ライフサイエンスコーパス: amazonensis

1 uzi , Plasmodium falciparum , and Leishmania amazonensis .

2 lowing intradermal infection with Leishmania amazonensis.

3 complicated pathogenic immune response of L. amazonensis.

4 scription-PCR in all life-cycle stages of L. amazonensis.

5 loads when they are infected with Leishmania amazonensis.

6 cognize macrophages infected with Leishmania amazonensis.

7 40L knockout (CD40L-/-) mice with Leishmania amazonensis.

8 genic nematode natural enemy Heterorhabditis amazonensis.

9 ATP-treated macrophages eliminate Leishmania amazonensis.

10 arginase enzyme from Leishmania (Leishmania) amazonensis.

11 y more potent than amphotericin B against L. amazonensis.

12 an important effector function in killing L. amazonensis.

13 adding it to cells infected with Leishmania amazonensis.

14 ctivity exposed on the surface of Leishmania amazonensis.

15 ls exposed to SGE prior to infection with L. amazonensis.

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

17 In cutaneous leishmaniasis, Leishmania amazonensis activates macrophage double-stranded, RNA-ac

18 infected BALB/c mice to screen a Leishmania amazonensis amastigote cDNA expression library and obtai

19 nd interleukin-12p40 production following L. amazonensis amastigote infection compared with non-treat

20 Notably, L. amazonensis amastigote infection failed to activate DCs,

21 ised to find that IFN-gamma could promote L. amazonensis amastigote replication in macrophages (Mphis

22 ously reported that the growth of Leishmania amazonensis amastigotes in murine macrophages (Mphis) wa

23 hat infection of macrophages with Leishmania amazonensis amastigotes led to the activation of the MAP

24 This was supported by the fact that L. amazonensis amastigotes limited the production of IL-12p

25 These results suggest that L. amazonensis amastigotes may condition DCs of a susceptib

26 bone marrow-derived dendritic cells with L. amazonensis amastigotes resulted in rapid and significan

27 rigger for the differentiation of Leishmania amazonensis amastigotes, independently of temperature an

28 L. amazonensis amastigotes, through activation of extracell

29 t Leishmania spp promastigotes as well as L. amazonensis and L. infantum amastigotes.

30 L. major (LV39), L. amazonensis and L. mexicana were the most efficient util

31 otective response in mice challenged with L. amazonensis and L. pifanoi.

32 tween MHC class II -/- mice infected with L. amazonensis and Leishmania major suggest that these para

33 mania mexicana complex parasites (Leishmania amazonensis and Leishmania pifanoi) is impaired in the a

34 liensis , Leishmania guyanensis , Leishmania amazonensis , and Trypanosoma cruzi .

35 th of Trypanosoma cruzi, Leishmania mexicana amazonensis, and Pneumocystis carinii in culture.

36 parison of draining lymph node cells from L. amazonensis- and L. major-infected mice at 10 weeks post

37 uld be enhanced in vitro and in vivo with L. amazonensis antigen-pulsed bone marrow-derived dendritic

38 th phagocytosis and the uptake of Leishmania amazonensis by macrophages (Ms).

39 New World leishmaniasis caused by Leishmania amazonensis can be elicited by immunization with the dev

40 esponse of mice chronically infected with L. amazonensis can be enhanced towards a Th1 phenotype but

41 ction with the protozoan parasite Leishmania amazonensis can cause diverse clinical forms of leishman

42 Leishmania amazonensis can cause progressive disease in most inbred

43 Leishmania amazonensis can cause progressive disease in most inbred

44 nal sites of inoculation, indicating that L. amazonensis can persist in vivo independently of the abi

45 Transfection of L. mexicana amazonensis cells with this recombinant plasmid showed t

46 se and subsequently heal, whereas Leishmania amazonensis challenge leads to chronic lesions with high

47 tectively immunize mice against a Leishmania amazonensis challenge.

48 Infection of mammalian hosts with Leishmania amazonensis depends on the remarkable ability of these p

49 of the related protozoan parasite Leishmania amazonensis did not induce myosin autoimmunity.

50 /c mice to infection with L. mexicana and L. amazonensis, does play a significant role in regulating

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

52 a are relatively indiscriminate, and that H. amazonensis en-tomopathogenic nematodes recruit to corn

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

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

55 re, we report the first isolation of L. (L.) amazonensis from dogs with clinical manifestations of vi

56 the macrophage parasite Leishmania mexicana amazonensis from intraphagolysosomal cytolysis was studi

57 ial of a DNA-based vaccine, we tested the L. amazonensis gene encoding P4 nuclease as well as adjuvan

58 Antiserum specific for Leishmania amazonensis GP63 specifically reacted with a 55-kDa TcGP

59 ncoding murine interleukin-12 (IL-12) and L. amazonensis HSP70.

60 phages from 5-LO knockout mice eliminated L. amazonensis in the presence of exogenous LTB4, and macro

61 ctional B cells are important for healing L. amazonensis in this infectious disease model.

62 ion of the macrophage-mediated killing of L. amazonensis in vitro and a less robust antibody response

63 Previous studies showed that L. amazonensis incorporates heme through the transmembrane

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

65 Leishmania amazonensis induces a nonhealing infection in C3H mice,

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

67 We have previously shown that L. amazonensis-infected C57BL/6 mice have profound impairme

68 Yet L. amazonensis-infected DCs produced elevated levels of IL-

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

70 ponsible for the susceptible phenotype in L. amazonensis-infected hosts and that this parasite may ha

71 uted partially to compromised immunity in L. amazonensis-infected hosts.

72 Upon contact with Leishmania amazonensis-infected macrophages, these FN-activated neu

73 After 2 to 4 weeks, L. amazonensis-infected mice had significantly delayed and

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

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

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

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

78 Treatment of L. amazonensis-infected mice with the highly-specific mitog

79 nterleukin-10 (IL-10), in CD4(+) cells of L. amazonensis-infected mice, we further examined whether L

80 ponses contributes to the pathogenesis in L. amazonensis-infected mice.

81 FN-gamma) production of CD4+ T cells from L. amazonensis-infected mice.

82 duction, may limit the immune response in L. amazonensis-infected mice.

83 In Leishmania amazonensis-infected patients, host SOD1 levels can be u

84 as local injection of IL-1beta following L. amazonensis infection accelerated Th cell activation and

85 tion established by promastigotes but not L. amazonensis infection established by amastigotes.

86 h1 transfer helped recipient mice control L. amazonensis infection established by promastigotes but n

87 The progressive disease following Leishmania amazonensis infection in mice requires functional CD4(+)

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

89 n in macrophages, and mouse resistance to L. amazonensis infection in vivo.

90 In addition, L. amazonensis infection induces an early increase in Toll-

91 ous leishmaniasis associated with Leishmania amazonensis infection is characterized by uncontrolled p

92 NADPH oxidase during the early stages of L. amazonensis infection is critical for inflammasome activ

93 t the CD4+ T-cell response during chronic L. amazonensis infection is limited during the transition f

94 The susceptibility of mice to Leishmania amazonensis infection is thought to result from an inabi

95 We identified that ROS production during L. amazonensis infection occurs upon engagement of Dectin-1

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

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

98 ause IL-4-/- mice remained susceptible to L. amazonensis infection, even after IL-12 administration,

99 ere injected locally with IP-10 following L. amazonensis infection, there was a significant delay in

100 scertain the role of IFN-gamma in Leishmania amazonensis infection, we were surprised to find that IF

101 not always be indicative of protection to L. amazonensis infection.

102 nhibiting PERK kinase activity diminished L. amazonensis infection.

103 s (SGE) of Lutzomyia longipalpis enhances L. amazonensis infection.

104 DNA vaccine to induce protection against L. amazonensis infection.

105 in downmodulating the Th1 response after L. amazonensis infection.

106 trains of mice are susceptible to Leishmania amazonensis infection.

107 thology, and therefore, susceptibility to L. amazonensis infection.

108 and this pathway is important for Leishmania amazonensis infection.

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

110 nd tested against Leishmania donovani and L. amazonensis intracellular amastigotes.

111 The protozoan parasite Leishmania amazonensis is a heme auxotroph and must acquire this es

112 or surface glycoprotein (gp63) of Leishmania amazonensis is a metalloprotease implicated in the infec

113 e species in Brazil, Leishmania (Leishmania) amazonensis is an important etiological agent of human c

114 L. amazonensis is endemic in South America, where it causes

115 han 8% of all cases in endemic regions. (L.) amazonensis is generally found in the north and northeas

116 y, inflammasome activation in response to L. amazonensis is impaired by inhibitors of NADPH oxidase,

117 f LTB4 in neutrophil infection by Leishmania amazonensis is not clear.

118 ticular, neutrophil-derived LTB4 controls L. amazonensis killing, degranulation, and reactive oxygen

119 opica; and the species L (L) mexicana, L (L) amazonensis, L (L) major, and L (L) aethiopica in aggreg

120 prevalent in Brazil [Leishmania (Leishmania) amazonensis, L (Viannia) braziliensis, and L (V) guyanen

121 T cells mediates pathogenesis in Leishmania amazonensis (La)-infected mice, these susceptible mice d

122 Although L. amazonensis lacking LIT1 grew normally in axenic culture

123 ce with both Leishmania major and Leishmania amazonensis leads to a healed footpad lesion, whereas co

124 opeptidase (lap) were cloned from Leishmania amazonensis, Leishmania donovani, and Leishmania major,

125 nstrated after expression in yeast and in L. amazonensis LIT1-null amastigotes.

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

127 e identify and characterize LIT1, a novel L. amazonensis membrane protein with extensive similarity t

128 L. amazonensis metacyclic promastigotes lacking one SODA al

129 Lesions caused by Leishmania amazonensis normally heal, but relapses occur due to par

130 Infection with Leishmania amazonensis, on the other hand, causes progressive cutan

131 In this study, we show that L. amazonensis or its lipophosphoglycan can induce neutroph

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

133 endritic cells (DCs) of C57BL/6 mice with L. amazonensis or Leishmania major promastigotes and assess

134 the mitochondrial SOD isoform in Leishmania amazonensis Our inability to generate L. amazonensis SOD

135 s reveal a quite unexpected aspect of the L. amazonensis parasite and have important implications for

136 One possibility is that the L. amazonensis parasite modulates antigen-presenting cells,

137 aques containing large numbers of Leishmania amazonensis parasites and few lymphoid elements.

138 nctions at early stages of infection with L. amazonensis parasites and provide a compelling rationale

139 esponses following infection with Leishmania amazonensis parasites.

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

141 ant amount of the Ca2+ stored in L. mexicana amazonensis promastigotes and amastigotes is present in

142 of DCs that were preinfected with Leishmania amazonensis promastigotes and that these activated DCs,

143 d challenge infection with 107 metacyclic L. amazonensis promastigotes at 4 wk demonstrated protectiv

144 PAD4 in the netosis stimulated by Leishmania amazonensis promastigotes in human neutrophils.

145 Infection with L. amazonensis promastigotes led to increased 1/2 phosphory

146 and avirulent clones of Leishmania mexicana amazonensis promastigotes or amastigotes were loaded wit

147 growth of Leishmania chagasi and Leishmania amazonensis promastigotes, by impairing the flagellar po

148 L-12, or P4/HSP70 prior to challenge with L. amazonensis promastigotes.

149 fection of C3HeB/FeJ mice for 7 days with L. amazonensis promoted an immature CD11c(+) DC phenotype c

150 with recombinant shewasin A from Shewanella amazonensis provided the first documentation of this act

151 e importance of efficient heme uptake for L. amazonensis replication and vertebrate host infectivity,

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

153 These experiments indicated that L. amazonensis resistance to killing in vivo is only partia

154 inhibit Plasmodium falciparum and Leishmania amazonensis, respectively.

155 The crystal structure of Hda from Shewanella amazonensis SB2B at 1.75 A resolution reveals that Hda r

156 nia amazonensis Our inability to generate L. amazonensis SODA null mutants and the lethal phenotype o

157 ticle will increase our knowledge of L. (L.) amazonensis-specific adaptations to infection, parasite

158 Adoptive transfer of L. amazonensis-specific Th1 cells prior to infection overca

159 mastigotes in IFN-gamma-stimulated Mphis, L. amazonensis-specific Th1 transfer helped recipient mice

160 1-complemented (LHR1/Deltalhr1 plus LHR1) L. amazonensis strains.

161 tion and membrane association of FCaBP in L. amazonensis suggest that the mechanisms for flagellar ta

162 ar with 10(5) metacyclic promastigotes of L. amazonensis together with SGE (equivalent to 0.5 gland)

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

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

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

166 om P2X7 receptor knockout mice eliminated L. amazonensis when incubated with ionomycin.

167 BP was expressed in the protozoan Leishmania amazonensis, which lacks FCaBP.

168 ected a gp63-deficient variant of Leishmania amazonensis with constructs expressing gp63 and various

169 f a vaccine combining heat-killed Leishmania amazonensis with human rIL-12 (rhIL-12) and alum (alumin