ライフサイエンスコーパス: chabaudi

1 ent antigens or infection with plasmodium C. chabaudi.

2 with either fraction and challenged with P. chabaudi.

3 infection with the rodent malaria Plasmodium chabaudi.

4 virulent, genetically distinct strain of P. chabaudi.

5 etectible NP(+) GCs in mice infected with P. chabaudi.

6 blood-stage malaria of the genus Plasmodium chabaudi.

7 infected with erythrocytic-stage Plasmodium chabaudi.

8 , P. knowlesi, P. berghei, P. yoelii, and P. chabaudi.

9 that after infection of mice with Plasmodium chabaudi, a c-Kit(hi) progenitor subset positive for int

10 S globin are well-protected from Plasmodium chabaudi adami and partially protected against P berghei

11 Plasmodium chabaudi adami causes a nonlethal infection in mice.

12 P chabaudi adami causes a nonlethal infection, mainly in m

13 pleen-dependent parasite killing during a P. chabaudi adami infection in mice.

14 In gamma transgenic mice infected with P chabaudi adami, the parasitemia rose more quickly (in ag

15 ythrocytes and bacteria in the spleens of P. chabaudi adami-infected mice during precrisis (a period

16 munized with purified recombinant Plasmodium chabaudi AMA-1 (PcAMA-1) and/or the 42-kDa C-terminal pr

17 he transformation of mature blood-stage P.c. chabaudi and a description of a vector that targets effi

18 d to maintain protective immunity against P. chabaudi and aid in establishing the molecular basis of

19 cient (J(H(-/-))) mice were infected with P. chabaudi and depleted of NK cells or gammadelta T cells

20 P chabaudi and P berghei iRBCs with apoptotic parasites (T

21 sites Plasmodium falciparum and P. vivax: P. chabaudi and P. falciparum infect red blood cells (RBC)

22 een two rodent malaria parasites, Plasmodium chabaudi and P. yoelii.

23 n mice demonstrated oral efficacy against P. chabaudi and the absence of obvious toxicity.

24 i.e. mice infected with malaria (Plasmodium chabaudi) and nematodes (Nippostrongylus brasiliensis).

25 ring the ascending parasitemia in Plasmodium chabaudi- and Plasmodium berghei-infected mice and the 4

26 II and have limited ability to present the P chabaudi antigen, merozoite surface protein-1, to specif

27 er antibody levels against P. berghei and P. chabaudi antigens than P. berghei-infected or P. chabaud

28 Plasmodium berghei and Plasmodium chabaudi are widely used model malaria species.

29 lethal malaria infection model of Plasmodium chabaudi AS in combination with the gastrointestinal nem

30 Plasmodium chabaudi AS infection during early pregnancy results in

31 We investigated this question for Plasmodium chabaudi AS infection in C57BL/6 mice.

32 chabaudi AS infection or production of isotype-switched

33 ffective immune response to and surviving P. chabaudi AS infection, pregnant mice cannot produce viab

34 chabaudi AS infection, the absence of ICOS resulted in a

35 e, we demonstrate that, in response to P. c. chabaudi AS infection, the absence of ICOS resulted in a

36 -term protective immunity against Plasmodium chabaudi AS malaria.

37 esis, A/J mice were infected with Plasmodium chabaudi AS, treated with intravenous ferric carboxymalt

38 the roles of IFN-gamma and TNF in Plasmodium chabaudi AS-induced fetal loss in mice were directly inv

39 C57BL/6 mice were inoculated with Plasmodium chabaudi AS-infected erythrocytes, and the responses to

40 r to our previous observations in Plasmodium chabaudi AS-infected mice.

41 mbryos on day 7 of gestation phagocytosed P. chabaudi AS-infected red blood cells and secreted tumor

42 parasitemia in mice infected with Plasmodium chabaudi AS.

43 alaria during pregnancy using the Plasmodium chabaudi AS/C57BL/6 mouse model.

44 pression of an avirulent clone of Plasmodium chabaudi (AS) by a virulent clone (AJ) in immuno-deficie

45 Four strains of P. c. chabaudi, AS, AJ, AQ, and CB, were studied.

46 Analysis of SBP P. c. chabaudi before and after mosquito transmission demonstr

47 Immunization with Plasmodium chabaudi by mosquito bite under chloroquine cover does n

48 me of the rodent malaria parasite Plasmodium chabaudi chabaudi (Pcc) isolate CB was characterized.

49 Blood-stage Plasmodium chabaudi chabaudi AS infection requires cell- and Ab-med

50 e against pathology during acute Plasmodium0 chabaudi chabaudi AS model of malaria.

51 ransgenic mice were infected with Plasmodium chabaudi chabaudi clone AS.

52 s" of the rodent malaria parasite Plasmodium chabaudi chabaudi in mice.

53 The rodent malaria parasite Plasmodium chabaudi chabaudi shares many features with human malari

54 regimen is protective against a nonlethal P. chabaudi chabaudi strain AS blood-stage challenge, resul

55 ra vectors encoding AMA1 from the Plasmodium chabaudi chabaudi strain AS.

56 of serially blood passaged (SBP) Plasmodium chabaudi chabaudi to interrogate regulation of parasite

57 and noncerebral malaria (clone AS Plasmodium chabaudi chabaudi), we quantified disease severity, para

58 primary erythrocytic infection of Plasmodium chabaudi chabaudi.

59 ted efficacy in a mouse model infected by P. chabaudi chabaudi.

60 deltao/o double KO mice passively against P. chabaudi challenge infection.

61 nsfer provided partial protection against P. chabaudi challenge, suggesting that the elimination of b

62 esis (FAS) in Tmem development in Plasmodium chabaudi chronic mouse malaria infection.

63 parasitemia during infection with Plasmodium chabaudi Concentrations of the closely related protein a

64 te membrane in the rodent malaria parasite P.chabaudi, demonstrates phenotypic similarity to the prod

65 d antigen on the malaria parasite Plasmodium chabaudi evolving in laboratory mice.

66 mental data in mice infected with Plasmodium chabaudi, finding that dying mice trace a large arc in r

67 del of SMA by infecting C57BL/6 mice with P. chabaudi followed after recovery by P. berghei infection

68 , single crossover integration into the P.c. chabaudi genome.

69 ent malaria species Plasmodium yoelii and P. chabaudi have been widely used to validate vaccine appro

70 Intact females also had higher anti-P. chabaudi immunoglobulin G (IgG) and IgG1 responses than

71 fection with the malaria parasite Plasmodium chabaudi, implying that another MYD88-dependent receptor

72 We examine the rodent malaria Plasmodium chabaudi in laboratory mice, a parasite-host system in w

73 also inhibits blood stage development of P. chabaudi in mice.

74 es of the rodent-malaria parasite Plasmodium chabaudi in vivo.

75 ed the percentage of plasma cells in both P. chabaudi-infected and uninfected groups but decreased th

76 mAb markedly reduced viral expression in P. chabaudi-infected animals.

77 MIF was detected in the sera of P. chabaudi-infected BALB/c mice, and circulating levels co

78 n this study, we report that ingestion of P. chabaudi-infected erythrocytes or malarial pigment (hemo

79 P-OVA were significantly decreased in the P. chabaudi-infected group compared with the uninfected gro

80 jection with T-independent NP-Ficoll, the P. chabaudi-infected group had significantly increased NP-s

81 G2c Ab was significantly increased in the P. chabaudi-infected group.

82 fourfold in the spleen and bone marrow of P. chabaudi-infected mice with active disease, as compared

83 cell responses in the spleens of Plasmodium chabaudi-infected mice.

84 tly, splenic CD11b(high)Ly6C(+) cells from P chabaudi-infected wild-type mice significantly reduce ac

85 on of the NP-specific IgG2c Ab induced by P. chabaudi infection but did not affect other NP-specific

86 tivate CMI against the parasite, suppress P. chabaudi infection by a redundant Ab-mediated process.

87 ta indicate that the suppression of acute P. chabaudi infection by CMI is gammadelta T cell dependent

88 During Plasmodium chabaudi infection in mice, a population of CD11b(high)L

89 data indicate that the early response to P. chabaudi infection of the blood is marked by a primary w

90 mediating sex differences in response to P. chabaudi infection, responses to infection were compared

91 These data suggest that during P. chabaudi infection, there is a shift toward an extrafoll

92 protects susceptible mice against lethal P. chabaudi infection.

93 to identify TLR7 as a key sensor of early P. chabaudi infection.

94 Blood-stage Plasmodium chabaudi infections are suppressed by antibody-mediated

95 e deficient in gammadelta T cells resolve P. chabaudi infections, we immunized deltao/o mice by infec

96 We propose that resistance to P. chabaudi is mediated by increased RBC turnover and highe

97 parasitemia of acute blood-stage Plasmodium chabaudi malaria by an antibody- or T-cell-dependent cel

98 es, we first compared the time courses of P. chabaudi malaria in CD28-deficient (CD28(-/-)) and CD28-

99 e in cell-mediated immunity (CMI) against P. chabaudi malaria, but delta-chain knockout (KO) (deltao/

100 SP-1(42) were partially protected against P. chabaudi malaria, indicating a role for protective antib

101 easured as protection against blood-stage P. chabaudi malaria.

102 is not necessary or sufficient to resolve P. chabaudi malaria.

103 gammadelta T cells during chronic Plasmodium chabaudi malaria.

104 on to vaccine blood-stage efficacy in the P. chabaudi model.

105 ne here the parallels between the Plasmodium chabaudi mouse model of malaria and human malaria.

106 Using the Plasmodium chabaudi mouse model of malaria and immunization with mo

107 42-kDa C-terminal processing fragment of P. chabaudi MSP-1 (MSP-1(42)).

108 n transgenic P. falciparum expressing the P. chabaudi MSP-1(19) orthologue, individuals with high-lev

109 misinin- and artesunate-resistant Plasmodium chabaudi mutants, AS-ART and AS-ATN, were previously sel

110 t chronic exposure to blood-stage Plasmodium chabaudi offers the best protection from parasitemia and

111 onkeys and humans (P. yoelii, P. berghei, P. chabaudi, P. knowlesi and P. vivax).

112 Red cells from P. chabaudi/P. berghei-infected animals had increased surfa

113 P. chabaudi/P. berghei-infected animals had more intense sp

114 nce microscopy showed that red cells from P. chabaudi/P. berghei-infected animals were removed at an

115 P. chabaudi/P. berghei-infected mice had an initial 9- to 1

116 -derived NO have a similar time course of P. chabaudi parasitemia as P. acnes-treated NOS20/0 mice, w

117 not required for the suppression of acute P. chabaudi parasitemia by AMI, CD28 costimulation is essen

118 ay contribute to the control of ascending P. chabaudi parasitemia during acute malaria but alone are

119 t that the time course shows that Plasmodium chabaudi parasitemia in NADPH oxidase KO (p47phox-/-) mi

120 roduction of NO during descending Plasmodium chabaudi parasitemia, a period when parasites are killed

121 n is not necessary for the suppression of P. chabaudi parasitemia.

122 ant fitness-determining trait and Plasmodium chabaudi parasites adjust their sex allocation in respon

123 oducible method to generate transformed P.c. chabaudi parasites expressing fluorescent, bioluminescen

124 tive oxygen intermediates, and phagocytose P chabaudi parasites in vitro, and in a proportion of the

125 This suggests that P. chabaudi parasites use kin discrimination to evaluate th

126 of the HIV-transgenic mice with PLASMODIUM: chabaudi parasites.

127 ease and lymphomagenesis, we used Plasmodium chabaudi (Pc) to produce chronic malaria infection in mi

128 P chabaudi primary and secondary parasitemia was similar i

129 audi antigens than P. berghei-infected or P. chabaudi-recovered animals.

130 rted that isolated, permeabilized Plasmodium chabaudi, releases Ca(2+) upon addition of exogenous IP(

131 fection of MIF knockout mice with Plasmodium chabaudi resulted in less severe anemia, improved erythr

132 on profiles in mice infected with Plasmodium chabaudi revealed and validated similar responses and hi

133 from mice infected with a single Plasmodium chabaudi strain, we estimate that transmission investmen

134 ns of the rodent malaria parasite Plasmodium chabaudi that differ in virulence.

135 We will highlight the contribution of P. chabaudi to our understanding of malaria in particular,

136 ozoite surface protein (MSP)-1 of Plasmodium chabaudi to show that activated T cells generate three d

137 sing the rodent model of malaria, Plasmodium chabaudi, we show that individual CIR proteins have diff

138 icial selection for resistance in Plasmodium chabaudi, we tested resilience of WP against drug resist

139 od cells from the rodent parasite Plasmodium chabaudi with seco-cyclopropyl pyrrolo indole analogs.