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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 rate that a dose of 250 mg/kg reduced the T. spiralis abundance in the digestive tract by 49%.
16  explain the effects of compound 1 on the T. spiralis adult worm.
17  hydraulic conductivity although Vallisneria spiralis affected photosynthetic activity of biofilm.
18 ippostrongylus brasiliensis, and Trichinella spiralis) alters intestinal epithelial cell function by
19 gnificantly delayed expulsion of Trichinella spiralis and increased deposition of muscle larvae in BA
20 wo other gut-dwelling nematodes (Trichinella spiralis and Nippostrongylus brasiliensis).
21 genes downstream of the first gene in the T. spiralis and T. muris operons are trans-spliced to splic
22 ected in the parasitic nematodes Trichinella spiralis and Trichinella pseudospiralis.
23 ity to larvae) in immunity to a helminth, T. spiralis, and defines the essential requirement for CCR3
24 Hg using 446 samples of Fucus ceranoides, F. spiralis, and F. vesiculosus collected between 1990 and
25 g hepatitis after infection with Trichinella spiralis, and inflammation is dependent on the migration
26 e used a natural mouse parasite, Trichinella spiralis, and multipoint intravital time-lapse confocal
27 OS-/- and iNOS-/+ mice were infected with T. spiralis, and parasite expulsion and intestinal patholog
28 ights still unresolved in the reaction to T. spiralis are the means by which mast cells respond to pa
29 ) and the muscle-stage larvae of Trichinella spiralis as a representative parasitic nematode.
30 ment coincides with expulsion of Trichinella spiralis, at a time when the majority of the MMCs are lo
31 st protection against N. brasiliensis and T. spiralis but contributes to expulsion of these two worms
32 re required for IL-4-induced expulsion of T. spiralis but not N. brasiliensis.
33 ts show that the intestinal life cycle of T. spiralis can be supported entirely by host epithelial ce
34 here that the parasitic nematode Trichinella spiralis can catalyze the conversion and thus modulate b
35 e forthcoming genome sequence of Trichinella spiralis can provide invaluable comparative information
36 mmalian skeletal muscle cells by Trichinella spiralis causes host nuclei to become polyploid (ca. 4N)
37                                  Trichinella spiralis creates a unique intracellular habitat in stria
38  stage of the parasitic nematode Trichinella spiralis displays on its surface glycoproteins that are
39 sly to intestinal infection with Trichinella spiralis, eliminating a role for T-bet in MC recruitment
40 tion with the parasitic nematode Trichinella spiralis, eosinophils play an important immune regulator
41       Because mice infected with Trichinella spiralis experience a pronounced, but transient, mastocy
42                                  Although T. spiralis expulsion required IL-4Ralpha expression by bot
43 endent, these observations suggested that T. spiralis expulsion would be Stat6 independent.
44  cells are required for IL-4 induction of T. spiralis expulsion.
45 secondary infection, rats expel 90-99% of T. spiralis first-stage larvae from the intestine in a matt
46 cal responses of Fucus vesiculosus and Fucus spiralis from Portugal and Wales (UK), representing, res
47  a critical role in clearance of Trichinella spiralis from the intestinal tract.
48 xpulsion of the related nematode Trichinella spiralis from these animals.
49 sion of the intestinal nematode, Trichinella spiralis, from the small intestine.
50                              We find that T. spiralis genes located in operons have an increased like
51  meat products contaminated with Trichinella spiralis had entered the food chain in Germany in March
52 rial DNA (mtDNA) of the nematode Trichinella spiralis has been amplified in four overlapping fragment
53 body response to the L1 stage of Trichinella spiralis has been described as biphasic.
54 udies with rodents infected with Trichinella spiralis, Heligmosomoides polygyrus, Nippostronglyus bra
55 earing antigens in immune defense against T. spiralis; however, the potency of the immune response in
56 rvival of the parasitic nematode Trichinella spiralis in an intracellular environment are poorly char
57 lated early (day 3) during infection with T. spiralis in BALB/c mice, suggesting an innate response,
58  by the intraepithelial nematode Trichinella spiralis in jejunal epithelium from BALB/c mice.
59 ctor phase of protective immunity against T. spiralis in rats.
60 d especially highlights the importance of F. spiralis in the food chain of Mediterranean countries.
61 flammation during development of Trichinella spiralis in the muscle.
62 asion, reflecting the broad host range of T. spiralis in vivo.
63 or of protective immune responses against T. spiralis in vivo.
64  mice with the nematode parasite Trichinella spiralis induces changes in the proteome of the jejunal
65           Primary intestinal infection by T. spiralis induces mastocytosis, and mast cell degranulati
66 ion with the parasitic nematode, Trichinella spiralis, induces a pronounced eosinophilia that coincid
67  properties were evaluated using Trichinella spiralis infected mice.
68  IgE production and consumption in 10-day T. spiralis infected rats showed that about 4.67 microg IgE
69 rved in the jejunal submucosa of Trichinella spiralis-infected BALB/c mice.
70 rvival, was significantly up-regulated in T. spiralis-infected beta(6)(-/-) mice compared with infect
71                                     Using T. spiralis-infected beta(6)(-/-) mice, we show accumulatio
72                      In vivo treatment of T. spiralis-infected IFN-gamma knockout mice with rIL-18 de
73 Cs in the jejunal submucosa and spleen of T. spiralis-infected mice expressed this serine protease du
74 6 activation by IL-4/IL-13 is required in T. spiralis-infected mice for the mast cell responses that
75 HT metabolism whilst afferent activity in T. spiralis-infected mice was studied by extracellular reco
76   Jejunal segments isolated from Trichinella spiralis-infected mice were used to assess 5-HT metaboli
77  mesenteric lymph nodes (mLN) of Trichinella spiralis-infected mice.
78  MC responses and parasite elimination in T. spiralis-infected mice.
79     Previous work has shown that Trichinella spiralis-infected rats transport IgE from plasma to inte
80  2,617 were present in all uninfected and T. spiralis-infected replicates, 8% of which were notably u
81                 Anthelmintic treatment of T. spiralis-infected rodents with mebendazole (MBZ) causes
82 parasite expulsion from the gut following T. spiralis infection and participates in the response to l
83 l antigens during the intestinal phase of T. spiralis infection and to test the antiparasitic effects
84                                  Trichinella spiralis infection elicits a vigorous IgE response and p
85 nduction of IL4 responses during Trichinella spiralis infection enhance the presence of nTh1 cells.
86 ansport to the gut and circulation during T. spiralis infection in rats.
87 We tested the influence of eosinophils on T. spiralis infection in two mouse strains in which the eos
88                                           T. spiralis infection increased mucosal 5-HT bioavailabilit
89                                  Trichinella spiralis infection induces a strong type 2 cytokine-medi
90  We previously demonstrated that Trichinella spiralis infection inhibits host inducible NO synthase (
91                            After Trichinella spiralis infection of mice, we show that basophil respon
92 n-2, and compare expression levels during T. spiralis infection of resistant (BALB/c) with susceptibl
93 responses and inflammation after Trichinella spiralis infection or the induction of food allergy-like
94    The IgE present in serum 10 days after T. spiralis infection originated in the gut and/or associat
95  the kinetics of its up-regulation during T. spiralis infection suggest that this novel lectin may se
96  therefore investigated the role of NO in T. spiralis infection using iNOS-deficient mice.
97 -18 knockout mice are highly resistant to T. spiralis infection, expel the worms rapidly and subseque
98                    Secreted proteins from T. spiralis infective larvae inhibit nucleotide-induced mas
99 roteins contributes to protection against T. spiralis invasion but that surface binding alone is not
100                                  Trichinella spiralis is a highly destructive parasitic nematode that
101                                  Trichinella spiralis is an obligate parasite of animals that has an
102 of the gastrointestinal nematode Trichinella spiralis is associated with pronounced mastocytosis medi
103 tion with the parasitic nematode Trichinella spiralis is initiated when the L1 larva invades host int
104 Nippostrongylus brasiliensis and Trichinella spiralis, is similar in that both require IL-4Ralpha exp
105  (introduction of the macrophyte Vallisneria spiralis (L.) or the gastropod Viviparus viviparus (Linn
106 tect intracellular, muscle-stage Trichinella spiralis larvae against NO-mediated killing.
107 phil lineage is ablated, large numbers of T. spiralis larvae are killed by NO, implicating the eosino
108 gnificant difference in their response to T. spiralis larvae in chronically infected skeletal muscle
109                        We have found that T. spiralis larvae molt, ecdyse, develop to adulthood, and
110                             The number of T. spiralis larvae present in the skeletal muscle of IgE(-/
111                                  Trichinella spiralis larvae were identified in wild boar meat sample
112                          Actively growing T. spiralis larvae were susceptible to killing by NO in vit
113                            Roberts and Fucus spiralis Linnaeus are among the most active species, whi
114 ra usneoides (Linnaeus) M. Roberts and Fucus spiralis Linnaeus are among the most active species, whi
115 SLE) of three brown macroalgae, namely Fucus spiralis Linnaeus, Pelvetia canaliculata (Linnaeus) Deca
116 ens (NA) recognized by antibodies against T. spiralis localized to infected cell nuclei.
117 the expulsion of the GI parasite Trichinella spiralis may be dependent on IL-4 and mediated by TNF, p
118 e; however, in the absence of eosinophils T. spiralis muscle larvae died in large numbers.
119                                        Fucus spiralis, Porphyra sp. and Osmundea pinnatifida are macr
120                   Infection with Trichinella spiralis rarely leads to significant morbidity.
121 From its intracellular habitat in muscle, T. spiralis secretes potent glycoprotein antigens that elic
122 lid standing, 'P. telluritireducens' and 'P. spiralis', should be associated with the validly publish
123 d peritonitis and infection with Trichinella spiralis, stimulated similar responses in Galpha15(-/-)
124  enzymes in secreted products of Trichinella spiralis suggests that endoparasites use similar mechani
125  1) local jejunal inflammation induced by T. spiralis systemically inhibits NOS-2 gene transcription,
126      In parasitic infection with Trichinella spiralis, the immune response incorporates both lymphocy
127 are targeted by rat antibodies that cause T. spiralis to be expelled from the intestine.
128  have used the parasite helminth Trichinella spiralis to study the generation and differentiation of
129 aused by an intestinal parasite, Trichinella spiralis, to study the relationship between intestinal i
130 s used to examine molecular mechanisms in T. spiralis treated with quercetin.
131  We have surveyed the genomes of Trichinella spiralis, Trichuris muris, and Romanomermis culicivorax
132 ection of mice with the nematode Trichinella spiralis triggers recruitment and differentiation of int
133                                    The 22 T. spiralis tRNA genes fall into three categories: (i) thos
134     Molecular docking analysis showed the T. spiralis tubulin beta chain and glutamate-gated channels
135 other gastrointestinal nematode, Trichinella spiralis, unlike N. brasiliensis expulsion, is mast cell
136  chymase efficiently degrade the Trichinella spiralis virulence factor heat shock protein 70 (Hsp70)
137  stage of the parasitic nematode Trichinella spiralis was shown to invade epithelial cell monolayers
138 d in BALB/c mice following infection with T. spiralis was significantly diminished in IgE(-/-) mice w
139 choline-related antibody response against T. spiralis was T independent.
140 ejunum of BALB/c mice exposed to Trichinella spiralis were assessed during the course of the infectio
141 uced in rats 16 days after infection with T. spiralis were specific for phosphorylcholine-bearing pro
142 t contribute to immunity against Trichinella spiralis, which lives within IEC.
143 across all C. elegans strains and against T. spiralis, while demonstrating minimal cytotoxicity in hu

 
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