69               Airway hyperresponsiveness and peribronchial fibrosis in Stat6-/- mice were significant
70 bolished airway hyperresponsiveness, but not peribronchial fibrosis in Stat6-/- mice.
71  of airway remodelling (mucus metaplasia and peribronchial fibrosis).
72 , squamous metaplasia, chronic inflammation, peribronchial fibrosis, and bullous disease were assesse
73  hyperresponsiveness, mucus cell metaplasia, peribronchial fibrosis, and fungus retention were marked
74 to naive WT mice led to airway eosinophilia, peribronchial fibrosis, and increased thickness of the a
75 trophy and hyperplasia, airway inflammation, peribronchial fibrosis, and increases in bronchial lymph
76 g eosinophilia, goblet cell metaplasia, mild peribronchial fibrosis, and peribronchial smooth muscle
77 ls were counted; and goblet cell metaplasia, peribronchial fibrosis, and smooth muscle hypertrophy we
78 erstitial fibrosis, goblet cell hyperplasia, peribronchial fibrosis, and vascular sclerosis.
79 eatures, such as goblet cell hyperplasia and peribronchial fibrosis, compared with CCR5+/+ mice at th
80 lergen had significantly increased levels of peribronchial fibrosis, increased thickening of the smoo
81 atically altered airway structure and caused peribronchial fibrosis, resulting in airway hyperreactiv
82 pulmonary disease (COPD) is characterized by peribronchial fibrosis.
83 iator was associated with the development of peribronchial fibrosis.
84 rized by diffuse alveolar damage with marked peribronchial fibrosis.
85 reated mice contributed to reduced levels of peribronchial fibrosis.
86 ytes that express Th2 cytokines that promote peribronchial fibrosis.
87  but not in term infants, which may indicate peribronchial fluid or overdistension of compliant lung
88 onstitutively expressed in the epithelium of peribronchial glands and conducting airways in normal lu
89 significant immediate changes manifesting as peribronchial ground glass opacities, consolidations, ai
90  with invasive hyphal elements and a compact peribronchial infiltrate of predominantly polymorphonucl
91            In lung tissue, we observed large peribronchial infiltrates with T and B cells in close co
92 ical analysis of the lungs revealed a marked peribronchial infiltration of eosinophils, but no eosino
93 with the histologic development of a patchy, peribronchial infiltration of mononuclear and polymorpho
94 ion of CCL18 led to massive perivascular and peribronchial infiltration of T lymphocytes.
95  P- and E-selectin contribute to CRA-induced peribronchial inflammation and airway hyperreactivity.
96  the role of selectins in the development of peribronchial inflammation and airway hyperreactivity.
97  role in the development of allergen-induced peribronchial inflammation and airway hyperreactivity.
98  conidia challenge significantly reduced the peribronchial inflammation and airway hyperresponsivenes
99                 This resulted in spontaneous peribronchial inflammation and led to a systemic and loc
100 al surface proteins, specifically E, induced peribronchial inflammation and pulmonary vasculitis in a
101 s in airway Th2 cytokines, eosinophilia, and peribronchial inflammation compared with IL-33 alone.
102                                              Peribronchial inflammation contributes to the pathophysi
103                                  A score for peribronchial inflammation in lung histology was used.
104 let cell hyperplasia and markedly diminished peribronchial inflammation in Stat6-/- mice in contrast
105  and brain, and protection from alveolar and peribronchial inflammation in the lung, thereby limiting
106 istologic evidence for both perivascular and peribronchial inflammation in the lungs, increased tissu
107 age, and it is likely due to the preexisting peribronchial inflammation present at the time of the se
108 erum OVA-specific IgE (P = 0.035), and lower peribronchial inflammation score (P < 0.0001) than nontr
109 70-85% reductions in airway hyperreactivity, peribronchial inflammation, and eosinophil accumulation.
110 nt, because TLR9(-/-) mice displayed reduced peribronchial inflammation, decreased accumulation and/o
111 a is dependent, in part, on the intensity of peribronchial inflammation.
112 amster infection with wt Ad14 caused minimal peribronchial inflammation.
113 ation leads to local Th2 cell activation and peribronchial inflammation.
114 el of ovalbumin (OVA)-induced asthma that 1) peribronchial inflammatory cells expressed large amounts
115 ited histopathological changes consisting of peribronchial inflammatory infiltrates.
116  IL-4-secreting cells, elevated perivascular/peribronchial inflammatory responses in the lung, and gr
117 d leukocytic infiltrates in the alveolar and peribronchial interstitial spaces that were consistent w
118                                 In contrast, peribronchial, intrapulmonary, Peyer's patch, and spleni
119 rgic airway inflammation is characterized by peribronchial leukocyte accumulation within the airway.
120 d inflammatory injury, as evidenced by fewer peribronchial leukocytes, significantly less protein in
121 e same interactions occurred in the draining peribronchial LN.
122                              In the draining peribronchial LNs, small numbers of beads were present i
123 s recently emerged as a therapy for treating peribronchial lung cancers.
124             Most interestingly, the level of peribronchial lung tissue eosinophils in IL-13-treated e
125 g trafficking in the mouse lung and draining peribronchial lymph node (LN).
126 d, and in vitro, following Ag stimulation of peribronchial lymph node (PBLN) cells in culture.
127 IgE serum levels, Th2 cytokine production by peribronchial lymph node (PBLN) cells, increased numbers
128 ive response of spleen mononuclear cells and peribronchial lymph node cells demonstrated that the res
129 ominant production of Th-1-type cytokines in peribronchial lymph node cells in vitro.
130 ction of interleukin-5 (IL-5) in cultures of peribronchial lymph node cells.
131 s, T lymphocytes, or CD4 or CD8 T cells from peribronchial lymph nodes (PBLN) of RSV-infected mice we
132 ease in T cells and a decrease in B cells in peribronchial lymph nodes and in spleens of immunized CD
133 accelerated migration of RDC to the draining peribronchial lymph nodes occurs only during the first 2
134            Migration of BLT1(-/-) BMDCs into peribronchial lymph nodes was significantly impaired com
135 ma, IL-4, and IL-5 by mononuclear cells from peribronchial lymph nodes were monitored.
136 ile at late times they appeared healthy with peribronchial lymphoid aggregates.
137 lec-F Ab significantly reduced the number of peribronchial major basic protein(+)/TGF-beta(+) cells,
138 most common finding in group 1 was prominent peribronchial markings with hyperinflation (n = 17), whe
139 n normal, but they may demonstrate prominent peribronchial markings with hyperinflation.
140 hyma and airways were evaluated for pattern (peribronchial markings, consolidation, and ground-glass,
141 acute OVA challenge, have an accumulation of peribronchial mast cells and express increased levels of
142  significantly inhibited the accumulation of peribronchial mast cells and the expression of IL-4 and
143                                          Few peribronchial mast cells are noted either in the lungs o
144 suggesting that ISS inhibits accumulation of peribronchial mast cells in vivo by indirect mechanism(s
145                         This accumulation of peribronchial mast cells is associated with increased ex
146 or 1-6 mo have a significant accumulation of peribronchial mast cells.
147 XF1 crosstalk and expansion of this specific peribronchial MC population in chronically rejecting fib
148 ory distress, and the pathologic findings of peribronchial mononuclear cell infiltration and release
149 on with RSV is characterized by a pronounced peribronchial mononuclear infiltrate, with eosinophilic
150 oblasts in vivo, we determined the number of peribronchial myofibroblasts (Col-1(+) and alpha-smooth
151 was a significant reduction in the number of peribronchial myofibroblasts in OVA-challenged Smad 3-de
152                       Although the number of peribronchial myofibroblasts increased significantly in
153  < 0.05) to methacholine, BAL (p < 0.05) and peribronchial (p < 0.01) eosinophilia, and BAL fluid IL-
154             COPD is characterized by chronic peribronchial, perivascular, and alveolar inflammation.
155  inducible BALT (iBALT), which is located in peribronchial, perivascular, and interstitial areas thro
156 anulomas in Rgs16(-/-) mice, instead forming peribronchial/perivascular aggregates.
157 ha smooth muscle actin-positive cells in the peribronchial region of OB.
158 ment of nodular granulomatous lesions in the peribronchial region or cavitary peripheral disease in s
159 n fibril disorganization was observed in the peribronchial regions of HDM-exposed neonatal mice.
160 role in regulating eosinophil recruitment to peribronchial regions of the lung possibly by coordinate
161 of eosinophils (predominantly located in the peribronchial regions of the lungs), and increased airwa
162 n and HA, especially in the perivascular and peribronchial regions, which were enriched in infiltrati
163 (iEos), which were defined as IL-5-dependent peribronchial Siglec-FhiCD62L-CD101hi cells with a segme
164  collagens III and V) and significantly less peribronchial smooth muscle (thickness of peribronchial
165 metaplasia, mild peribronchial fibrosis, and peribronchial smooth muscle hypertrophy; increased level
166 ss peribronchial smooth muscle (thickness of peribronchial smooth muscle layer, alpha-smooth muscle a
167 richrome staining), reduced thickness of the peribronchial smooth muscle layer, and reduced epithelia
168  of its receptor DR3 restricted increases in peribronchial smooth muscle mass and accumulation of lun
169 helial cell mucus metaplasia, an increase in peribronchial smooth muscle mass, subepithelial fibrosis
170 lial height (EH) and perimeters and areas of peribronchial smooth muscle, epithelium, and subepitheli
171 form for healing of dehiscence and, in time, peribronchial soft tissue grows in to cover the defect,
172 lls adjacent to neurovascular bundles in the peribronchial stroma, and in the wall of the large and s
173    CCR5-/- mice exhibited significantly less peribronchial T-cell and eosinophil accumulation and air
174                                              Peribronchial TE constructs embedded with EPs or ECs lim
175 levels of activin A and increased numbers of peribronchial TGF-beta1(+) cells were detected in WT and
176  subscores for mucous plugging (P = 0.0018), peribronchial thickening (P = 0.0004), or parenchymal in
177                                              Peribronchial thickening was the most common abnormal fi
178 levant structural change in cystic fibrosis) peribronchial thickening, mucous plugging and many other
179 severity of bronchiectasis, mucous plugging, peribronchial thickening, parenchymal anomalies, and air
180  The most common abnormalities were nodules, peribronchial thickening, pleural thickening and bronchi
181 ared with littermate controls as assessed by peribronchial trichrome staining and total lung collagen
182 position (assessed by lung collagen content, peribronchial trichrome staining, and immunostaining wit
183 s with anti-AQP1 demonstrated the protein in peribronchial vessels and visceral pleura at E21 with in

 
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