Helminthiase

Résumé

Une helminthiase est un terme désignant les maladies parasitaires, causées par des vers parasites intestinaux, les helminthes. Ces vers constituent un important problème de santé publique dans les pays en voie de développement puisque plus de deux milliards de personnes en sont infectées. L’helminthiase transmise par contact avec le sol et la schistosomiase sont les formes les plus courantes de cette maladie tropicale négligée. La contamination peut avoir lieu par voie orale, par contact avec des insectes vecteurs, de la terre souillée et des animaux. L'eau souillée et le sol sont les principales voies de transmission de ces parasites. De nombreuses espèces sont concernées, on distingue les plathelminthes ou vers plats et les némathelminthes ou vers ronds. Ces parasites vivent très souvent dans les voies gastro-intestinales de leur hôte ou parfois s’installent dans d’autres organes où ils causent des dommages physiologiques plus ou moins importants. L’helminthias

Source officielle

https://fr.wikipedia.org/wiki/Helminthiase

À propos de ce résultat

Cette page est générée automatiquement et peut contenir des informations qui ne sont pas correctes, complètes, à jour ou pertinentes par rapport à votre recherche. Il en va de même pour toutes les autres pages de ce site. Veillez à vérifier les informations auprès des sources officielles de l'EPFL.

Publications associées (27)

Publications associées

Chargement

Personnes associées (10)

, , , , , , , , ,

Personnes associées

Chargement

Unités associées (3)

Unités associées

Chargement

Concepts associés (18)

Concepts associés

Chargement

Cours associés (1)

Cours associés

Chargement

Séances de cours associées (1)

Séances de cours associées

Chargement

Interactions between fibroblastic reticular cells and B cells promote mesenteric lymph node lymphangiogenesis

Lalit Kumar Dubey, Nicola Harris, Praneeth Karempudi

Lymphatic growth (lymphangiogenesis) within lymph nodes functions to promote dendritic cell entry and effector lymphocyte egress in response to infection or inflammation. Here we demonstrate a crucial role for lymphotoxin-beta receptor (LT beta R) signaling to fibroblastic reticular cells (FRCs) by lymphotoxin-expressing B cells in driving mesenteric lymph node lymphangiogenesis following helminth infection. LT beta R ligation on fibroblastic reticular cells leads to the production of B-cell-activating factor (BAFF), which synergized with interleukin-4 (IL-4) to promote the production of the lymphangiogenic factors, vascular endothelial growth factors (VEGF)-A and VEGF-C, by B cells. In addition, the BAFF-IL-4 synergy augments expression of lymphotoxin by antigen-activated B cells, promoting further B cell-fibroblastic reticular cell interactions. These results underlie the importance of lymphotoxin-dependent B cell-FRC cross talk in driving the expansion of lymphatic networks that function to promote and maintain immune responsiveness.

Springer Nature2017

Chargement

The microbiota provides colonisation resistance against intestinal helminths by regulating intestinal physiology

Luc Xavier Marie Lebon

Intestinal helminth infections are a global health problem affecting particularly people living in poor countries. Heavy worm burdens can lead to nutritional and cognitive deficiencies. Type-two immunity plays a crucial role in promoting tissue repair and limiting parasite burdens; however, our knowledge as to how these responses lead to protection is limited. Moreover, intestinal helminths have co-evolved with their mammalian hosts and are well known to possess potent immuno-modulatory capacities allowing them to establish chronic and repeated infections. As adult worms reside in the gut, we asked whether the presence of intestinal bacterial communities (commonly referred to as the microbiota) impacted on worm burdens or type-two immunity following infection. For this purpose, we infected germ-free (living in a sterile environment) or antibiotic-treated mice with the natural murine parasite Heligmosomoides polygyrus bakeri. As worms are normally hatched from faecal cultures and carry their own microbiota, we first developed a system to generate bacteriologically-sterile (axenic) infective larvae. In germ-free and antibiotic-treated mice, the number of adult worms and their egg production were both increased, despite the presence of a slightly increased helminth-elicited type-two immune response, as shown by cytokine and antibody responses. The increased worm fitness in the absence of microbiota was already detected early following infection and was associated with a more anterior distribution of larvae along the intestinal tract. Thus, we hypothesised that the microbiota may impact on parasite burdens through observed alterations of intestinal physiology, such as increased bile acid production and deregulated smooth muscle cell contractility. To test the importance of these factors, we performed experiments in which we treated mice with an excess of bile acids or altered intestinal transit through drug treatment. Both interventions lead to changes in worm infectivity or location, mirroring different observations generated in our germ-free and antibiotic-treated mice. In summary, our data indicate that a complex microbiota affords 'colonisation resistance' against intestinal helminths, in a manner that is independent of the immune response but dependent on changes to intestinal physiology.

EPFL2017

Chargement

, , ,

Approximately 2 billion people worldwide and a significant part of the domestic livestock are infected with soil-transmitted helminths, of which many establish chronic infections causing substantial eco-nomic and welfare burdens. Beside intensive research on helminth-triggered mucosal and systemic immune responses, the local mechanism that enables infective larvae to cross the intestinal epithelial barrier and invade mucosal tissue remains poorly addressed. Here, we show that Heligmosomoides poly-gyrus infective L3s secrete acetate and that acetate potentially facilitates paracellular epithelial tissue invasion by changed epithelial tight junction claudin expression. In vitro, impedance-based real-time epithelial cell line barrier measurements together with ex vivo functional permeability assays in intesti-nal organoid cultures revealed that acetate decreased intercellular barrier function via the G-protein cou-pled free fatty acid receptor 2 (FFAR2, GPR43). In vivo validation experiments in FFAR2-/-mice showed lower H. polygyrus burdens, whereas oral acetate-treated C57BL/6 wild type mice showed higher burdens. These data suggest that locally secreted acetate - as a metabolic product of the energy metabolism of H. polygyrus L3s - provides a significant advantage to the parasite in crossing the intestinal epithelial barrier and invading mucosal tissues. This is the first and a rate-limiting step for helminths to establish chronic infections in their hosts and if modulated could have profound consequences for their life cycle.(c) 2022 Australian Society for Parasitology. Published by Elsevier Ltd. All rights reserved.

2022

Chargement

The microbiota provides colonisation resistance against intestinal helminths by regulating intestinal physiology

Luc Xavier Marie Lebon

EPFL2017