ライフサイエンスコーパス: eosinophil recruitment

1 of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment.

2 other IL-13-mediated mechanisms critical for eosinophil recruitment.

3 s 1 and 2 lesions, with negligible effect on eosinophil recruitment.

4 antibody induced near complete inhibition of eosinophil recruitment.

5 and participate in lymphocyte activation and eosinophil recruitment.

6 in vivo and thereby mediate T cell-dependent eosinophil recruitment.

7 receptors were essential for LTC4 to induce eosinophil recruitment.

8 as epithelial cells, are thought to initiate eosinophil recruitment.

9 oactive intestinal peptide (VIP), CRTH2, and eosinophil recruitment.

10 xpression of VIP in association with intense eosinophil recruitment.

11 creased mucin production and bronchoalveolar eosinophil recruitment.

12 and found that necrotic liver cells induced eosinophil recruitment.

13 ent mice demonstrates an identical defect in eosinophil recruitment.

14 -4-producing Th2 cells in ICOS-/- mice or in eosinophil recruitment.

15 levels, antigen-specific IgG1 response, and eosinophil recruitment.

16 g by regulation of lymphocyte activation and eosinophil recruitment.

17 more effective in blocking allergen-induced eosinophil recruitment.

18 veness to inhaled Ag, despite a reduction in eosinophil recruitment.

19 rotein, G(q), in the regulation of pulmonary eosinophil recruitment.

20 uitment was replaced by augmentation of lung eosinophil recruitment.

21 es the magnitude of the early (but not late) eosinophil recruitment after antigen challenge in models

22 Histologic indices of lung inflammation (eg, eosinophil recruitment, airway and vessel wall thickenin

23 L11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airwa

24 3) has been shown to play a critical role in eosinophil recruitment and airway allergic inflammation

25 uation of cellular mediators associated with eosinophil recruitment and airway remodeling revealed th

26 ion, mice deficient in eotaxin have impaired eosinophil recruitment and are protected from gastromega

27 We demonstrate that aeroallergen-induced eosinophil recruitment and chemokine production were lar

28 s, and injections of anti-IL-5 mAb prevented eosinophil recruitment and crystal deposition but did no

29 ngs suggest a possible role for TNF-alpha in eosinophil recruitment and cytokine expression in this d

30 Lack of GM-CSF also resulted in reduced eosinophil recruitment and delayed recruitment of mononu

31 Eosinophil recruitment and enhanced nitric oxide (NO) pr

32 Eosinophil recruitment and enhanced production of NO are

33 nary fibrosis via induction of IL-5-mediated eosinophil recruitment and fibrogenic cytokine productio

34 ion through IL-17-independent suppression of eosinophil recruitment and IL-17-dependent regulation of

35 Eosinophil recruitment and inhibition of fungal clearanc

36 ice, lead us to suggest that deficiencies in eosinophil recruitment and isotype switching to IgE prod

37 The potent inhibitory effects on eosinophil recruitment and late-phase inflammation sugge

38 odulated ongoing AHRs considerably, reducing eosinophil recruitment and methacholine responsiveness,

39 Eosinophil recruitment and mucus hypersecretion are char

40 istration of IL-5 restored the impairment of eosinophil recruitment and mucus production in OVA-chall

41 A2BAR exhibited decreased M2 macrophage and eosinophil recruitment and reduced IL-4 and IL-13 cytoki

42 ethasone, which has been reported to inhibit eosinophil recruitment and shrink GBM lesions on contras

43 However, the kinetics of eosinophil recruitment and the development of AHR are no

44 re of chitin in germinating conidia promotes eosinophil recruitment and ultimately induces Th2-skewed

45 of chemokine-, IL-13-, and allergen-induced eosinophil recruitment and, conversely, neutralization o

46 o orally available drugs aimed at preventing eosinophil recruitment and, hence, the pathogenesis asso

47 cient mice ( approximately 75% inhibition of eosinophil recruitment) and ICAM-1-deficient mice ( appr

48 nteract to increase Th2 cytokine production, eosinophil recruitment, and airway hyperresponsiveness i

49 creased Th2 cytokine production, IgE levels, eosinophil recruitment, and airway mucus, demonstrating

50 secreting cells, diminished allergen-induced eosinophil recruitment, and decreased the number of ragw

51 cludes macrophage activation, neutrophil and eosinophil recruitment, and elevated KC, TNF-alpha, and

52 ling on proinflammatory cytokine production, eosinophil recruitment, and hepatocellular apoptosis.

53 otype, including airway hyperresponsiveness, eosinophil recruitment, and mucus overproduction.

54 reatment efficacy was assessed by evaluating eosinophil recruitment, antibody, and cytokine productio

55 Such impairment of eosinophil recruitment appeared to take place after IgE

56 Since the molecular mechanisms controlling eosinophil recruitment are incompletely understood, we p

57 ary and sufficient chemokine responsible for eosinophil recruitment around TEBs.

58 current with a restoration of macrophage and eosinophil recruitment around the growing ducts.

59 t to date dissecting compartmentalization of eosinophil recruitment as it unfolds during allergic inf

60 To contrast eosinophil recruitment between these two compartments, w

61 suggest that PARP-1 plays a critical role in eosinophil recruitment by specifically regulating the ca

62 Eosinophil recruitment, cytokine production, serum immun

63 and inflammation defects, but the granuloma eosinophil recruitment defect persisted when donor cells

64 ediators and adhesion molecules orchestrates eosinophil recruitment during allergic inflammation in t

65 make MCP-4 a candidate for playing a role in eosinophil recruitment during allergic respiratory disea

66 In summary, CXCR4 blockade inhibited eosinophil recruitment during type-2 granuloma formation

67 ment and activation of Th2 cells, leading to eosinophil recruitment, even in the absence of challenge

68 elial cells require H2R to produce CCL24, an eosinophil recruitment factor, whereas H2R blockade redu

69 Bronchial inflammatory cell (lymphocyte and eosinophil) recruitment has been demonstrated.

70 ddress the endogenous mechanisms involved in eosinophil recruitment in a late-phase allergic reaction

71 or endogenous eotaxin in mediating the 111In-eosinophil recruitment in allergic inflammation, and sug

72 The mechanisms of selective eosinophil recruitment in allergic reactions are not ful

73 The accelerated eosinophil recruitment in allergic subjects provides sup

74 Eosinophil recruitment in asthma is a multistep process,

75 ion of allergic inflammation with diminished eosinophil recruitment in BAL and lung and reduced mucus

76 Eosinophil recruitment in BAL was significantly reduced

77 1 plays a critical role in the regulation of eosinophil recruitment in colonic eosinophilic disease s

78 These results demonstrate that eosinophil recruitment in EAE is dependent on LTB4 recep

79 damental role of the eotaxin/CCR3 pathway in eosinophil recruitment in experimental asthma.

80 endothelium contributed to the inhibition of eosinophil recruitment in IL-1 receptor type 1-deficient

81 Bronchoalveolar lavage (BAL) eosinophil recruitment in IL-1 receptor type 1-deficient

82 -5, or mMIP-1beta, induced significant 111In-eosinophil recruitment in mouse skin.

83 caspofungin that was associated with airway eosinophil recruitment in neutropenic mice with invasive

84 kine eotaxin is likely to be associated with eosinophil recruitment in onchodermatitis, DEC was appli

85 Eosinophil recruitment in P-selectin-deficient mice ( ap

86 Eosinophil recruitment in response to conidial aspiratio

87 ith metRANTES, significantly inhibited 111In-eosinophil recruitment in the allergic reaction.

88 -3 contributes to a significant component of eosinophil recruitment in the type-2 interstitial granul

89 an antiMIP-1alpha antibody, suppressed 111In-eosinophil recruitment in this delayed-onset allergic re

90 and may play an important role in mediating eosinophil recruitment in various allergic conditions in

91 of the hookworm Necator americanus inhibited eosinophil recruitment in vivo in response to eotaxin, b

92 The role of selectins in mediating eosinophil recruitment in vivo was assessed in a model o

93 5 production by lung leukocytes in vitro and eosinophil recruitment in vivo.

94 hil is essential for chemoattractant-induced eosinophil recruitment in vivo.

95 osinophil aggregation in vitro and cutaneous eosinophil recruitment in vivo.

96 Here, we describe a novel mouse model of eosinophil recruitment in which we have compared the in

97 d type 2 T cell-dependent responses (IgE and eosinophil recruitment) in a model of allergic pulmonary

98 injection and subsequently declined, whereas eosinophil recruitment increased as time elapsed and com

99 ODN in IFN-gamma -/- mice failed to inhibit eosinophil recruitment, indicating a critical role of IF

100 ted in P-selectin/ICAM-1 double-mutant mice (eosinophil recruitment inhibited approximately 62%).

101 and may play an important role in mediating eosinophil recruitment into inflammatory foci.

102 Eotaxin, which is a major mediator for eosinophil recruitment into lung, has regulatory effects

103 Allergen-induced eosinophil recruitment into the airway was abolished by

104 re was a fourfold increase in IL-13-mediated eosinophil recruitment into the airway.

105 CCL11, and CCL24 and for Th2 lymphocyte and eosinophil recruitment into the allergic airway.

106 re was a profound reduction in IL-13-induced eosinophil recruitment into the lung lumen.

107 Oral administration of 32 reduced eosinophil recruitment into the lungs in a dose-dependen

108 n and the RSV-G glycoprotein, suppressed the eosinophil recruitment into the lungs of these mice upon

109 ely expressed in the gastrointestinal tract, eosinophil recruitment into the small intestine was abla

110 Selective eosinophil recruitment into tissues is a characteristic

111 Eosinophil recruitment is a hallmark of parasitic infect

112 Furthermore, in the absence of eotaxin, eosinophil recruitment is attenuated, whereas in the abs

113 ce, suggesting that Aspergillus-induced lung eosinophil recruitment is regulated by IL-13-induced che

114 Selective eosinophil recruitment is the result of orchestrated eve

115 alization of interleukin-5 (IL-5) to inhibit eosinophil recruitment likewise had no effect on early c

116 n eosinophil development (Deltadbl-GATA) and eosinophil recruitment [mice deficient in CCR3 (CCR3 kno

117 Eosinophil recruitment occurred more rapidly in allergic

118 hase with expression of surface integrins on eosinophils, recruitment of eosinophils from the bone ma

119 elial collagen deposition, but did not alter eosinophil recruitment or the alternative activation of

120 hil recruitment, but significantly inhibited eosinophil recruitment (p = 0.0032).

121 Eosinophil recruitment, Th2 and Th17 cytokine and chemok

122 ILC2 activation and eosinophil recruitment, TH2-related cytokine and chemoki

123 inking inflammatory cytokine mobilization to eosinophil recruitment that may be relevant to the patho

124 erized by ILC2 activation, proliferation and eosinophil recruitment that was associated with accelera

125 r signaling on platelets to markedly amplify eosinophil recruitment through pulmonary vascular adhesi

126 Thus, signaling via CCR3 mediates eosinophil recruitment to airway nerves and may be a pre

127 This study suggests that Gal-1 can limit eosinophil recruitment to allergic airways and suppresse

128 Moreover, eosinophil recruitment to both the lung and peritoneum i

129 , CCL28 appears to play a role in regulating eosinophil recruitment to peribronchial regions of the l

130 , an integrin counter-receptor implicated in eosinophil recruitment to the airway in asthma.

131 bronchoconstriction, since it would decrease eosinophil recruitment to the airway nerves.

132 ism appears to be by specifically inhibiting eosinophil recruitment to the airway nerves.

133 phenotype in lung tissue was associated with eosinophil recruitment to the airways, as all BAL eosino

134 s lower in CXCR2(-/-) mice than BALB/c mice, eosinophil recruitment to the cornea was not impaired.

135 ustained O. volvulus keratitis by regulating eosinophil recruitment to the cornea.

136 that P-selectin is an important mediator of eosinophil recruitment to the cornea.

137 iver blindness (Onchocerca volvulus) induces eosinophil recruitment to the corneal stroma at the time

138 rast, CCR3 disruption significantly curtails eosinophil recruitment to the lung after allergen challe

139 , significantly reduced the intensity of the eosinophil recruitment to the lung and airway during the

140 Eosinophil recruitment to the lung was also significantl

141 CAR4-deficient mice did not have a defect in eosinophil recruitment to the lung, nor a change in eosi

142 generation and is associated with decreased eosinophil recruitment to the lung.

143 induced airway hyperreactivity and decreased eosinophil recruitment to the lungs as effectively as de

144 , OVA, in mice, including Ag-specific recall eosinophil recruitment to the peritoneum.

145 f the adaptive immune system, contributes to eosinophil recruitment to the site of larval infection,

146 suggest that CCR3 plays an essential role in eosinophil recruitment to the skin and the lung and in t

147 t helminths may employ mechanisms to inhibit eosinophil recruitment, to prolong worm survival in the

148 Significant 111In-eosinophil recruitment was also observed in an active cu

149 and eotaxin-1/2(-/-) mice demonstrated that eosinophil recruitment was dependent on eotaxin-1.

150 developed normally and that the reduction in eosinophil recruitment was likely due to systemic reduct

151 Eosinophil recruitment was not completely inhibited in P

152 psies at 30 min and 6 h, whereas significant eosinophil recruitment was observed in allergic subjects

153 Eosinophil recruitment was partially reduced (54%) by th

154 d to mature for 3 wk, the inhibition of lung eosinophil recruitment was replaced by augmentation of l

155 cient mice ( approximately 67% inhibition of eosinophil recruitment) was significantly reduced compar

156 mice to synthesize GM-CSF, a key cytokine in eosinophil recruitment, was reestablished by replenishme

157 ht to be the principal orchestrating cell in eosinophil recruitment, we evaluated its presence in the

158 like molecule beta (RELMbeta) expression and eosinophil recruitment, which are two mechanisms that el