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Spiralis Infection (spirali + infection)

Distribution by Scientific Domains

Medical Sciences	83%

Selected Abstracts

Long-lasting changes in small intestinal transport following the recovery from Trichinella spiralis infection

NEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2006
K. Venkova
Abstract, Changes in intestinal motility and visceral sensitivity are found after resolution of acute enteric inflammation. The study investigates whether a transient nematode-induced intestinal inflammation may result in long-lasting remodelling of epithelial transport. Ferrets infected with Trichinella spiralis or sham-infected animals were euthanized on day 10, 30 or 60 postinfection (PI) and the jejunum was isolated. The net transport of electrolytes was measured electrophysiologically as transmucosal short-circuit current (Isc) and responses to electrical field stimulation (EFS: 1,32 Hz) or secretagogues were investigated. Myeloperoxidase (MPO) activity, a marker of mucosal inflammation, was maximal during the enteric stage of T. spiralis infection (day 10 PI) and returned to normal on days 30 and 60 PI. Mucosal inflammation caused a reduction in basal Isc, increased electrical conductance (G) and decreased the maximal responses to EFS, carbachol or histamine. On days 30 and 60 PI the inflammation resolved and basal electrogenic transport appeared normal; however, the secretion induced by EFS, carbachol or histamine remained suppressed. Moreover, EFS-induced responses were shifted from predominantly cholinergic in controls to non-cholinergic in the infected animals. The results suggest that a transient small intestinal inflammation causes a long-term remodelling of epithelial function. [source]

Enterochromaffin cell hyperplasia and decreased serotonin transporter in a mouse model of postinfectious bowel dysfunction

NEUROGASTROENTEROLOGY & MOTILITY, Issue 6 2005
J. Wheatcroft
Abstract, Patients with postinfective irritable bowel syndrome and Trichinella spiralis -infected mice share many features including visceral hypersensitivity and disordered motility. We assessed enterochromaffin (EC) numbers and serotonin transporter (SERT) using National Institute of Health (NIH) female mice studied for up to 56 days post- T. spiralis infection. The effects of steroid treatment and the T-cell dependence of the observed responses were assessed by infection of hydrocortisone-treated or T-cell receptor knock out [TCR (,×,) KO] animals. Enterochromaffin cell density in uninfected animals increased from duodenum 10.0 cells mm,2 (5.9,41.0) to colon 61.8. (46.3,162) cells mm,2P < 0.0001. Infection increased duodenal and jejunal counts which rose to 37.3 (22,57.7) cells mm,2 and 50.6 (7,110.8) cells mm,2, respectively, at day 14. Infection significantly reduced jejunal SERT expression, with luminance values falling from 61.0 (45.1,98.3) to a nadir of 11.6 (0,36.0) units at day 9, P < 0.001. Specific deficiencies in all T cells reduced EC hyperplasia and abrogated infection-induced mastocytosis. Thus infection induced inflammation increases EC numbers, as has been reported in PI-IBS, and reduces SERT. This may increase mucosal 5HT availability and contribute to the clinical presentation of PI-IBS. [source]

Interleukin-5 deficient mice exhibit impaired host defence against challenge Trichinella spiralis infections

PARASITE IMMUNOLOGY, Issue 10 2000
B.A. Vallance
Enteric nematode infections are characterized by both peripheral and tissue eosinophilia. The cytokine interleukin (IL)-5 is considered a critical factor in the proliferation and recruitment of eosinophils, however, studies suggest it plays little role in host defence, at least during primary Trichinella spiralis infections. Less is known concerning its role in host defence or in the inflammatory response that develops against challenge infections with the same parasite. We examined these questions by infecting IL-5 deficient and wild-type mice, with T. spiralis parasites. Both strains expelled the primary infection by day 21. Forty days after the primary infection, we challenged the mice with a second T. spiralis infection and counted tissue eosinophils and worms in the intestine. While wild-type mice developed a large tissue eosinophilia, IL-5 deficient mice showed little increase in eosinophil numbers within the intestine. Throughout the challenge infection, significantly larger worm burdens were recovered from IL-5 deficient mice, and worm expulsion was also significantly slower (day 21) compared to wild-type mice (day 14). Thus, unlike in a primary infection, IL-5 is not only essential for the onset of intestinal eosinophilia, but also makes a significant contribution to enteric host defence during challenge T. spiralis infections. [source]

Secretion of IL-12 by murine macrophages activated by immunoglobulin receptor-mediated internalization of the surface coat of Trichinella spiralis larvae

PARASITE IMMUNOLOGY, Issue 3 2000
Modha
Trichinella spiralis larvae incubated with a rabbit antiserum raised against the larval surface coat bound murine macrophages to the parasite surface. Cell binding was not observed without the antisurface coat serum, or with incubation of larvae in normal rabbit serum, or with antibodies to keyhole limpet haemocyanin which identify a cryptic T. spiralis larval antigen. Cell adherence to the larval surface was lost by treatment of the cells with the lysosomotropic drug primaquine, implicating a receptor-mediated mechanism. Cells adhering to the parasite surface internalized parasite surface coat material, which was subsequently concentrated into endosomes. Culture supernatants from these cells contained enhanced levels of IL-12. Thus, the initial Th1 response to T. spiralis infection may be explained by these data. [source]

Epithelial stem cell-related alterations in Trichinella spiralis -infected small intestine

CELL PROLIFERATION, Issue 3 2009
R. Walsh
Objectives:, Infection of mice with the parasite Trichinella spiralis leads to small intestinal inflammation, characterized by changes in mucosal architecture and subpopulations of epithelial cells. This model has been used to explore changes in the epithelial proliferative cell population and expression of transforming growth factor-beta (TGF-,). Materials and methods:, Histochemical and immunohistochemical studies were undertaken in duodenal samples. Location and number of Ki-67-positive cells were assessed using Score and Wincrypts program. Changes in mRNA transcripts were studied by real-time RT-PCR. Results:,T. spiralis infection induced an increase in total number of proliferative (Ki-67-positive) cells per half crypt on day 2 post-infection. Transcription of Math1, a transcription factor required for secretory cell differentiation in the intestine, was up-regulated on days 6,18 post-infection. At these time points, numbers of Paneth cells at the crypt base were also increased and the epithelial proliferative zone was shifted up the crypt-villus axis. Transcription of TGF-, isoforms within the small intestine was up-regulated on days 6 and 12 post-infection, but anti-TGF-, antibody treatment had no effect on T. spiralis -induced changes in mucosal architecture or increase in Paneth/intermediate cells. Conclusions:,T. spiralis infection promotes an initial increase in small intestinal epithelial proliferation and subsequent cell differentiation along the secretory cell lineage. The resulting increase in numbers of Paneth cells at the crypt base causes the proliferative zone to move up the crypt-villus axis. Further studies are required to determine the significance of an increase in the expression of TGF-, transcripts. [source]