ライフサイエンスコーパス: peribronchial

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 associated with airway hyperresponsiveness, peribronchial allergic inflammation, and goblet cell hyp

4 A major reduction in peribronchial and airway eosinophilia was observed in CC

5 ungs but less so in St3gal3 mutants, whereas peribronchial and BALF eosinophil numbers were greater i

6 Peribronchial and bronchoalveolar lavage eosinophils, ke

7 irway eosinophilia, histological evidence of peribronchial and perivascular airway inflammation, clus

8 Histological analysis revealed peribronchial and perivascular eosinophilic inflammation

9 issues with dense, B cell (B220(+))-enriched peribronchial and perivascular infiltrates with germinal

10 pulmonary disease (COPD) is characterized by peribronchial and perivascular inflammation and largely

11 Peribronchial and perivascular inflammation and mucus pr

12 ory response to the recall Ag, inhibition of peribronchial and perivascular lung inflammation, and in

13 The proliferative peribronchial and perivascular mesenchymal cells appear

14 ted abnormal histopathology characterized by peribronchial and perivascular mononuclear infiltrates.

15 organized accumulation of eosinophils in the peribronchial and perivascular regions of allergen-chall

16 for 3 days causes a slightly more pronounced peribronchial and perivascular spindle cell proliferatio

17 heal injection in rats causes an increase in peribronchial and perivascular stromal cells on days 2 a

18 was associated histologically with enhanced peribronchial and/or perivascular cellularity (score of

19 ere pneumonia characterized by perivascular, peribronchial, and interstitial infiltrates of lymphocyt

20 the role of HIF-1alpha in the development of peribronchial angiogenesis and inflammation in a murine

21 During the development of asthma, peribronchial angiogenesis is induced in response to aer

22 othelial progenitor cells and a reduction of peribronchial angiogenesis.

23 elial fibrosis, smooth muscle thickness, and peribronchial angiogenesis.

24 influx of eosinophils and lymphocytes in the peribronchial area, and severe airway hyperreactivity th

25 n cells extracted from the lungs, and in the peribronchial areas of BALB/c mice passively sensitized

26 Broncholithiasis occurs when peribronchial calcific nodes produce bronchial obstructi

27 ation-regulated chemokine and the numbers of peribronchial CD4(+) lymphocytes that drive the ongoing

28 egulated chemokine, as well as the number of peribronchial CD4(+) lymphocytes that express Th2 cytoki

29 els of airway mucus, airway eosinophils, and peribronchial CD4+ cells in ovalbumin-challenged mice we

30 aminin alpha1 chain exhibited alterations in peribronchial cell shape and decreased smooth muscle dev

31 resolution of lung eosinophilia, and reduced peribronchial-cell apoptosis.

32 The number of peribronchial cells expressing TGF-beta1, as well as TGF

33 eosinophils, as well as increased numbers of peribronchial cells expressing TGF-beta1.

34 had a significant reduction in the number of peribronchial cells staining positive for major basic pr

35 had a significant increase in the number of peribronchial cells staining positive for major basic pr

36 with increased airway smooth muscle mass and peribronchial collagen deposition.

37 chial fibrosis (total lung collagen content, peribronchial collagens III and V) and significantly les

38 n = 1) or nodules following perivascular and peribronchial distributions (n = 5).

39 /-) T cells, particularly those derived from peribronchial draining lymph nodes, revealed a dramatic

40 oblet cell hyperplasia, mucus secretion, and peribronchial edema and also inhibited the release of IL

41 -18 was instilled, a significant increase in peribronchial eosinophil accumulation was observed in al

42 cantly attenuated airway hyperreactivity and peribronchial eosinophil accumulation, and significantly

43 , or leukotriene levels at 24 hours although peribronchial eosinophilia was significantly reduced.

44 Furthermore, chemokine production and peribronchial eosinophilia were not restored during the

45 ignificantly reduced airway hyperreactivity, peribronchial eosinophilia, and the overall inflammatory

46 Experimental ABPA was associated with severe peribronchial eosinophilia, bronchial hyperresponsivenes

47 y hyperresponsiveness (AHR) to methacholine, peribronchial eosinophilic and lymphocytic inflammation,

48 thacholine (MCh), and histologic evidence of peribronchial eosinophilic infiltration and mucoid cell

49 lec-F Ab had significantly reduced levels of peribronchial eosinophilic inflammation and significantl

50 allergen-induced airway hyperreactivity and peribronchial eosinophilic inflammation in a murine mode

51 okine resulted in a dramatic accumulation of peribronchial eosinophils and striking pathologic change

52 ecreases in airway hyperreactivity (AHR) and peribronchial eosinophils compared with wild-type contro

53 ich was associated with increased numbers of peribronchial eosinophils, as well as increased numbers

54 e challenged with OVA had significantly less peribronchial fibrosis (total lung collagen content and

55 IL-5-deficient mice had significantly less peribronchial fibrosis (total lung collagen content, per

56 Peribronchial fibrosis and goblet cell hyperplasia were

57 , established by the presence of pleural and peribronchial fibrosis and impaired lung mechanics deter

58 llergen-induced airway remodeling, including peribronchial fibrosis and mucus production.

59 yperreactivity, goblet cell hyperplasia, and peribronchial fibrosis at day 28 after conidia.

60 ed airway hyperreactivity, eosinophilia, and peribronchial fibrosis compared with nonsensitized mice

61 After 11 challenges, airway eosinophilia and peribronchial fibrosis further declined and the cytokine

62 lial cells, resulting in significantly lower peribronchial fibrosis in CC10-Cre(tg)/Ikkbeta(delta/del

63 Airway hyperresponsiveness and peribronchial fibrosis in Stat6-/- mice were significant

64 bolished airway hyperresponsiveness, but not peribronchial fibrosis in Stat6-/- mice.

65 of airway remodelling (mucus metaplasia and peribronchial fibrosis).

66 , squamous metaplasia, chronic inflammation, peribronchial fibrosis, and bullous disease were assesse

67 hyperresponsiveness, mucus cell metaplasia, peribronchial fibrosis, and fungus retention were marked

68 to naive WT mice led to airway eosinophilia, peribronchial fibrosis, and increased thickness of the a

69 trophy and hyperplasia, airway inflammation, peribronchial fibrosis, and increases in bronchial lymph

70 g eosinophilia, goblet cell metaplasia, mild peribronchial fibrosis, and peribronchial smooth muscle

71 ls were counted; and goblet cell metaplasia, peribronchial fibrosis, and smooth muscle hypertrophy we

72 erstitial fibrosis, goblet cell hyperplasia, peribronchial fibrosis, and vascular sclerosis.

73 eatures, such as goblet cell hyperplasia and peribronchial fibrosis, compared with CCR5+/+ mice at th

74 lergen had significantly increased levels of peribronchial fibrosis, increased thickening of the smoo

75 atically altered airway structure and caused peribronchial fibrosis, resulting in airway hyperreactiv

76 rized by diffuse alveolar damage with marked peribronchial fibrosis.

77 reated mice contributed to reduced levels of peribronchial fibrosis.

78 pulmonary disease (COPD) is characterized by peribronchial fibrosis.

79 ytes that express Th2 cytokines that promote peribronchial fibrosis.

80 but not in term infants, which may indicate peribronchial fluid or overdistension of compliant lung

81 onstitutively expressed in the epithelium of peribronchial glands and conducting airways in normal lu

82 with invasive hyphal elements and a compact peribronchial infiltrate of predominantly polymorphonucl

83 ical analysis of the lungs revealed a marked peribronchial infiltration of eosinophils, but no eosino

84 with the histologic development of a patchy, peribronchial infiltration of mononuclear and polymorpho

85 ion of CCL18 led to massive perivascular and peribronchial infiltration of T lymphocytes.

86 P- and E-selectin contribute to CRA-induced peribronchial inflammation and airway hyperreactivity.

87 the role of selectins in the development of peribronchial inflammation and airway hyperreactivity.

88 role in the development of allergen-induced peribronchial inflammation and airway hyperreactivity.

89 conidia challenge significantly reduced the peribronchial inflammation and airway hyperresponsivenes

90 s in airway Th2 cytokines, eosinophilia, and peribronchial inflammation compared with IL-33 alone.

91 Peribronchial inflammation contributes to the pathophysi

92 A score for peribronchial inflammation in lung histology was used.

93 let cell hyperplasia and markedly diminished peribronchial inflammation in Stat6-/- mice in contrast

94 istologic evidence for both perivascular and peribronchial inflammation in the lungs, increased tissu

95 age, and it is likely due to the preexisting peribronchial inflammation present at the time of the se

96 erum OVA-specific IgE (P = 0.035), and lower peribronchial inflammation score (P < 0.0001) than nontr

97 70-85% reductions in airway hyperreactivity, peribronchial inflammation, and eosinophil accumulation.

98 nt, because TLR9(-/-) mice displayed reduced peribronchial inflammation, decreased accumulation and/o

99 a is dependent, in part, on the intensity of peribronchial inflammation.

100 amster infection with wt Ad14 caused minimal peribronchial inflammation.

101 el of ovalbumin (OVA)-induced asthma that 1) peribronchial inflammatory cells expressed large amounts

102 ited histopathological changes consisting of peribronchial inflammatory infiltrates.

103 IL-4-secreting cells, elevated perivascular/peribronchial inflammatory responses in the lung, and gr

104 d leukocytic infiltrates in the alveolar and peribronchial interstitial spaces that were consistent w

105 In contrast, peribronchial, intrapulmonary, Peyer's patch, and spleni

106 rgic airway inflammation is characterized by peribronchial leukocyte accumulation within the airway.

107 d inflammatory injury, as evidenced by fewer peribronchial leukocytes, significantly less protein in

108 e same interactions occurred in the draining peribronchial LN.

109 In the draining peribronchial LNs, small numbers of beads were present i

110 Most interestingly, the level of peribronchial lung tissue eosinophils in IL-13-treated e

111 g trafficking in the mouse lung and draining peribronchial lymph node (LN).

112 d, and in vitro, following Ag stimulation of peribronchial lymph node (PBLN) cells in culture.

113 IgE serum levels, Th2 cytokine production by peribronchial lymph node (PBLN) cells, increased numbers

114 ive response of spleen mononuclear cells and peribronchial lymph node cells demonstrated that the res

115 ominant production of Th-1-type cytokines in peribronchial lymph node cells in vitro.

116 ction of interleukin-5 (IL-5) in cultures of peribronchial lymph node cells.

117 s, T lymphocytes, or CD4 or CD8 T cells from peribronchial lymph nodes (PBLN) of RSV-infected mice we

118 ease in T cells and a decrease in B cells in peribronchial lymph nodes and in spleens of immunized CD

119 accelerated migration of RDC to the draining peribronchial lymph nodes occurs only during the first 2

120 Migration of BLT1(-/-) BMDCs into peribronchial lymph nodes was significantly impaired com

121 ma, IL-4, and IL-5 by mononuclear cells from peribronchial lymph nodes were monitored.

122 ile at late times they appeared healthy with peribronchial lymphoid aggregates.

123 lec-F Ab significantly reduced the number of peribronchial major basic protein(+)/TGF-beta(+) cells,

124 most common finding in group 1 was prominent peribronchial markings with hyperinflation (n = 17), whe

125 n normal, but they may demonstrate prominent peribronchial markings with hyperinflation.

126 hyma and airways were evaluated for pattern (peribronchial markings, consolidation, and ground-glass,

127 acute OVA challenge, have an accumulation of peribronchial mast cells and express increased levels of

128 significantly inhibited the accumulation of peribronchial mast cells and the expression of IL-4 and

129 Few peribronchial mast cells are noted either in the lungs o

130 suggesting that ISS inhibits accumulation of peribronchial mast cells in vivo by indirect mechanism(s

131 This accumulation of peribronchial mast cells is associated with increased ex

132 or 1-6 mo have a significant accumulation of peribronchial mast cells.

133 ory distress, and the pathologic findings of peribronchial mononuclear cell infiltration and release

134 on with RSV is characterized by a pronounced peribronchial mononuclear infiltrate, with eosinophilic

135 oblasts in vivo, we determined the number of peribronchial myofibroblasts (Col-1(+) and alpha-smooth

136 was a significant reduction in the number of peribronchial myofibroblasts in OVA-challenged Smad 3-de

137 Although the number of peribronchial myofibroblasts increased significantly in

138 < 0.05) to methacholine, BAL (p < 0.05) and peribronchial (p < 0.01) eosinophilia, and BAL fluid IL-

139 COPD is characterized by chronic peribronchial, perivascular, and alveolar inflammation.

140 inducible BALT (iBALT), which is located in peribronchial, perivascular, and interstitial areas thro

141 anulomas in Rgs16(-/-) mice, instead forming peribronchial/perivascular aggregates.

142 ha smooth muscle actin-positive cells in the peribronchial region of OB.

143 ment of nodular granulomatous lesions in the peribronchial region or cavitary peripheral disease in s

144 role in regulating eosinophil recruitment to peribronchial regions of the lung possibly by coordinate

145 of eosinophils (predominantly located in the peribronchial regions of the lungs), and increased airwa

146 n and HA, especially in the perivascular and peribronchial regions, which were enriched in infiltrati

147 (iEos), which were defined as IL-5-dependent peribronchial Siglec-FhiCD62L-CD101hi cells with a segme

148 collagens III and V) and significantly less peribronchial smooth muscle (thickness of peribronchial

149 metaplasia, mild peribronchial fibrosis, and peribronchial smooth muscle hypertrophy; increased level

150 ss peribronchial smooth muscle (thickness of peribronchial smooth muscle layer, alpha-smooth muscle a

151 richrome staining), reduced thickness of the peribronchial smooth muscle layer, and reduced epithelia

152 helial cell mucus metaplasia, an increase in peribronchial smooth muscle mass, subepithelial fibrosis

153 lial height (EH) and perimeters and areas of peribronchial smooth muscle, epithelium, and subepitheli

154 form for healing of dehiscence and, in time, peribronchial soft tissue grows in to cover the defect,

155 lls adjacent to neurovascular bundles in the peribronchial stroma, and in the wall of the large and s

156 CCR5-/- mice exhibited significantly less peribronchial T-cell and eosinophil accumulation and air

157 Peribronchial TE constructs embedded with EPs or ECs lim

158 levels of activin A and increased numbers of peribronchial TGF-beta1(+) cells were detected in WT and

159 levant structural change in cystic fibrosis) peribronchial thickening, mucous plugging and many other

160 The most common abnormalities were nodules, peribronchial thickening, pleural thickening and bronchi

161 ared with littermate controls as assessed by peribronchial trichrome staining and total lung collagen

162 position (assessed by lung collagen content, peribronchial trichrome staining, and immunostaining wit

163 s with anti-AQP1 demonstrated the protein in peribronchial vessels and visceral pleura at E21 with in