Inhibitory Effects of Human Neutrophil Functions by the 45-kD Glycoprotein Derived from the Parasitic Nematode &lt;i&gt;Trichinella spiralis&lt;/i&gt;

Bruschi, Fabrizio; Carulli, Giovanni; Azzarà, Antonio; Homan, Wieger; Minnucci, S; Rizzuti‐Gullaci, Angela; Sbrana, Silverio; Angiolini, Claudia

doi:10.1159/000024359

Cited by 24 publications

(21 citation statements)

References 18 publications

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“…For example, nematode infection influences the neuropeptide content of the gut (9), and it has been reported that infecting nematodes can modulate their environment by immunosuppression through the release of immunoreactive neuropeptides (14). It has also recently been reported that the 45-kDa glycoprotein derived from T. spiralis has an anti-inflammatory effect (6). In addition, goblet cell hyperplasia is a hallmark of T. spiralis infection (31).…”

Section: Discussionmentioning

confidence: 99%

Intestinal Nematode Infection Ameliorates Experimental Colitis in Mice

et al. 2002

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Epidemiological studies suggest that inflammatory bowel disease (IBD) is common in developed countriesIn the present study, we investigated the effect of polarizing the immune response toward the Th2 type, using intestinal nematode infection, on subsequent experimental colitis. Mice were infected with the intestinal nematode Trichinella spiralis and allowed to recover before colitis was induced with dinitrobenzene sulfonic acid. The mice were sacrificed postcolitis to assess colonic damage macroscopically, histologically, and by myeloperoxidase (MPO) activity and Th cytokines. Prior nematode infection reduced the severity of colitis both macroscopically and histologically together with a decreased mortality and was correlated with a downregulation of MPO activity, Th1-type cytokine expression in colonic tissue, and emergence of a Th2-type immune response. These results indicate a protective role of nematode infection in Th1 cell-driven inflammation and prompt consideration of a novel therapeutic strategy in IBD based on immunological distraction.

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Section: Discussionmentioning

confidence: 99%

Intestinal Nematode Infection Ameliorates Experimental Colitis in Mice

et al. 2002

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“…Clarifying the host immune response will make it easier to identify the critical measures taken by parasites for evasion and prolonged infestation. Increasing evidence shows that parasite-derived substances play an important role in initiating or maintaining the parasite's advantage, directly suppressing the function of certain subsets of immune cells as well as stimulating other cell populations related to immunopathology (7,12,23).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Human Immune Response byEchinococcus granulosusAntigen B and Its Possible Role in Evading Host Defenses

Riganò

Profumo

Bruschi³

et al. 2001

Infect Immun

143

117

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). AgB skewed the Th1/Th2 cytokine ratios towards a preferentially immunopathology-associated Th2 polarization, predominantly in patients with progressive disease. AgB-stimulated patients' PBMC also proliferated less than SHF-stimulated PBMC (P ‫؍‬ 9 ؋ 10 ؊3 ). In vitro Th2 cytokine production was reflected in vivo by elevated specific immunoglobulin E (IgE) and IgG4 antibodies binding to AgB. These findings confirm that AgB plays a role in the escape from early immunity by inhibiting PMN chemotaxis. They also add new information on the host-parasite relationship, suggesting that AgB exploits the activation of T helper cells by eliciting a nonprotective Th2 cell response.Cystic echinococcosis (CE) is a widely endemic helminthic disease caused by infection with metacestodes (larval stage) of the tapeworm Echinococcus granulosus. It affects humans and a wide range of livestock species (28). The disease is characterized by the growth in the host internal organs, mostly liver and lungs, of steadily growing fluid-filled, unilocular cysts surrounded by a two-layered hydatid cyst wall. The main feature of the host-parasite relationship is the coexistence of the chronic infection with detectable humoral and cellular responses against the parasite. Parasite survival in vivo depends on efficient evasion mechanisms starting to operate as the parasite develops toward a hydatid cyst. A fibrotic host capsule of variable thickness usually develops, thus forming together with the parasite-derived acellular laminated layer a formidable cystic structure. As a consequence, the actively dividing germinal layer within the cyst along with its associated brood capsule and enclosed protoscoleces are effectively sequestered from the host immune responses. In addition to this physical barrier, the hydatid cyst has probably evolved other strategies for immune evasion. Although older models suggested a more passive role for parasites in immune evasion-for example sequestration, antigenic masking by host proteins, and global immunosuppression-later studies suggest in human parasitoses the active deployment of strategies that manipulate and exploit the host response (12, 30).

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“…Eggs hatch inside the female uterus and new larvae migrate through blood vessels to the striated muscles, where new cysts are formed. During this process, products excreted/secreted (ES) by T. spiralis induce profound effects on the host immune system, deviating Th1 responses to Th2 by inducing dendritic cells (DCs) and macrophages to acquire an immature, tolerogenic phenotype [34][35][36][37]. In addition to Th2 biasing, T. spiralis induces secretion of IL-10 and TGF-β by both innate and adaptive immune populations, contributing to regulation and containment of host tissue inflammation and fostering tissue repair [34,38].…”

Section: Abbreviationsmentioning

confidence: 99%

Helminth Infection and Type 1 Diabetes

Zaccone¹,

Hall²

2012

Rev Diabet Stud

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■ AbstractThe increasing incidence of type 1 diabetes (T1D) and autoimmune diseases in industrialized countries cannot be exclusively explained by genetic factors. Human epidemiological studies and animal experimental data provide accumulating evidence for the role of environmental factors, such as infections, in the regulation of allergy and autoimmune diseases. The hygiene hypothesis has formally provided a rationale for these observations, suggesting that our coevolution with pathogens has contributed to the shaping of the present-day human immune system. Therefore, improved sanitation, together with infection control, has removed immunoregulatory mechanisms on which our immune system may depend. Helminths are multicellular organisms that have developed a wide range of strategies to manipulate the host immune system to survive and complete their reproductive cycles successfully. Immunity to helminths involves profound changes in both the innate and adaptive immune compartments, which can have a protective effect in inflammation and autoimmunity. Recently, helminth-derived antigens and molecules have been tested in vitro and in vivo to explore possible applications in the treatment of inflammatory and autoimmune diseases, including T1D. This exciting approach presents numerous challenges that will need to be addressed before it can reach safe clinical application. This review outlines basic insight into the ability of helminths to modulate the onset and progression of T1D, and frames some of the challenges that helminth-derived therapies may face in the context of clinical translation.

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Inhibitory Effects of Human Neutrophil Functions by the 45-kD Glycoprotein Derived from the Parasitic Nematode <i>Trichinella spiralis</i>

Cited by 24 publications

References 18 publications

Intestinal Nematode Infection Ameliorates Experimental Colitis in Mice

Intestinal Nematode Infection Ameliorates Experimental Colitis in Mice

Modulation of Human Immune Response byEchinococcus granulosusAntigen B and Its Possible Role in Evading Host Defenses

Helminth Infection and Type 1 Diabetes

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