ライフサイエンスコーパス: eotaxin-1

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

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

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

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

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

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

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

8 that eosinophil recruitment was dependent on eotaxin-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 3 (CCR3 knockout) and mice deficient in both eotaxin-1 and eotaxin-2 (eotaxin-1/2 double knockout)] w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 -25-induced expression of IL-4, IL-5, IL-13, eotaxin-1 (CCL11), and pulmonary eosinophilia.

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

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

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

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

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

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

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

57 0; monocyte chemoattractant protein (MCP)-3; eotaxin-1; CCR5; CXCR3; and CCR3 in the cornea and conju

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

59 3-induced EE was significantly diminished in eotaxin-1-deficient mice (48.7 +/- 10.3 vs. 14.1 +/- 12.

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

61 +/- 12.5 eosinophils/mm(2) in wild-type and eotaxin-1-deficient mice, respectively).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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