ライフサイエンスコーパス: eotaxin-1

1 ine CC motif ligand 11 (CCL11, also known as eotaxin-1).

2 when stimulated with CC chemokine ligand 11 (eotaxin-1).

3 ty), but is only 38.9% identical with murine eotaxin-1.

4 phils, accompanied by a decrease in IL18 and eotaxin-1.

5 he critical roles of the charged residues in eotaxin-1.

6 eticulum and is induced by interleukin-3 and eotaxin-1.

7 ergic airways disease is directed in part by eotaxin-1.

8 that eosinophil recruitment was dependent on eotaxin-1.

9 ion, and synthesis of procollagen type I and eotaxin-1.

10 tg mice, including 800-fold higher levels of eotaxin-1.

11 d that despite the expression of its ligands eotaxin-1, -2 and -3, neither eosinophils nor mast cells

12 alogue of CCR3 (CROSS(5)-N(3)E3(3)) binds to eotaxin-1, -2, and -3 but not to MCP-1.

13 the cognate chemokines of the receptor CCR3 (eotaxin-1, -2, and -3).

14 with eosinophil selectivity, referred to as eotaxin-1, -2, and -3.

15 in the mRNA expression and protein levels of eotaxin-1, -2, and -3.

16 lergen-challenged wild-type mice was lost in eotaxin-1/2 DKO and CCR3-deficient mice.

17 However, eotaxin-1/2 DKO mice had a marked decrease in tissue eos

18 e deficient in both eotaxin-1 and eotaxin-2 (eotaxin-1/2 double knockout)] were subjected to Aspergil

19 airway was abolished by 98%, 94%, and 99% in eotaxin-1/2 double knockout, CCR3 knockout, and Deltadbl

20 for eotaxin-2 and a synergistic reduction in eotaxin-1/2 double-deficient (DKO) and CCR3-deficient mi

21 DSS treatment of eotaxin-2(-/-) and eotaxin-1/2(-/-) mice demonstrated that eosinophil recru

22 ic studies, wild-type mice transplanted with eotaxin-1/2-deficient bone marrow had markedly less angi

23 type mice in an atopic asthma model into the eotaxin-1/2-deficient mice led to angiogenesis and airwa

24 Chemokine analysis demonstrated that eotaxin 1 and 2 secretion in response to repeated allerg

25 3 (CCR3 knockout) and mice deficient in both eotaxin-1 and eotaxin-2 (eotaxin-1/2 double knockout)] w

26 S treatment of mice strongly induced colonic eotaxin-1 and eotaxin-2 expression and eosinophil levels

27 Notably, ovalbumin-induced expressions of eotaxin-1 and eotaxin-2 mRNA in the lungs were almost co

28 cally ablating eotaxin-1 or eotaxin-2 alone, eotaxin-1 and eotaxin-2 together, and CCR3.

29 In BALF, the levels of IL-5, IL-13, eotaxin-1 and eotaxin-2 were significantly lower in FHL2

30 with asthma, leptin augmented IL-13-induced eotaxin-1 and eotaxin-3 production and IL13RA2 expressio

31 olved in binding to CCR3 are mimicked on the eotaxin-1 and MCP-3 surface.

32 petent: they undergo chemotaxis toward mouse eotaxin-1 and produce characteristic cytokines, includin

33 vated levels of eosinophil chemoatttractants eotaxin-1 and RANTES in the muscle tissue of all three d

34 LPA (1 microM, 6 h) attenuated IL-13-induced eotaxin-1 and SOCS-1 gene expression.

35 of NF-kappaB-regulated chemokines, including eotaxin-1 and thymus- and activation-regulated chemokine

36 n, increase of thymic stromal lymphopoietin, eotaxin-1 and type 2 cytokine circuits, and even showed

37 tion of the Th2-associated chemokines CCL11 (eotaxin-1) and CCL22 (macrophage-derived chemokine).

38 tor receptor 2, CCR3, CC chemokine ligand 11/eotaxin-1, and CC chemokine ligand 24/eotaxin-2 all redu

39 s had reduced expression of CCL7/MCP-3, CC11/eotaxin-1, and CCL24/eotaxin-2.

40 nophil-directed cytokines (e.g., IL-5, CCL11/eotaxin-1, and CCL5/RANTES) and IL-17 ex vivo.

41 In contrast, levels of MCP-3, eotaxin-1, and CCR3 transcripts increased in both tissue

42 omarkers (TARC, PARC, periostin, and IL-22), eotaxin-1, and eotaxin-3 significantly decreased.

43 kinase (ERK) phosphorylation caused by IL-5, eotaxin-1, and fMLP.

44 scopy revealed colocalization of rhinovirus, eotaxin-1, and IL-4 in CD68-positive cells.

45 delivery to the lung induces EE by an IL-5, eotaxin-1, and STAT6-dependent mechanism.

46 Altogether, these results suggest eotaxin-1 as a novel modifier of Alzheimer's disease AAO

47 Administration of anti-eotaxin-1 attenuated rhinovirus-induced airway eosinophi

48 rovides a basis for targeting the eosinophil/eotaxin-1 axis in UC.

49 ced esophageal eosinophilia was dependent on eotaxin-1 (but not eotaxin-2).

50 Chemokines, eotaxin-1 (CCL11) and eotaxin-2 (CCL24), which are known

51 The CC chemokine eotaxin-1 (CCL11) is chemotactic for eosinophils, basoph

52 se eosinophils stimulated with the chemokine eotaxin-1 (CCL11) secreted enzymatically active EARs (EC

53 In the discovery cohort, eotaxin-1 (CCL11) was associated with disease duration p

54 py to study the interaction between vCCI and eotaxin-1 (CCL11), a CC chemokine that is an important f

55 -25-induced expression of IL-4, IL-5, IL-13, eotaxin-1 (CCL11), and pulmonary eosinophilia.

56 ha), the chemoattractant IP-10 (CXCL10), and eotaxin-1 (CCL11), previously involved in brain disorder

57 eosinophil spreading on VCAM-1 but inhibited eotaxin-1 (CCL11)-mediated eosinophil migration, calcium

58 e eosinophil-selective chemokines, eotaxins (eotaxin-1/CCL11 and eotaxin-2/CCL24), eosinophils, and t

59 m showed up-regulation of Th2 (IL-13, CCL17, eotaxin-1/CCL11, CCL13, CCL4, IL-10), Th1 (CXCL10, CXCL1

60 nstead, the eosinophil-recruiting chemokines eotaxin-1/CCL11, eotaxin-2/CCL24, and eotaxin-3/CCL26 ar

61 kines activating the receptor CCR3 including eotaxin-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26, RANTE

62 eased lung expression of cytokines including eotaxin-1/CCL11, IL-4, IL-13, and IFN-gamma.

63 showed that most Th2-related markers (e.g., Eotaxin-1, CCL13, and CCL18) were upregulated in GC-naiv

64 CXCL8/IL-8, CXCL10/IP-10, CCL5/RANTES, CCL11/eotaxin-1, CCL2/MCP-1, CCL4/MIP-1beta, CCL7/MCP-3, and C

65 0; monocyte chemoattractant protein (MCP)-3; eotaxin-1; CCR5; CXCR3; and CCR3 in the cornea and conju

66 of C-C motif chemokine ligand 11 (CCL11; or eotaxin-1) characterized by eosinophil infiltration and

67 e of all three dystrophin-deficient strains; eotaxin-1 concentration in muscle correlated inversely w

68 that correlated with ME/CFS severity: CCL11 (Eotaxin-1), CXCL1 (GROalpha), CXCL10 (IP-10), IFN-gamma,

69 3-induced EE was significantly diminished in eotaxin-1-deficient mice (48.7 +/- 10.3 vs. 14.1 +/- 12.

70 Notably, in contrast to observations made in eotaxin-1-deficient mice, eotaxin-2-deficient mice had n

71 +/- 12.5 eosinophils/mm(2) in wild-type and eotaxin-1-deficient mice, respectively).

72 player in the signaling pathway activated by eotaxin-1 during eosinophil migration.

73 d locus harbors several chemokines including eotaxin-1 encoded by CCL11, and the haplotype includes a

74 ent in eosinophil chemoattractant molecules (eotaxin-1, eotaxin-2, and their receptor CCR3) and with

75 beta1 and IL-13 alone or in combination, and eotaxin-1 expression and production were evaluated.

76 lergen had significantly increased levels of eotaxin-1 expression in airway epithelium which was asso

77 u and immunofluorescence analysis-identified eotaxin-1 expression was restricted to intestinal F4/80(

78 uorescence anisotropy results on variants of eotaxin-1 further confirm the critical roles of the char

79 with A. alternata in wild-type, Gm-csf- and eotaxin-1-gene-deleted mice, while eosinophils are recru

80 Other cytokines, including eotaxin-1, growth related oncogene (GRO), interleukin (I

81 ologues; however, only one murine homologue, eotaxin-1, has been identified.

82 mice, nor on weight loss or levels of CCL11 (eotaxin-1), IFN-gamma, IL-5, or IL-13 in bronchoalveolar

83 not PBS-treated, mice induced expression of eotaxin-1, IL-4, and IL-13 ex vivo.

84 nd airway remodeling revealed that levels of eotaxin-1, IL-5, IL-13, found in inflammatory zone 1, an

85 -regulating expression of chemokines such as eotaxin-1 in airway epithelium with resultant recruitmen

86 ls of Th2 cytokines such as IL-5, IL-13, and eotaxin-1 in bronchoalveolar lavage fluid after OVA chal

87 type (SASP) reveals elevated levels of CCL11/Eotaxin-1 in lesions of aged mice, which is found to inh

88 NF-alpha, IFN-gamma, GM-CSF, MIP-1alpha, and Eotaxin-1 in patients with MDD based on validated depres

89 Immunohistochemical analysis showed eotaxin-1 in the lung macrophages of virus-infected, OVA

90 ering, but inhibited ERK(1/2) activation and eotaxin-1-induced migration.

91 matrix metalloprotease with BB-94 inhibited eotaxin-1-induced TrkA activation and eosinophil migrati

92 ith ASD had significantly elevated levels of eotaxin-1, interferon-gamma, and IL-12p70 relative to ch

93 ice and, more importantly, delivery of CCL11/eotaxin-1 into the lung during the development of this d

94 CCL11/eotaxin-1 is a potent eosinophilic CC chemokine expresse

95 CCL11, also known as eotaxin-1, is described as an eosinophil chemoattractant

96 mycin also suppressed IgE, although IL-4 and eotaxin 1 levels were augmented.

97 eplaced by neutrophilia in adult mice, while eotaxin-1 levels decreased and GRO-alpha levels increase

98 Validating this association, we found plasma eotaxin-1 levels were correlated with disease AAO in an

99 upted the typical age-associated increase of eotaxin-1 levels, suggesting a complex regulatory role f

100 ated bronchoalveolar lavage fluid leptin and eotaxin-1 levels.

101 ray and quantitative PCR, elevated levels of eotaxin-1 mRNA in the rectosigmoid colon of pediatric UC

102 We show that elevated levels of eotaxin-1 mRNA positively correlated with rectosigmoid e

103 Intravenous injection of eotaxin (1 nmol/kg) into guinea pigs in vivo stimulated

104 ine the consequences of genetically ablating eotaxin-1 or eotaxin-2 alone, eotaxin-1 and eotaxin-2 to

105 ealed a modest role for individually ablated eotaxin-1 or eotaxin-2.

106 TNF-alpha (but not IL5, IL-3, eotaxin-1 or GM-CSF) was detected in supernatants of ex

107 IL-5, eotaxin-1, or fMLP caused 1) change of Mac-1 to its acti

108 cer and activator of transcription (STAT) 6, eotaxin-1, or IL-5-deficient mice.

109 Eotaxin-1 (P = 0.01), eosinophil cationic protein (P < 0

110 tinal macrophage and epithelial cell-derived eotaxin-1 plays a critical role in the regulation of eos

111 Finally, eotaxin-1-positive fibroblasts were identified in severe

112 At 48 h, eotaxin-1 production was markedly increased with the com

113 and eosinophilia while suppressing IL-5 and eotaxin-1 production.

114 factor, transforming growth factor-beta(1), eotaxin-1, RANTES (regulated on activation, normal T-cel

115 ectrostatic potential of vMIP-II to those of eotaxin-1, RANTES, and MCP-3, three CCR3 physiological a

116 ent from that for the physiological agonists eotaxin-1, RANTES, and MCP-3.

117 IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recru

118 m healthy subjects increased cell spreading, eotaxin-1 release and proliferation.

119 cell spreading, cellular proliferation, and eotaxin-1 release were measured.

120 Similarly, AFs produced more eotaxin-1 than did DLFs at baseline (2.5-fold higher; p

121 In contrast, in the absence of eotaxin-1, there was a fourfold increase in IL-13-mediat

122 sinophilia, associated with up-regulation of eotaxin-1, was present in the bronchoalveolar lavage flu

123 t (luminal inflammatory cells) compared with eotaxin-1, which was expressed solely in the tissue.