ライフサイエンスコーパス: amazonensis

1 uzi , Plasmodium falciparum , and Leishmania amazonensis .

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

3 lowing intradermal infection with Leishmania amazonensis.

4 complicated pathogenic immune response of L. amazonensis.

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

6 loads when they are infected with Leishmania amazonensis.

7 cognize macrophages infected with Leishmania amazonensis.

8 40L knockout (CD40L-/-) mice with Leishmania amazonensis.

9 in its activity against intramacrophagic L. amazonensis.

10 genic nematode natural enemy Heterorhabditis amazonensis.

11 ATP-treated macrophages eliminate Leishmania amazonensis.

12 arginase enzyme from Leishmania (Leishmania) amazonensis.

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

14 an important effector function in killing L. amazonensis.

15 d successful intracellular replication of L. amazonensis.

16 adding it to cells infected with Leishmania amazonensis.

17 ctivity exposed on the surface of Leishmania amazonensis.

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

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

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

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

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

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

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

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

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

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

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

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

30 L. amazonensis amastigotes, through activation of extracell

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

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

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

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

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

36 nce in Caenorhabditis elegans and Leishmania amazonensis and predicted sensitivity in Aedes sp., Schi

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

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

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

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

41 hat cause cutaneous disease, L. major and L. amazonensis, are poorly understood.

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

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

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

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

46 Leishmania amazonensis can cause progressive disease in most inbred

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

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

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

50 tectively immunize mice against a Leishmania amazonensis challenge.

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

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

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

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

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

56 s reported for L. major, APX depletion in L. amazonensis enhanced differentiation of metacyclic proma

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

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

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

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

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

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

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

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

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

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

67 effect on their efficacy against Leishmania amazonensis in vitro infection.

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

69 In this study, we observed that L. amazonensis induced PD-1 expression on both CD4(+) and C

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

71 Leishmania amazonensis induces a nonhealing infection in C3H mice,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 antibodies (MoAbs) against a non-healing L. amazonensis infection in BALB/c mice, and that anti-PD-1

94 -1 and PD-L1 in the immunopathogenesis of L. amazonensis infection in C57BL/6 mice.

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

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

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

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

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

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

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

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

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

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

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

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

107 regulating local immune responses during L. amazonensis infection, providing new insights into immun

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

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

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

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

112 and this pathway is important for Leishmania amazonensis infection.

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

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

115 trains of mice are susceptible to Leishmania amazonensis infection.

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

117 nhibiting PERK kinase activity diminished L. amazonensis infection.

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

119 Lecoeur et al. show us how Leishmania amazonensis inhibits macrophage inflammasomes by modifyi

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

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

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

123 Leishmania amazonensis is an etiological agent of diffuse cutaneous

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

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

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

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

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

129 Leishmania amazonensis is the etiological agent of cutaneous and di

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

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

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

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

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

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

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

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

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

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

140 L. amazonensis metacyclic promastigotes lacking one SODA al

141 In phagocytic cells such as macrophages, L. amazonensis modulates endosomal/lysosomal trafficking pa

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

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

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

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

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

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

148 on of virulent forms in both L. major and L. amazonensis Our results also uncover a unique requiremen

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

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

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

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

153 esponses following infection with Leishmania amazonensis parasites.

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

155 mpound 4 exhibited better results against L. amazonensis promastigotes (IC(50) = 15.52 3.782 uM) and

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

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

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

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

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

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

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

163 drial alterations and lipid inclusions in L. amazonensis promastigotes, upregulated tumor necrosis fa

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

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

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

167 In L. amazonensis, reactive oxygen species (ROS) signaling dri

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

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

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

171 inhibit Plasmodium falciparum and Leishmania amazonensis, respectively.

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

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

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

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

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

177 1-complemented (LHR1/Deltalhr1 plus LHR1) L. amazonensis strains.

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

179 bset of phagocytic B (termed B-1P) cells, L. amazonensis survives and proliferates at high rates insi

180 In contrast, we found that in L. amazonensis, the ROS-inducible APX is essential for surv

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

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

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

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

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

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

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

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