ライフサイエンスコーパス: spiralis

1 rs of invasion and niche establishment by T. spiralis.

2 tibodies protect epithelial cells against T. spiralis.

3 ct rats against intestinal infection with T. spiralis.

4 0 to 289 h) of an infection with Trichinella spiralis.

5 f a secondary immune response to Trichinella spiralis.

6 is following oral infection with Trichinella spiralis.

7 ive when C57BL/10 mice were infected with T. spiralis.

8 f eosinophils in secondary infection with T. spiralis.

9 llular responses to muscle-stage Trichinella spiralis.

10 n the mouse after infection with Trichinella spiralis.

11 estigation of intracellular parasitism by T. spiralis.

12 tage of tools for in vitro cultivation of T. spiralis.

13 eport a draft genome sequence of Trichinella spiralis, a food-borne zoonotic parasite, which is the m

14 The mouse is a natural host for Trichinella spiralis, a worm that establishes chronic infection in s

15 hydraulic conductivity although Vallisneria spiralis affected photosynthetic activity of biofilm.

16 ippostrongylus brasiliensis, and Trichinella spiralis) alters intestinal epithelial cell function by

17 gnificantly delayed expulsion of Trichinella spiralis and increased deposition of muscle larvae in BA

18 wo other gut-dwelling nematodes (Trichinella spiralis and Nippostrongylus brasiliensis).

19 genes downstream of the first gene in the T. spiralis and T. muris operons are trans-spliced to splic

20 ected in the parasitic nematodes Trichinella spiralis and Trichinella pseudospiralis.

21 ity to larvae) in immunity to a helminth, T. spiralis, and defines the essential requirement for CCR3

22 g hepatitis after infection with Trichinella spiralis, and inflammation is dependent on the migration

23 e used a natural mouse parasite, Trichinella spiralis, and multipoint intravital time-lapse confocal

24 OS-/- and iNOS-/+ mice were infected with T. spiralis, and parasite expulsion and intestinal patholog

25 ights still unresolved in the reaction to T. spiralis are the means by which mast cells respond to pa

26 ment coincides with expulsion of Trichinella spiralis, at a time when the majority of the MMCs are lo

27 st protection against N. brasiliensis and T. spiralis but contributes to expulsion of these two worms

28 re required for IL-4-induced expulsion of T. spiralis but not N. brasiliensis.

29 ts show that the intestinal life cycle of T. spiralis can be supported entirely by host epithelial ce

30 here that the parasitic nematode Trichinella spiralis can catalyze the conversion and thus modulate b

31 e forthcoming genome sequence of Trichinella spiralis can provide invaluable comparative information

32 mmalian skeletal muscle cells by Trichinella spiralis causes host nuclei to become polyploid (ca. 4N)

33 Trichinella spiralis creates a unique intracellular habitat in stria

34 stage of the parasitic nematode Trichinella spiralis displays on its surface glycoproteins that are

35 sly to intestinal infection with Trichinella spiralis, eliminating a role for T-bet in MC recruitment

36 tion with the parasitic nematode Trichinella spiralis, eosinophils play an important immune regulator

37 Because mice infected with Trichinella spiralis experience a pronounced, but transient, mastocy

38 Although T. spiralis expulsion required IL-4Ralpha expression by bot

39 endent, these observations suggested that T. spiralis expulsion would be Stat6 independent.

40 cells are required for IL-4 induction of T. spiralis expulsion.

41 secondary infection, rats expel 90-99% of T. spiralis first-stage larvae from the intestine in a matt

42 cal responses of Fucus vesiculosus and Fucus spiralis from Portugal and Wales (UK), representing, res

43 a critical role in clearance of Trichinella spiralis from the intestinal tract.

44 xpulsion of the related nematode Trichinella spiralis from these animals.

45 sion of the intestinal nematode, Trichinella spiralis, from the small intestine.

46 We find that T. spiralis genes located in operons have an increased like

47 meat products contaminated with Trichinella spiralis had entered the food chain in Germany in March

48 rial DNA (mtDNA) of the nematode Trichinella spiralis has been amplified in four overlapping fragment

49 body response to the L1 stage of Trichinella spiralis has been described as biphasic.

50 udies with rodents infected with Trichinella spiralis, Heligmosomoides polygyrus, Nippostronglyus bra

51 earing antigens in immune defense against T. spiralis; however, the potency of the immune response in

52 rvival of the parasitic nematode Trichinella spiralis in an intracellular environment are poorly char

53 lated early (day 3) during infection with T. spiralis in BALB/c mice, suggesting an innate response,

54 by the intraepithelial nematode Trichinella spiralis in jejunal epithelium from BALB/c mice.

55 ctor phase of protective immunity against T. spiralis in rats.

56 d especially highlights the importance of F. spiralis in the food chain of Mediterranean countries.

57 flammation during development of Trichinella spiralis in the muscle.

58 asion, reflecting the broad host range of T. spiralis in vivo.

59 or of protective immune responses against T. spiralis in vivo.

60 mice with the nematode parasite Trichinella spiralis induces changes in the proteome of the jejunal

61 Primary intestinal infection by T. spiralis induces mastocytosis, and mast cell degranulati

62 ion with the parasitic nematode, Trichinella spiralis, induces a pronounced eosinophilia that coincid

63 IgE production and consumption in 10-day T. spiralis infected rats showed that about 4.67 microg IgE

64 rved in the jejunal submucosa of Trichinella spiralis-infected BALB/c mice.

65 rvival, was significantly up-regulated in T. spiralis-infected beta(6)(-/-) mice compared with infect

66 Using T. spiralis-infected beta(6)(-/-) mice, we show accumulatio

67 In vivo treatment of T. spiralis-infected IFN-gamma knockout mice with rIL-18 de

68 Cs in the jejunal submucosa and spleen of T. spiralis-infected mice expressed this serine protease du

69 6 activation by IL-4/IL-13 is required in T. spiralis-infected mice for the mast cell responses that

70 HT metabolism whilst afferent activity in T. spiralis-infected mice was studied by extracellular reco

71 Jejunal segments isolated from Trichinella spiralis-infected mice were used to assess 5-HT metaboli

72 mesenteric lymph nodes (mLN) of Trichinella spiralis-infected mice.

73 MC responses and parasite elimination in T. spiralis-infected mice.

74 Previous work has shown that Trichinella spiralis-infected rats transport IgE from plasma to inte

75 2,617 were present in all uninfected and T. spiralis-infected replicates, 8% of which were notably u

76 Anthelmintic treatment of T. spiralis-infected rodents with mebendazole (MBZ) causes

77 parasite expulsion from the gut following T. spiralis infection and participates in the response to l

78 l antigens during the intestinal phase of T. spiralis infection and to test the antiparasitic effects

79 Trichinella spiralis infection elicits a vigorous IgE response and p

80 nduction of IL4 responses during Trichinella spiralis infection enhance the presence of nTh1 cells.

81 ansport to the gut and circulation during T. spiralis infection in rats.

82 We tested the influence of eosinophils on T. spiralis infection in two mouse strains in which the eos

83 T. spiralis infection increased mucosal 5-HT bioavailabilit

84 Trichinella spiralis infection induces a strong type 2 cytokine-medi

85 We previously demonstrated that Trichinella spiralis infection inhibits host inducible NO synthase (

86 After Trichinella spiralis infection of mice, we show that basophil respon

87 n-2, and compare expression levels during T. spiralis infection of resistant (BALB/c) with susceptibl

88 responses and inflammation after Trichinella spiralis infection or the induction of food allergy-like

89 The IgE present in serum 10 days after T. spiralis infection originated in the gut and/or associat

90 the kinetics of its up-regulation during T. spiralis infection suggest that this novel lectin may se

91 therefore investigated the role of NO in T. spiralis infection using iNOS-deficient mice.

92 -18 knockout mice are highly resistant to T. spiralis infection, expel the worms rapidly and subseque

93 Secreted proteins from T. spiralis infective larvae inhibit nucleotide-induced mas

94 roteins contributes to protection against T. spiralis invasion but that surface binding alone is not

95 Trichinella spiralis is a highly destructive parasitic nematode that

96 Trichinella spiralis is an obligate parasite of animals that has an

97 of the gastrointestinal nematode Trichinella spiralis is associated with pronounced mastocytosis medi

98 tion with the parasitic nematode Trichinella spiralis is initiated when the L1 larva invades host int

99 Nippostrongylus brasiliensis and Trichinella spiralis, is similar in that both require IL-4Ralpha exp

100 (introduction of the macrophyte Vallisneria spiralis (L.) or the gastropod Viviparus viviparus (Linn

101 tect intracellular, muscle-stage Trichinella spiralis larvae against NO-mediated killing.

102 phil lineage is ablated, large numbers of T. spiralis larvae are killed by NO, implicating the eosino

103 gnificant difference in their response to T. spiralis larvae in chronically infected skeletal muscle

104 We have found that T. spiralis larvae molt, ecdyse, develop to adulthood, and

105 The number of T. spiralis larvae present in the skeletal muscle of IgE(-/

106 Trichinella spiralis larvae were identified in wild boar meat sample

107 Actively growing T. spiralis larvae were susceptible to killing by NO in vit

108 Roberts and Fucus spiralis Linnaeus are among the most active species, whi

109 ra usneoides (Linnaeus) M. Roberts and Fucus spiralis Linnaeus are among the most active species, whi

110 SLE) of three brown macroalgae, namely Fucus spiralis Linnaeus, Pelvetia canaliculata (Linnaeus) Deca

111 ens (NA) recognized by antibodies against T. spiralis localized to infected cell nuclei.

112 the expulsion of the GI parasite Trichinella spiralis may be dependent on IL-4 and mediated by TNF, p

113 e; however, in the absence of eosinophils T. spiralis muscle larvae died in large numbers.

114 Fucus spiralis, Porphyra sp. and Osmundea pinnatifida are macr

115 Infection with Trichinella spiralis rarely leads to significant morbidity.

116 From its intracellular habitat in muscle, T. spiralis secretes potent glycoprotein antigens that elic

117 d peritonitis and infection with Trichinella spiralis, stimulated similar responses in Galpha15(-/-)

118 enzymes in secreted products of Trichinella spiralis suggests that endoparasites use similar mechani

119 1) local jejunal inflammation induced by T. spiralis systemically inhibits NOS-2 gene transcription,

120 In parasitic infection with Trichinella spiralis, the immune response incorporates both lymphocy

121 are targeted by rat antibodies that cause T. spiralis to be expelled from the intestine.

122 have used the parasite helminth Trichinella spiralis to study the generation and differentiation of

123 aused by an intestinal parasite, Trichinella spiralis, to study the relationship between intestinal i

124 We have surveyed the genomes of Trichinella spiralis, Trichuris muris, and Romanomermis culicivorax

125 ection of mice with the nematode Trichinella spiralis triggers recruitment and differentiation of int

126 The 22 T. spiralis tRNA genes fall into three categories: (i) thos

127 other gastrointestinal nematode, Trichinella spiralis, unlike N. brasiliensis expulsion, is mast cell

128 chymase efficiently degrade the Trichinella spiralis virulence factor heat shock protein 70 (Hsp70)

129 stage of the parasitic nematode Trichinella spiralis was shown to invade epithelial cell monolayers

130 d in BALB/c mice following infection with T. spiralis was significantly diminished in IgE(-/-) mice w

131 choline-related antibody response against T. spiralis was T independent.

132 ejunum of BALB/c mice exposed to Trichinella spiralis were assessed during the course of the infectio

133 uced in rats 16 days after infection with T. spiralis were specific for phosphorylcholine-bearing pro

134 t contribute to immunity against Trichinella spiralis, which lives within IEC.