ライフサイエンスコーパス: L. amazonensis

1 L. amazonensis amastigotes, through activation of extrac

2 L. amazonensis is endemic in South America, where it cau

3 L. amazonensis metacyclic promastigotes lacking one SODA

4 Inhibition of arginase I or ODC abrogates L. amazonensis replication in infected human macrophages

5 In addition, L. amazonensis infection induces an early increase in To

6 ole in downmodulating the Th1 response after L. amazonensis infection.

7 htly more potent than amphotericin B against L. amazonensis.

8 sm underlying this enhanced immunity against L. amazonensis infection remains largely unresolved.

9 f a DNA vaccine to induce protection against L. amazonensis infection.

10 ed in the protective immune response against L. amazonensis infection in vaccinated mice.

11 Although L. amazonensis lacking LIT1 grew normally in axenic cult

12 s encoding murine interleukin-12 (IL-12) and L. amazonensis HSP70.

13 d and tested against Leishmania donovani and L. amazonensis intracellular amastigotes.

14 ALB/c mice to infection with L. mexicana and L. amazonensis, does play a significant role in regulati

15 ed by the New World species, L. mexicana and L. amazonensis, we analyzed their course of infection in

16 plex parasites (L. mexicana, L. pifanoi, and L. amazonensis), a critical role for immunoglobulin G-me

17 inst Leishmania spp promastigotes as well as L. amazonensis and L. infantum amastigotes.

18 that the CD4+ T-cell response during chronic L. amazonensis infection is limited during the transitio

19 c Th1 transfer helped recipient mice control L. amazonensis infection established by promastigotes bu

20 particular, neutrophil-derived LTB4 controls L. amazonensis killing, degranulation, and reactive oxyg

21 In comparison to L. major controls, L. amazonensis-infected DCs secreted lower levels of int

22 All phenotypes observed in LHR1/Deltalhr1 L. amazonensis were rescued by expression of episomal LH

23 r inhibiting PERK kinase activity diminished L. amazonensis infection.

24 of the Dectin-1/Syk/ROS/NLRP3 pathway during L. amazonensis phagocytosis is important for macrophage

25 We identified that ROS production during L. amazonensis infection occurs upon engagement of Decti

26 ression in C57BL/6 mice infected with either L. amazonensis or L. major (a healing model).

27 crophages from 5-LO knockout mice eliminated L. amazonensis in the presence of exogenous LTB4, and ma

28 from P2X7 receptor knockout mice eliminated L. amazonensis when incubated with ionomycin.

29 acts (SGE) of Lutzomyia longipalpis enhances L. amazonensis infection.

30 es revealed that Retro-2 curbed experimental L. amazonensis infections in a dose-dependent manner.

31 e were injected locally with IP-10 following L. amazonensis infection, there was a significant delay

32 ls, as local injection of IL-1beta following L. amazonensis infection accelerated Th cell activation

33 n and interleukin-12p40 production following L. amazonensis amastigote infection compared with non-tr

34 ion represents a required upstream event for L. amazonensis-induced LTB4 synthesis.

35 ads to LTB4 formation, which is required for L. amazonensis elimination.

36 the importance of efficient heme uptake for L. amazonensis replication and vertebrate host infectivi

37 comparison of draining lymph node cells from L. amazonensis- and L. major-infected mice at 10 weeks p

38 Antigen stimulation of CD4+ T cells from L. amazonensis-infected mice in vitro in the presence of

39 (IFN-gamma) production of CD4+ T cells from L. amazonensis-infected mice.

40 However, these cells isolated from L. amazonensis-infected mice were not skewed toward eith

41 hmania amazonensis Our inability to generate L. amazonensis SODA null mutants and the lethal phenotyp

42 functional B cells are important for healing L. amazonensis in this infectious disease model.

43 emonstrated after expression in yeast and in L. amazonensis LIT1-null amastigotes.

44 The disease-promoting CD4+ T cells in L. amazonensis-infected mice have the characteristics of

45 ization and membrane association of FCaBP in L. amazonensis suggest that the mechanisms for flagellar

46 ributed partially to compromised immunity in L. amazonensis-infected hosts.

47 responses contributes to the pathogenesis in L. amazonensis-infected mice.

48 responsible for the susceptible phenotype in L. amazonensis-infected hosts and that this parasite may

49 production, may limit the immune response in L. amazonensis-infected mice.

50 ver, the adoptive transfer of ANK cells into L. amazonensis-infected mice markedly increased DC and T

51 ng an important effector function in killing L. amazonensis.

52 LHR1-complemented (LHR1/Deltalhr1 plus LHR1) L. amazonensis strains.

53 L. major (LV39), L. amazonensis and L. mexicana were the most efficient u

54 head challenge infection with 107 metacyclic L. amazonensis promastigotes at 4 wk demonstrated protec

55 d amastigotes in IFN-gamma-stimulated Mphis, L. amazonensis-specific Th1 transfer helped recipient mi

56 fection established by promastigotes but not L. amazonensis infection established by amastigotes.

57 Notably, L. amazonensis amastigote infection failed to activate D

58 , we identify and characterize LIT1, a novel L. amazonensis membrane protein with extensive similarit

59 f interleukin-10 (IL-10), in CD4(+) cells of L. amazonensis-infected mice, we further examined whethe

60 The failure of L. amazonensis-infected C3H mice to respond to IL-12 was

61 lation of the macrophage-mediated killing of L. amazonensis in vitro and a less robust antibody respo

62 e ear with 10(5) metacyclic promastigotes of L. amazonensis together with SGE (equivalent to 0.5 glan

63 he complicated pathogenic immune response of L. amazonensis.

64 via NADPH oxidase during the early stages of L. amazonensis infection is critical for inflammasome ac

65 ranscription-PCR in all life-cycle stages of L. amazonensis.

66 Adoptive transfer of L. amazonensis-specific Th1 cells prior to infection ove

67 Treatment of L. amazonensis-infected mice with the highly-specific mi

68 ent mice infected with either L. mexicana or L. amazonensis failed to control the lesion progression,

69 rprised to find that IFN-gamma could promote L. amazonensis amastigote replication in macrophages (Mp

70 we observed that ATP was not able to reduce L. amazonensis load.

71 This was supported by the fact that L. amazonensis amastigotes limited the production of IL-

72 These experiments indicated that L. amazonensis resistance to killing in vivo is only par

73 iginal sites of inoculation, indicating that L. amazonensis can persist in vivo independently of the

74 In this study, we show that L. amazonensis or its lipophosphoglycan can induce neutr

75 Previous studies showed that L. amazonensis incorporates heme through the transmembra

76 We have previously shown that L. amazonensis-infected C57BL/6 mice have profound impai

77 These results suggest that L. amazonensis amastigotes may condition DCs of a suscep

78 ults reveal a quite unexpected aspect of the L. amazonensis parasite and have important implications

79 ential of a DNA-based vaccine, we tested the L. amazonensis gene encoding P4 nuclease as well as adju

80 One possibility is that the L. amazonensis parasite modulates antigen-presenting cel

81 Moreover, we immunized mice with the L. amazonensis vaccines to determine if this vaccine reg

82 ay not always be indicative of protection to L. amazonensis infection.

83 tion in macrophages, and mouse resistance to L. amazonensis infection in vivo.

84 ngly, inflammasome activation in response to L. amazonensis is impaired by inhibitors of NADPH oxidas

85 pathology, and therefore, susceptibility to L. amazonensis infection.

86 because IL-4-/- mice remained susceptible to L. amazonensis infection, even after IL-12 administratio

87 After 2 to 4 weeks, L. amazonensis-infected mice had significantly delayed a

88 se mechanism of pathogenesis associated with L. amazonensis infection remains largely unresolved.

89 of bone marrow-derived dendritic cells with L. amazonensis amastigotes resulted in rapid and signifi

90 4/IL-12, or P4/HSP70 prior to challenge with L. amazonensis promastigotes.

91 protective response in mice challenged with L. amazonensis and L. pifanoi.

92 infection of C3HeB/FeJ mice for 7 days with L. amazonensis promoted an immature CD11c(+) DC phenotyp

93 between MHC class II -/- mice infected with L. amazonensis and Leishmania major suggest that these p

94 e response of mice chronically infected with L. amazonensis can be enhanced towards a Th1 phenotype b

95 We found that C3H mice infected with L. amazonensis exhibited decreased IL-12 production, whi

96 functions at early stages of infection with L. amazonensis parasites and provide a compelling ration

97 Infection with L. amazonensis promastigotes led to increased 1/2 phosph

98 cells exposed to SGE prior to infection with L. amazonensis.

99 d dendritic cells (DCs) of C57BL/6 mice with L. amazonensis or Leishmania major promastigotes and ass

100 could be enhanced in vitro and in vivo with L. amazonensis antigen-pulsed bone marrow-derived dendri

101 Yet L. amazonensis-infected DCs produced elevated levels of