ライフサイエンスコーパス: peribronchiolar

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1 bronchiolar epithelium and mild to moderate peribronchiolar alveolitis.

2 extravasate to orchestrate the formation of peribronchiolar and interstitial lymphohistiocytic granu

3 ly, we had shown that T cells accumulated in peribronchiolar and perivascular areas of lungs soon aft

4 transfer of LT1, but not LT3, caused marked peribronchiolar and perivascular inflammation in isograf

5 rulent SchuS4 strain of Ft engenders intense peribronchiolar and perivascular inflammation, but fails

6 C57BL/6 mice developed a chronic alveolar, peribronchiolar, and perivascular eosinophilia following

7 in situ hybridization in the bronchiolar and peribronchiolar areas and the vascular endothelium after

8 endotoxin) and later in the bronchiolar and peribronchiolar areas and vascular endothelium (1 day af

9 of CRAMP(-/-) mice, DC trafficking into the peribronchiolar areas was diminished.

10 At 3 days, asbestos-induced peribronchiolar cell proliferation in wild-type mice was

11 ulation of PKC-delta has multiple effects on peribronchiolar cell proliferation, proinflammatory and

12 s of distal bronchiolar epithelial cells and peribronchiolar cells incorporating the proliferation ma

13 d bronchoalveolar lavage fluid eosinophilia, peribronchiolar cellular cuffing, and Ig subclass switch

14 cient mice were significantly protected from peribronchiolar collagen deposition and increases in air

15 lly challenged Pin1(-/-) mice showed reduced peribronchiolar collagen deposition compared with wild-t

16 bated airway remodelling, typified by excess peribronchiolar collagen deposition.

17 anges were also seen, mostly in a patchy and peribronchiolar distribution.

18 thickness after fluid administration reflect peribronchiolar edema formation.

19 hickness of the airway wall, consistent with peribronchiolar edema formation.

20 astance parameters, in association will less peribronchiolar fibrosis and decreases in nuclear RelB i

21 Peribronchiolar fibrosis is a prominent feature of airwa

22 in inflammation, AHR, mucus metaplasia, and peribronchiolar fibrosis.

23 more lung inflammation with perivascular and peribronchiolar infiltrates compared with controls.

24 veloped dense, pseudo-follicular lymphocytic peribronchiolar infiltrates that resembled the histologi

25 and no change in the amounts of perivascular/peribronchiolar infiltration compared with wild-type-Ad-

26 he major basic protein of eosinophils showed peribronchiolar infiltration of eosinophils.

27 onchoalveolar lavage fluid and caused slight peribronchiolar inflammation in WT mice.

28 ntation and is characterized by a persistent peribronchiolar inflammation that eventually gives way t

29 SPM caused increased T helper 2 cells (Th2), peribronchiolar inflammation, and increased airway mucus

30 rway epithelial thickening, perivascular and peribronchiolar inflammation, and structural airway remo

31 nduced by RSV infection in HIS mice included peribronchiolar inflammation, neutrophil predominance in

32 bronchoalveolar lavage and perivascular and peribronchiolar inflammation.

33 temporal sequence that proceeds from initial peribronchiolar inflammatory lesions to characteristic,

34 During the first 24 hours, severe peribronchiolar injury involving edema, intra-alveolar p

35 evels in cells throughout the lung including peribronchiolar interstitial cells, blood vessels, and c

36 to moderate staining in the early silicotic peribronchiolar lesions.

37 nical syndrome characterized by perivascular/peribronchiolar leukocyte infiltration leading to the de

38 BOS is characterized by persistent peribronchiolar leukocyte recruitment leading to airway

39 expectations, BEC enhanced perivascular and peribronchiolar lung inflammation, mucus metaplasia, NF-

40 ebster mice developed prominent perivascular/peribronchiolar lymphocytic cuffing and well-formed gran

41 n mice; they also had prominent perivascular/peribronchiolar lymphocytic infiltrates not present in t

42 bacteria induced granulomatous lung lesions, peribronchiolar lymphocytosis, increased cell concentrat

43 tected, which was limited almost entirely to peribronchiolar lymphoid aggregates.

44 llergic airways inflammation, an increase in peribronchiolar MCs was associated with increased concen

45 IL-11 transgene (+) animals manifest nodular peribronchiolar mononuclear cell infiltrates and impress

46 ssion of IL-10 and Foxp3 in perivascular and peribronchiolar mononuclear cells, and constitutive prod

47 to adulthood, subepithelial airway fibrosis, peribronchiolar mononuclear nodules, and alveolar enlarg

48 alveoli) and independent (airway remodeling, peribronchiolar nodules) of lung growth and development,

49 the mature lung caused airway remodeling and peribronchiolar nodules, but alveolar enlargement was no

50 lar enlargement without airway remodeling or peribronchiolar nodules.

51 to the alveolar spaces in association with a peribronchiolar organizing pneumonia.

52 ted of hypertrophic alveolar macrophages and peribronchiolar-perivascular monocytic infiltrates.

53 ile duct proliferation, and a nondestructive peribronchiolar pulmonary infiltration.

54 +) T cells are found, including perivascular/peribronchiolar regions and within lymphoid aggregates o

55 total number of infections and perivascular/peribronchiolar rejections were assessed from transplant

56 from BALB/c mice showed PMN accumulation at peribronchiolar sites but no germinating conidia.

57 We further show that FGF9 represses peribronchiolar smooth muscle differentiation and stimul

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