Trichinella spiralis: An Intracellular Parasite in the Intestinal Phase

Wright, K. A.

doi:10.2307/3280292

Cited by 107 publications

(49 citation statements)

References 6 publications

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“…The T. spiralis life cycle is completed when these immature L1 larvae invade the striated muscle cells of the host (Bruschi & Murrel 2000;Schantz & Dietz 2001). During the intestinal phase of infection, larvae and adult parasites establish an intramulticellular niche composed by serial rows of enterocytes (Despommier et al 1978;Wright 1979). The tyvelose-bearing excretory/secretory products (ESP) of L1 larvae probably help the process of invasion (McVay et al 1998).…”

Section: Introductionmentioning

confidence: 99%

Glycosylation changes in different developmental stages of Trichinella

et al. 2009

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Abstract:The in situ identification of carbohydrate structures in Trichinella spiralis intestinal larvae, adults and L1 muscular larvae was carried out by lectin histochemistry, with emphasis on the O-linked glycans. The absence of reactivity with two lectins-TML and MAL indicated thatTrichinella spiralis does not synthesize sialic acid. Reactivity with HPA, VVL-B4, PNA and UEA-I staining suggested that T. spiralis synthesizes and expresses on its cuticle O-linked glycans analogous to Tn-antigen (GalNAc-α-Ser/Thr), T-antigen (Gal-β1,3-GalNAc-α-Ser/Thr) and also structures analogous to A-blood group antigens (GalNAc-α1,3-Gal-β1,3(4)-(Fuc-α1,2-)-R). Expression of the saccharidic moieties is stage-specific. Blood group-A and T-antigen structures were identified on the cuticle of the intestinal and muscular larvae. The Tn-antigen structure was missing in the intestinal larvae. Appropriate ligands for WGA were not identified in the adult individuals. The obtained results may contribute to a better understanding of the glycobiology of this parasitic nematode in relation to occupation of its intracellular niche. The presence of saccharidic structures analogous to some of those expressed on the intestinal epithelial cells may serve as a protective shield on the surface of the parasite.

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Section: Introductionmentioning

confidence: 99%

Glycosylation changes in different developmental stages of Trichinella

et al. 2009

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“…The epithelium can itself respond to pathogens, for example, by the secretion of chloride ions and water by enterocytes (11, 51), by increased polyimmunoglobulin receptor-mediated transport of pathogen-specific immunoglobulin A (IgA) across the enterocytes (10), and by the release of mucus from goblet cells and of antimicrobial peptides from Paneth cells (37, 49). Thus, the resulting elimination of the pathogen and the associated pathology will be a complex product of both innate and pathogen-specific effector mechanisms.The intestinal nematode Trichinella spiralis dwells within epithelium and actively invades epithelial cells (36,69). This is associated with major pathological changes within the epithelial compartment such as villus atrophy and crypt hyperplasia, increased epithelial permeability, goblet cell and Paneth cell hyperplasia, and infiltration by mucosal mast cells (20,25).…”

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confidence: 99%

Expression Profiling Reveals Novel Innate and Inflammatory Responses in the Jejunal Epithelial Compartment during Infection withTrichinella spiralis

et al. 2004

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Infection with intestinal nematodes induces profound pathological changes to the gut that are associated with eventual parasite expulsion. We have applied expression profiling as an initial screening process with oligonucleotide microarrays (Affymetrix MG-U74AV2 gene chips) and time course kinetics to investigate gene transcription triggered by the intraepithelial nematode Trichinella spiralis in jejunal epithelium from BALB/c mice. Of the 4,114 genes detected, 2,617 were present in all uninfected and T. spiralis-infected replicates, 8% of which were notably upregulated, whereas 12% were downregulated at the time of worm expulsion (day 14 postinfection). Upregulation of goblet cell mucin gene transcripts intestinal mucin gene 3 (MUC3), calcium chloride channel 5 (CLCA5), and goblet cell gene 4 (GOB4) is consistent with enhanced production and alteration of mucus, whereas a 60-to 70-fold upregulation of transcripts for mast cell proteases 1 and 2 (MCPT-1 and -2) is consistent with intraepithelial mucosal mast cell recruitment. Intestinal infection can induce substantial pathological changes in the epithelial compartment (1, 37, 59). These may be preceded by specific immune responses in the lamina propria, Peyer's patches and mesenteric lymph nodes (66) and may trigger the activation of intraepithelial lymphocytes and the recruitment of inflammatory cells into the epithelial compartment (7, 39). The epithelium can itself respond to pathogens, for example, by the secretion of chloride ions and water by enterocytes (11, 51), by increased polyimmunoglobulin receptor-mediated transport of pathogen-specific immunoglobulin A (IgA) across the enterocytes (10), and by the release of mucus from goblet cells and of antimicrobial peptides from Paneth cells (37, 49). Thus, the resulting elimination of the pathogen and the associated pathology will be a complex product of both innate and pathogen-specific effector mechanisms.The intestinal nematode Trichinella spiralis dwells within epithelium and actively invades epithelial cells (36,69). This is associated with major pathological changes within the epithelial compartment such as villus atrophy and crypt hyperplasia, increased epithelial permeability, goblet cell and Paneth cell hyperplasia, and infiltration by mucosal mast cells (20,25). Some of these profound changes are immunologically mediated and are temporally associated with the rejection of adult worms (25, 33). Infection of BALB/c mice with T. spiralis is a particularly well-characterized model of infection, where parasite expulsion is partially dependent on the recruitment and activity of mucosal mast cells (28,65) Although the molecular pathology of intestinal infection is generally studied in the context of specific mechanisms, a global approach such as that afforded by transcriptomics may highlight some of the molecular pathways involved or indeed bring novel mechanisms to light. The aim of the present study was to examine, by using oligonucleotide microarrays (Affymetrix MG-U74AV2), the effect of T. spiralis on ...

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“…Our results as well as morphological studies of different stages of T. spiralis by Wright (1979) and Despommier (1976) demonstrated that in addition lO the effect on membranous systems the larvae destruct cells and cause consequently a release of enzymes into extracellular space.…”

Section: Discussionmentioning

confidence: 55%

Activity of Aldolase in the Course of Experimental Trichinellosis in Guinea-pigs

Koudela¹

1983

Acta Vet. Brno

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Koudela B.: Activity of Aldolase in the Course of Experimental Trichinellosis in Guinea-pigs. Acta vet. Brno, 52, 1983; 169 -176. The activity of aldolase was determined in blood plasma and homogenates from the duodenal wall, masseter and heart musculature at different intervals after experimental infection of guinea pigs by Trichinella spiralis larvae. There were significant changes of enzymatic activity in all tissues studied. The dynamics of changes in the course of experimental trichinellosis was closely related to the life cycle of the parasite. The changes were due to altered permeability of cell membranes as well as to mechanical affection of surrounding tissue.

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Trichinella spiralis: An Intracellular Parasite in the Intestinal Phase

Cited by 107 publications

References 6 publications

Glycosylation changes in different developmental stages of Trichinella

Glycosylation changes in different developmental stages of Trichinella

Expression Profiling Reveals Novel Innate and Inflammatory Responses in the Jejunal Epithelial Compartment during Infection withTrichinella spiralis

Activity of Aldolase in the Course of Experimental Trichinellosis in Guinea-pigs

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