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The inflammatory effect of infection with Hymenolepis diminuta via the increased expression and activity of COX-1 and COX-2 in the rat jejunum and colon.

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The aim of this study was to determine whether Hymenolepis diminuta may affect the expression and activity of cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2), resulting in the altered levels of their main products - prostaglandins (PGE2) and thromboxane B2 (TXB2). The study used the same

Production and Use of Hymenolepis diminuta Cysticercoids as Anti-Inflammatory Therapeutics.

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Helminthic therapy has shown considerable promise as a means of alleviating some inflammatory diseases that have proven resistant to pharmaceutical intervention. However, research in the field has been limited by a lack of availability to clinician scientists of a helminth that is relatively benign,

Inflammatory responses in the intestine during tapeworm infections. Mucosal mast cells and mucosal mast cell proteases in Sprague-Dawley rats infected with Hymenolepis diminuta.

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Comparative studies were made of two populations of Sprague-Dawley rats infected with Hymenolepis diminuta. The time course of infection, the development of mucosal mastocytosis and the levels of rat mucosal mast cell (MMC) protease (RMCP II) in serum and in jejunal mucosal tissues were monitored at

Young mice expel the tapeworm Hymenolepis diminuta and are protected from colitis by triggering a memory response with worm antigen.

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Infection with helminth parasites reduces the severity of concomitant inflammatory disease in adult mice. There is an alarming increase of inflammatory bowel disease (IBD) in children. It is important to determine whether helminth therapy would be of value in pediatric IBD and whether triggering

Mast cell responses to Hymenolepis microstoma infection in mice.

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Murine mast cells (MC) responded strongly to Hymenolepis microstoma infection. Starting day 7 postinfection (PI) and continuing until the end of the experiment (35 days PI), significantly larger numbers of MC were present in both the duodenum and bile duct of infected mice than in uninfected

A nuclear magnetic resonance study of the glucose metabolism of Hymenolepis diminuta exposed to histamine and serotonin in vitro.

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The direct effects of the inflammatory mediators, histamine (HI) and serotonin (SE), on the glucose metabolism of Hymenolepis diminuta in vitro were studied by analyzing the excretory products from culture media, containing D-1-13C-glucose and various concentrations of HI and/or SE, by 1H-nuclear

Kinetics of mast cells, eosinophils and phospholipase B activity in the spontaneous-cure response of two strains of mice (rapid and slow responder) to the cestode Hymenolepis nana.

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Primary egg-derived infection of Hymenolepis nana (100 eggs) in BALB/c (rapid responder) and C3H (slow responder) mice resulted in increased levels of mucosal mast cells (MMCs), eosinophilia (bone marrow, peripheral, tissue) and phospholipase B activity. The response appeared to be similar in both

Lymphokine production by mesenteric lymph node cells from BALB/C mice during Hymenolepis nana infection.

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Mesenteric lymph node cells (MLNC) prepared from BALB/c mice during infection with Hymenolepis nana proliferated extensively when cultured in the presence of soluble egg antigen, as assessed by measuring 3H-thymidine incorporation. Analysis of Hymenolepis-specific proliferative cells in MLNC by

Immunoprotective Effect of Chitosan Particles on Hymenolepis nana - Infected Mice.

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Hymenolepis nana is the most commonly known intestinal cestode infecting mainly human. This study aimed to investigate the potential effect of chitosan particles (CSP) to enhance the immune system against H. nana infection. Determination of worm burden, egg output, histopathological changes,

Murine autoimmune arthritis is exaggerated by infection with the rat tapeworm, Hymenolepis diminuta.

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Infection with helminth parasites triggers strong and stereotypic immune responses in humans and mice, which can protect against specific experimentally-induced autoimmune diseases. We have shown that infection with the rat tapeworm, Hymenolepis diminuta, confers a protective effect on FCA-induced

Hymenolepis diminuta: analysis of the expression of Toll-like receptor genes (TLR2 and TLR4) in the small and large intestines of rats.

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Toll receptors play a critical role in the rapid activation of innate immune responses to a variety of pathogens. In mammals, Toll-like receptors (TLR) have been found in both immune related cells and other cells. At present little is known about the participation of TLR in host defense mechanisms

Immunoproteomics and Surfaceomics of the Adult Tapeworm Hymenolepis diminuta.

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In cestodiasis, mechanical and molecular contact between the parasite and the host activates the immune response of the host and may result in inflammatory processes, leading to ulceration and intestinal dysfunctions. The aim of the present study was to identify antigenic proteins of the adult

Hymenolepis nana: A case report of a perfect IBD camouflage warrior.

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BACKGROUND There is evidence that parasitic helminths can ameliorate colitis in animal models and humans. Although infections with Hymenolepis sp. are clinically benign, the immunomodulatory interactions between host and parasite are largely unknown. UNASSIGNED In this study we examined the

A Trypsin-Sensitive Proteoglycan from the Tapeworm Hymenolepis diminuta Inhibits Murine Neutrophil Chemotaxis in vitro by Suppressing p38 MAP Kinase Activation.

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It has emerged that neutrophils can play important roles in the host response following infection with helminth parasites. Mice infected with the tapeworm, Hymenolepis diminuta, are protected from some inflammatory conditions, accompanied by reduced neutrophil tissue infiltration. Thus, the ability

Suppression of systemic lupus erythematosus in NZBWF1 mice infected with Hymenolepis microstoma.

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Intestinal helminths induce immune suppressive responses thought to regulate inflammatory diseases including allergies and autoimmune diseases. This study was designed to evaluate whether helminthic infections suppress the natural development of systemic lupus erythematosus (SLE) in NZBWF1 mice.

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