Nippostrongylus brasiliensis infections in mice: the immunological basis of worm expulsion

Parasitology ◽  
1975 ◽  
Vol 70 (1) ◽  
pp. 11-18 ◽  
Author(s):  
R. J. Love
Keyword(s):  
Immune Cells ◽  
Nippostrongylus Brasiliensis ◽  
Mesenteric Node ◽  
Worm Expulsion

Nippostrongylus brasiliensis infections in mice were terminated more rapidly than in rats and immunologically induced damage occurred earlier. Like rats, mice expelled damaged worms more rapidly than normal worms. Recipients of cells from the spleen or mesenteric node of immune mice expelled their worms by day 8 of the infection. Recipients of cells alone or antiserum alone did not expel their worms by day 5 but mice given both cells and antiserum expelled their worms by this stage of the infection. Damaged worms were expelled more rapidly than normal worms from mice given immune cells. This work indicates that antibodies and cells collaborate to expel N. brasiliensis from mice as has been shown to occur in rats.

Nippostrongylus brasiliensis: further properties of antibody-damaged worms and induction of comparable damage by maintaining worms in vitro

Parasitology ◽  
1975 ◽  
Vol 71 (2) ◽  
pp. 275-283 ◽  
Author(s):  
R. J. Love ◽  
Bridget M. Ogilvie ◽  
Diane J. McLaren
Keyword(s):  
Immune Response ◽  
Isoenzyme Pattern ◽  
Nippostrongylus Brasiliensis ◽  
Ultrastructural Morphology ◽  
Immature Rats ◽  
Normal Rat ◽  
Worm Expulsion ◽  
Anterior Migration

When adult Nippostrongylus brasiliensis were maintained in vitro they became damaged. Using the criteria of ultrastructural morphology, acetylcholinesterase isoenzyme pattern and the behaviour of the worms after transfer to a normal rat, this damage appeared to be similar to that produced by the in vivo action of antibodies.Antibodies were shown to be responsible for the anterior migration of adult worms which occurs during primary infections in mature rats and in the prolonged infections seen in lactating and immature rats.Antibody damaged worms and worms unaffected by antibodies were equally able to stimulate the immune response required for worm expulsion. Apparently antibody damage is not required for the initiation of the second immune component necessary for expulsion of this parasite.

Host–parasite interactions in rodent nematode infections

2003 ◽  
Vol 77 (2) ◽  
pp. 125-131 ◽  
Author(s):  
Y.R. Mahida
Keyword(s):  
Neutralizing Antibodies ◽  
Host Response ◽  
Trichinella Spiralis ◽  
Host Responses ◽  
Nippostrongylus Brasiliensis ◽  
Trichuris Muris ◽  
Epithelial Phenotype ◽  
Worm Expulsion ◽  
Genetically Manipulated ◽  
Host Parasite

AbstractIn rodents,Trichinella spiralisandNippostrongylus brasiliensisinfect the small intestine andTrichuris murisresides in the colon. The intestinal host response in these animals is characterized by changes in mucosal architecture and inflammation and is associated with worm expulsion. The requirement of T cell-mediated host response in worm expulsion has been demonstrated over many years. Subsequent studies have shown that Th2-type, but not Th1-type, responses mediate resistance to the nematodes. Investigations using neutralizing antibodies and genetically manipulated mice have characterized the contribution of individual Th2-type cytokines in not only worm expulsion, but also specific cellular changes that occur in the mucosa, such as alterations in epithelial phenotype and smooth muscle. There is also increasing appreciation of the contribution of non-bone marrow-derived cells in innate and adaptive host responses in these models.

Basophil effector function and homeostasis during helminth infection

Blood ◽  
2009 ◽  
Vol 113 (12) ◽  
pp. 2816-2825 ◽  
Author(s):  
Caspar Ohnmacht ◽  
David Voehringer
Keyword(s):  
De Novo ◽  
Allergic Inflammation ◽  
Lung Parenchyma ◽  
Effector Function ◽  
Nippostrongylus Brasiliensis ◽  
Helminth Parasites ◽  
Alternatively Activated Macrophages ◽  
Effector Cells ◽  
Worm Expulsion

AbstractBasophils are effector cells of the innate immune system that are associated with allergic inflammation and infections with helminth parasites. However, their development and in vivo functions are largely unknown. Here, we characterize basophil development, turnover, tissue localization, and effector function during infection with the helminth Nippostrongylus brasiliensis. Our results demonstrate that under homeostatic conditions basophils have a lifespan of about 60 hours. N brasiliensis–induced basophilia is caused by increased de novo production of basophils in the bone marrow. Basophils were found near the marginal zone in the red pulp of the spleen, in the lamina propria of the small intestine, and in the lung parenchyma. Activated basophils promoted systemic eosinophilia, were associated with differentiation of alternatively activated macrophages in the lung, and contributed to efficient worm expulsion, demonstrating that basophils play a crucial role as effector cells in type 2 immune responses.

scholarly journals Identification of an interleukin (IL)-25–dependent cell population that provides IL-4, IL-5, and IL-13 at the onset of helminth expulsion

2006 ◽  
Vol 203 (4) ◽  
pp. 1105-1116 ◽  
Author(s):  
Padraic G. Fallon ◽  
Sarah J. Ballantyne ◽  
Niamh E. Mangan ◽  
Jillian L. Barlow ◽  
Ayan Dasvarma ◽  
...  
Keyword(s):  
Nippostrongylus Brasiliensis ◽  
T Helper ◽  
T Helper 2 ◽  
Adaptive Immune ◽  
Type 2 Cytokines ◽  
Dependent Cell ◽  
Worm Expulsion ◽  
Draining Lymph Nodes

Type 2 immunity, which involves coordinated regulation of innate and adaptive immune responses, can protect against helminth parasite infection, but may lead to allergy and asthma after inappropriate activation. We demonstrate that il25−/− mice display inefficient Nippostrongylus brasiliensis expulsion and delayed cytokine production by T helper 2 cells. We further establish a key role for interleukin (IL)-25 in regulating a novel population of IL-4–, IL-5–, IL-13–producing non–B/non–T (NBNT), c-kit+, FcεR1− cells during helminth infection. A deficit in this population in il25−/− mice correlates with inefficient N. brasiliensis expulsion. In contrast, administration of recombinant IL-25 in vivo induces the appearance of NBNT, c-kit+, FcεR1− cells and leads to rapid worm expulsion that is T and B cell independent, but type 2 cytokine dependent. We demonstrate that these IL-25–regulated cells appear rapidly in the draining lymph nodes, implicating them as a source of type 2 cytokines during initiation of worm expulsion.

Nippostrongylus brasiliensis: Histamine and 5-hydroxytryptamine inhibition and worm expulsion

1971 ◽  
Vol 30 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Max Murray ◽  
W.D. Smith ◽  
A.H. Waddell ◽  
W.F.H. Jarrett
Keyword(s):  
Nippostrongylus Brasiliensis ◽  
Worm Expulsion

scholarly journals Bcl11b is essential for group 2 innate lymphoid cell development

2015 ◽  
Vol 212 (6) ◽  
pp. 875-882 ◽  
Author(s):  
Jennifer A. Walker ◽  
Christopher J. Oliphant ◽  
Alexandros Englezakis ◽  
Yong Yu ◽  
Simon Clare ◽  
...  
Keyword(s):  
Fetal Liver ◽  
Lymphoid Cells ◽  
Nippostrongylus Brasiliensis ◽  
Reporter Mice ◽  
Mucosal Surfaces ◽  
Gfp Reporter ◽  
Worm Expulsion ◽  
Group 2 ◽  
Cell Commitment

Group 2 innate lymphoid cells (ILC2s) are often found associated with mucosal surfaces where they contribute to protective immunity, inappropriate allergic responses, and tissue repair. Although we know they develop from a common lymphoid progenitor in the bone marrow (BM), the specific lineage path and transcriptional regulators that are involved are only starting to emerge. After ILC2 gene expression analysis we investigated the role of Bcl11b, a factor previously linked to T cell commitment, in ILC2 development. Using combined Bcl11b-tom and Id2-gfp reporter mice, we show that Bcl11b is expressed in ILC2 precursors in the BM and maintained in mature ILC2s. In vivo deletion of Bcl11b, by conditional tamoxifen-induced depletion or by Bcl11b−/− fetal liver chimera reconstitution, demonstrates that ILC2s are wholly dependent on Bcl11b for their development. Notably, in the absence of Bcl11b there is a concomitant expansion of the RORγt+ ILC3 population, suggesting that Bcl11b may negatively regulate this lineage. Using Nippostrongylus brasiliensis infection, we reveal that the absence of Bcl11b leads to impaired worm expulsion, caused by a deficit in ILC2s, whereas Citrobacter rodentium infection is cleared efficiently. These data clearly establish Bcl11b as a new factor in the differentiation of ILC2s.

scholarly journals The skin is an important bulwark of acquired immunity against intestinal helminths

2013 ◽  
Vol 210 (12) ◽  
pp. 2583-2595 ◽  
Author(s):  
Kazushige Obata-Ninomiya ◽  
Kenji Ishiwata ◽  
Hidemitsu Tsutsui ◽  
Yuichiro Nei ◽  
Soichiro Yoshikawa ◽  
...  
Keyword(s):  
Lung Injury ◽  
Intestinal Helminth ◽  
Nippostrongylus Brasiliensis ◽  
Arginase 1 ◽  
Helminthic Infections ◽  
Selective Ablation ◽  
Helminthic Infection ◽  
Worm Expulsion ◽  
Deficient Mice ◽  
Infected Skin

Once animals have experienced a helminthic infection, they often show stronger protective immunity against subsequent infections. Although helminthic infections are well known to elicit Th2-type immune responses, it remains ill-defined where and how acquired protection is executed. Here we show that skin-invading larvae of the intestinal helminth Nippostrongylus brasiliensis are surrounded by skin-infiltrating cells and are prevented from migrating out of infected skin during the second but not the first infection. B cell– or IgE receptor FcεRI–deficient mice showed impaired larval trapping in the skin. Selective ablation of basophils, but not mast cells, abolished the larval trapping, leading to increased worm burden in the lung and hence severe lung injury. Skin-infiltrating basophils produced IL-4 that in turn promoted the generation of M2-type macrophages, leading to the larval trapping in the skin through arginase-1 production. Basophils had no apparent contribution to worm expulsion from the intestine. This study thus reveals a novel mode of acquired antihelminth immunity, in which IgE-armed basophils mediate skin trapping of larvae, thereby limiting lung injury caused by larval migration.

scholarly journals Type 2 immunity is controlled by IL-4/IL-13 expression in hematopoietic non-eosinophil cells of the innate immune system

2006 ◽  
Vol 203 (6) ◽  
pp. 1435-1446 ◽  
Author(s):  
David Voehringer ◽  
Tiffany A. Reese ◽  
Xiaozhu Huang ◽  
Kanade Shinkai ◽  
Richard M. Locksley
Keyword(s):  
Airway Hyperreactivity ◽  
Th2 Cells ◽  
Nippostrongylus Brasiliensis ◽  
Lung Pathology ◽  
Cell Recruitment ◽  
Th2 Cell ◽  
Type 2 Immunity ◽  
Tissue Responses ◽  
Worm Expulsion

Nippostrongylus brasiliensis infection and ovalbumin-induced allergic lung pathology are highly interleukin (IL)-4/IL-13 dependent, but the contributions of IL-4/IL-13 from adaptive (T helper [Th]2 cells) and innate (eosinophil, basophils, and mast cells) immune cells remain unknown. Although required for immunoglobulin (Ig)E induction, IL-4/IL-13 from Th2 cells was not required for worm expulsion, tissue inflammation, or airway hyperreactivity. In contrast, innate hematopoietic cell–derived IL-4/IL-13 was dispensable for Th2 cell differentiation in lymph nodes but required for effector cell recruitment and tissue responses. Eosinophils were not required for primary immune responses. Thus, components of type 2 immunity mediated by IL-4/IL-13 are partitioned between T cell–dependent IgE and an innate non-eosinophil tissue component, suggesting new strategies for interventions in allergic immunity.

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