ライフサイエンスコーパス: pulmonary eosinophilia

1 uction, however, it significantly suppressed pulmonary eosinophilia.

2 ed Ag-induced airway hyperresponsiveness and pulmonary eosinophilia.

3 llular adhesion molecule-1 failed to develop pulmonary eosinophilia.

4 o induce the expression of eotaxin and cause pulmonary eosinophilia.

5 of IL-4, IL-5, IL-13, eotaxin-1 (CCL11), and pulmonary eosinophilia.

6 ts in diminished systemic disease as well as pulmonary eosinophilia.

7 the ability to inhibit RSV vaccine-enhanced pulmonary eosinophilia.

8 sociated with type 2 cytokine production and pulmonary eosinophilia.

9 had little impact on cytokine production or pulmonary eosinophilia.

10 lveolar lavage fluid (BALF) eosinophilia and pulmonary eosinophilia.

11 DNA vaccines were capable of sensitizing for pulmonary eosinophilia.

12 a severe asthmatic response termed tropical pulmonary eosinophilia.

13 s of human disease, including peripheral and pulmonary eosinophilia.

14 keyhole limpet hemocyanin showed significant pulmonary eosinophilia (39.5%) after challenge with live

15 Pulmonary eosinophilia, a hallmark pathologic feature of

16 gamma secreting spleen cells did not exhibit pulmonary eosinophilia after challenge.

17 and the CD4(+) T cell-mediated induction of pulmonary eosinophilia after live RSV challenge.

18 ) protein fail to inhibit the development of pulmonary eosinophilia after RSV challenge of mice previ

19 RSV attachment (G) protein develop extensive pulmonary eosinophilia after RSV challenge that mimics t

20 s secreted interleukin-5, and mice developed pulmonary eosinophilia after RSV challenge.

21 uced IL-5, IL-13, and eotaxin production and pulmonary eosinophilia after RSV challenge.

22 y RSV-specific CD8 T cell response abrogates pulmonary eosinophilia after subsequent RSV challenge.

23 nced enhanced respiratory disease, including pulmonary eosinophilia, after contracting a natural RSV

24 responsiveness correlated significantly with pulmonary eosinophilia among strains (r > 0.70, p < 0.00

25 of interleukin-5 (IL-5) in helminth-induced pulmonary eosinophilia and AHR.

26 roach inhibits both Ag- and Th2-cell-induced pulmonary eosinophilia and airway hyperreactivity.

27 h purified cockroach allergen, which induced pulmonary eosinophilia and airway hyperreactivity.

28 ecombinant interleukin-12 (IL-12) suppresses pulmonary eosinophilia and airway hyperresponsiveness (A

29 IL-5-overexpressing mice have increased pulmonary eosinophilia and are more susceptible to C. ne

30 e may have contributed to the development of pulmonary eosinophilia and augmented disease that occurr

31 of the ptges(-/-) lungs and sharply reduces pulmonary eosinophilia and basal secretion of MC product

32 e attachment (G) protein sensitizes mice for pulmonary eosinophilia and because Th2 cells are central

33 mmune response to C. neoformans by promoting pulmonary eosinophilia and by inhibiting the activation

34 the effect of an anti-CD3 mAb on Ag-induced pulmonary eosinophilia and correlated this with the expr

35 an directly induce IL-5 and IL-13, producing pulmonary eosinophilia and enhanced illness in RSV-chall

36 nd neutrophils, whereas mm IL-33 also caused pulmonary eosinophilia and goblet cell hyperplasia and i

37 for 10 consecutive d (20 min/d), as well as pulmonary eosinophilia and goblet cell metaplasia.

38 hanced pulmonary disease is characterized by pulmonary eosinophilia and is associated with a substant

39 The HLA-DQ transgenic mice developed pulmonary eosinophilia and lung tissue damage.

40 icant reduction in serum IgE levels, reduced pulmonary eosinophilia and peri-bronchiolar collagen dep

41 eficient ptges(-/-) mice develop exaggerated pulmonary eosinophilia and pulmonary arteriolar smooth-m

42 evels using ADA enzyme therapy decreased the pulmonary eosinophilia and resolved many of the lung his

43 The role of IL-5 in promoting the pulmonary eosinophilia and subsequent inflammatory damag

44 e of CCR8 does not affect the development of pulmonary eosinophilia and Th2 cytokine responses.

45 We now demonstrate that both pulmonary eosinophilia and vascular remodeling in the se

46 ice (increased IL-4, IL-5, and IL-10 levels, pulmonary eosinophilia, and decreased clearance).

47 allergen-induced airway hyperresponsiveness, pulmonary eosinophilia, and elevations in serum IgG1 and

48 cantly increased airway hyperresponsiveness, pulmonary eosinophilia, and enhanced chemokine and Th2 c

49 lating levels of total and OVA-specific IgE, pulmonary eosinophilia, and expression of IL-4, IL-5, an

50 oughing up thick mucus plugs, peripheral and pulmonary eosinophilia, and increased total serum IgE an

51 development of Th2 responses (elevated IgE, pulmonary eosinophilia, and lung cytokine levels of IL-4

52 nificant increases in airway responsiveness, pulmonary eosinophilia, and pulmonary Th2 cytokine expre

53 VAD reduced serum IgE and IgG1 responses, pulmonary eosinophilia, and the levels of IL-4 and IL-5

54 IL-5(-/-) mice did not induce peripheral or pulmonary eosinophilia, and these mice failed to show AH

55 Consistent with the pulmonary eosinophilia, anti-TNF-alpha-treated mice exhi

56 vaccination, SP appears to markedly enhance pulmonary eosinophilia as well as increase polymorphonuc

57 Anti-TNF-alpha-treated mice developed a pulmonary eosinophilia at day 14 postinfection.

58 is results in type 2 cytokine production and pulmonary eosinophilia, both hallmarks of vaccine-enhanc

59 aCD45 decreases allergen-induced pulmonary eosinophilia, bronchoalveolar lavage IL-13, Ig

60 This reduction in pulmonary eosinophilia correlated with the suppression o

61 in CCR2-/- mice was characterized by chronic pulmonary eosinophilia, crystal deposition in the lungs,

62 neutrophilia but resulted in ablation of the pulmonary eosinophilia, despite continued production of

63 eased neutrophil and macrophage numbers, and pulmonary eosinophilia did not develop.

64 Known causes of pulmonary eosinophilia (eg, drug exposures or parasitic

65 This strategy resulted in a pulmonary eosinophilia equivalent to that observed in OV

66 n of allergic inflammation and showed little pulmonary eosinophilia, few airway TH2 cells, and no ris

67 vaccine led to exacerbated disease including pulmonary eosinophilia following a natural RSV infection

68 the mm IL-33-induced Th2-associated effects (pulmonary eosinophilia, goblet cell hyperplasia, and inc

69 The IL-4/IL-13 deletion prevented pulmonary eosinophilia, goblet cell metaplasia in the ai

70 These studies show that pulmonary eosinophilia has dual outcomes: one linked to

71 nflammation are invariably associated with a pulmonary eosinophilia; however, this association has re

72 h, in turn, is required for allergen-induced pulmonary eosinophilia, identifying a novel pathway of e

73 lter the levels of vvGs-induced IL-5, IL-13, pulmonary eosinophilia, illness, or RSV titers upon RSV

74 ly heightened airway hyperresponsiveness and pulmonary eosinophilia in allergen-sensitized mice.

75 M2(82-90) epitope inhibit the development of pulmonary eosinophilia in either vacvG- or FI-RSV-immuni

76 Interestingly, OVA-induced pulmonary eosinophilia in eotaxin-knockout (Eot-/-) mice

77 The development of pulmonary eosinophilia in formalin-inactivated RSV-vacci

78 Mucosal peptide vaccination reduced pulmonary eosinophilia in mice subsequently immunized wi

79 in vivo depletion of CD4(+) cells abrogated pulmonary eosinophilia in mice vaccinated with the pepti

80 ntagonism attenuates house dust mite-induced pulmonary eosinophilia in mice.

81 h2 cells are known to be necessary to induce pulmonary eosinophilia in RSV-infected BALB/c mice previ

82 The induction of pulmonary eosinophilia in rVV-primed mice was also depen

83 llowing RSV challenge; however, the roles of pulmonary eosinophilia in the antiviral response and in

84 OVA-induced pulmonary eosinophilia in wild-type mice was significant

85 where following challenge there were reduced pulmonary eosinophilia, inflammation, Th2-type cytokine

86 o inflammatory diseases, the role of EBI2 in pulmonary eosinophilia is unknown.

87 ease outcome, focused on the hypothesis that pulmonary eosinophilia linked with allergic respiratory

88 /kg for prednisolone in the Sephadex-induced pulmonary eosinophilia model and an ED(50) = 15 mg/kg vs

89 found in D10-transferred mice, the levels of pulmonary eosinophilia, mucus goblet cells, and airway r

90 ne response: a Th2-shifted cytokine profile, pulmonary eosinophilia, severe lung pathology, elevated

91 57BL/6J x 129/Sv mice had significantly more pulmonary eosinophilia than IgG2a- and IgG3-treated C57B

92 bers (including CD4(+) T cells) and evoked a pulmonary eosinophilia that was associated with an incre

93 lenge) resulted in the development of marked pulmonary eosinophilia that was not seen in mice with an

94 sed a mouse model of OVA (ovalbumin)-induced pulmonary eosinophilia to study the cellular and molecul

95 Tropical pulmonary eosinophilia (TPE) is a severe asthmatic syndr

96 eosinophil-mediated inflammation of tropical pulmonary eosinophilia (TPE), bronchoalveolar lavage (BA

97 e experienced enhanced disease and exhibited pulmonary eosinophilia upon natural RSV infection.

98 the attachment (G) protein of RSV results in pulmonary eosinophilia upon RSV challenge, whereas immun

99 in mammalian cells has been shown to induce pulmonary eosinophilia upon RSV infection in a mouse mod

100 gy, decreased viral clearance, and increased pulmonary eosinophilia upon subsequent RSV challenge.

101 Pulmonary eosinophilia was absent in both IL-4 KO and IL

102 We found that Ag-induced pulmonary eosinophilia was associated with the induction

103 d-type mice, a significantly higher level of pulmonary eosinophilia was found in Ag-sensitized and ch

104 ry CD8 T cells to inhibit the development of pulmonary eosinophilia was largely due to an inadequate

105 ed 7 d after challenge (Day 9), a persistent pulmonary eosinophilia was noted accompanied by minimal

106 Importantly, pulmonary eosinophilia was significantly diminished in B

107 The pulmonary eosinophilia was similar to that induced by a

108 specific role of eotaxin-2 in IL-13-induced pulmonary eosinophilia, we generated eotaxin-2 gene-defi

109 EBI2 ligands and pulmonary eosinophilia were measured in the bronchoalveo

110 e, illness, RSV titers, cytokine levels, and pulmonary eosinophilia were measured.

111 SV) develop a Th2-type cytokine response and pulmonary eosinophilia when challenged with live RSV.

112 rleukin (IL)-4 and IL-5 response and develop pulmonary eosinophilia, whereas mice sensitized to RSV-F

113 chment (G) protein of RSV (vacvG) results in pulmonary eosinophilia, which mimics the response of for

114 tely abrogated granuloma development and the pulmonary eosinophilia, while it simultaneously increase

115 he lungs and spleens and developed extensive pulmonary eosinophilia, while mice sensitized to F glyco

116 imply that successful blockade of Ag-induced pulmonary eosinophilia will require antagonism of multip

117 on Th2-type airways responses with decreased pulmonary eosinophilia without augmenting neutrophilia,