ライフサイエンスコーパス: chagasi

1 Leishmania donovani and Leishmania infantum chagasi.

2 with fluorescent mCherry-labeled L. infantum chagasi.

3 presence and absence of Leishmania infantum chagasi.

4 urrounding the invading protozoan Leishmania chagasi.

5 but not human, macrophages infected with L. chagasi.

6 the visceralizing species of Leishmania, L. chagasi.

7 ceralizing species of Leishmania, Leishmania chagasi.

8 vestigated protective immunity to Leishmania chagasi, a cause of visceral leishmaniasis.

9 s analysis suggests that Leishmania infantum chagasi alters the expression profile of certain midgut

10 tained granulomas harboring intracellular L. chagasi amastigotes, whereas few amastigotes were presen

11 y inhibited the in vivo growth of Leishmania chagasi and Leishmania amazonensis promastigotes, by imp

12 te the clinical outcome of infection with L. chagasi and the function of infected macrophages.

13 idase coding region were transfected into L. chagasi, and beta-galactosidase activity and mRNA levels

14 antigen, recombinant (r) K39, of Leishmania chagasi are specific for members of the Leishmania donov

15 at s.c. inoculation of high doses of live L. chagasi causes a subclinical infection that elicits prot

16 e vector-borne protozoan Leishmania infantum chagasi causes minimal inflammation after inoculation in

17 Leishmania chagasi causes visceral leishmaniasis and, to a lesser e

18 pecies of such protozoa, Leishmania donovani chagasi causes visceral leishmaniasis.

19 From 3 days onward, total L. infantum chagasi-containing dermal leukocytes and total L. infant

20 Nonetheless, a second wave of L. infantum chagasi-containing neutrophils occurred 7 days after par

21 her this organ-specific multiplication of L. chagasi correlates with localized immune responses, we c

22 ne response of dogs infected with Leishmania chagasi, cytokine mRNA levels were measured in bone marr

23 ive patients infected with L. infantum or L. chagasi declined during treatment with meglumine antimon

24 or with L. major promastigotes, and s.c. L. chagasi did not protect against infection with L. major.

25 n BALB/c mice that were immunized against L. chagasi disease.

26 ta suggest that macrophages infected with L. chagasi exhibit a hybrid activation profile that is more

27 Transfection of promastigotes with L. chagasi HSP70 caused a heat-inducible increase in resist

28 om cutaneous leishmanial lesions, Leishmania chagasi in dermal scrapings of atypical cutaneous leishm

29 ch contribute to intracellular killing of L. chagasi in human and murine macrophages.

30 F-beta inhibited killing of intracellular L. chagasi in macrophages, although the phagocytosis-induce

31 f murine visceral leishmaniasis caused by L. chagasi, independently of Th2-type cytokines.

32 eta levels are significantly increased in L. chagasi-infected mice.

33 rgue that HO-1 has a critical role in the L. chagasi infection and is strongly associated with the in

34 Furthermore, L. chagasi infection caused an increase in biologically act

35 We found that L. chagasi infection or lipophosphoglycan isolated from pro

36 sentinel dogs exposed to natural Leishmania chagasi infection was assessed through time by xenodiagn

37 Upon L. chagasi infection, macrophages from Hmox1 knockout mice

38 mice, which are genetically resistant to L. chagasi infection, produce abundant IFN-gamma.

39 rrow macrophages with and without Leishmania chagasi infection.

40 locus are associated with the outcome of L. chagasi infection.

41 asymptomatic or symptomatic disease after L. chagasi infection.

42 vani, or L. major did not protect against L. chagasi infection.

43 become significantly more susceptible to L. chagasi infection.

44 r granuloma cells from BALB/c mice during L. chagasi infection.

45 asis (VL) caused by the protozoan Leishmania chagasi is ongoing outside Natal, northeast Brazil.

46 with DHFR-TS gene knockouts derived from L. chagasi, L. donovani, or L. major did not protect agains

47 Humans naturally infected with L. chagasi mounted both cellular and antibody responses to

48 late the parallel expression of these two L. chagasi mRNAs despite their lack of sequence identity.

49 s.c. immunization with either attenuated L. chagasi or with L. major promastigotes, and s.c. L. chag

50 Leishmania chagasi) parasite in the gut, but the extent to which th

51 ning dermal leukocytes and total L. infantum chagasi parasites in draining lymph nodes were similar i

52 flies, known vectors of Leishmania infantum/chagasi parasites, in a Brazilian city endemic with visc

53 ided an in vitro model of phagocytosis of L. chagasi promastigotes and intracellular conversion to am

54 GP46 mRNA increases >>30-fold as Leishmania chagasi promastigotes develop in vitro from a less infec

55 ng in about a 30-fold increase as Leishmania chagasi promastigotes grow in vitro from logarithmic pha

56 upon infection of human macrophages with L. chagasi promastigotes in vitro in the presence of IFN-ga

57 n site, we introduced metacyclic L. infantum chagasi promastigotes intradermally into BALB/c mouse ea

58 cytes infected with MBL-opsonized Leishmania chagasi promastigotes secreted higher levels of tumor ne

59 to L. major, a high dose s.c. inoculum of L. chagasi promastigotes was required to elicit protective

60 Metacyclic Leishmania infantum chagasi promastigotes were treated with methyl-beta-cycl

61 onclude that a unique pattern of selected L. chagasi proteins and RNAs is induced following phagocyto

62 developed a method to label live Leishmania chagasi short-term with fluorescent dyes.

63 However, L. chagasi that have been attenuated either by long-term pa

64 HO-1 in the infection by Leishmania infantum chagasi, the causative agent of VL cases in Brazil.

65 intracellular amastigote form of Leishmania chagasi, the cause of South American visceral leishmania

66 Leishmania chagasi, the cause of South American visceral leishmania

67 ce during development of Leishmania infantum chagasi to a virulent metacyclic stage, as did the expre

68 The ability of the protozoan Leishmania chagasi to infect a vertebrate host depends on its abili

69 even late after inoculation, and L. infantum chagasi trafficked through neutrophils in both neutrophi

70 eroxide and hydrogen peroxide, on Leishmania chagasi virulence.