<i>Echinostoma caproni</i> (<scp>T</scp>rematoda): differential <i>in vivo</i> mucin expression and glycosylation in high‐ and low‐compatible hosts

Cortés, Alba; Muñoz-Antolí, Carla; Sotillo, Javier; Fried, Bernard; Esteban, J. Guillermo; Toledo, Rafael

doi:10.1111/pim.12159

Cited by 20 publications

(14 citation statements)

References 47 publications

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“…Our results indicate that partial and complete resistance to E. caproni infections are associated with goblet cell hyperplasia and changes in mucus glycosylation at the time of challenge infection. Although previous studies have suggested that goblet cell hyperplasia has little effect on resistance to E. caproni infections 16 45 46 , our current results are somewhat confusing. Primary infection induced a goblet cell hyperplasia of about 4-fold greater than in negative controls from 4 wppi.…”

Section: Discussioncontrasting

confidence: 67%

Interleukin-25 Induces Resistance Against Intestinal Trematodes

Muñoz-Antolí

Cortés

Santano

et al. 2016

Sci Rep

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Echinostoma caproni is an intestinal trematode that has been extensively used as an experimental model to investigate the factors determining the resistance to intestinal helminths or the development of chronic infections. ICR mice are permissive hosts for E. caproni in which chronic infections are developed, concomitantly with local Th1 responses, elevated levels of local IFN-γ, inflammation and antibody responses. However, mice develop partial resistance to homologous challenge infections after cure of a primary infection, which converts this subject into an adequate model for the study of the mechanisms generating resistance against intestinal helminths. The purpose of the present study was to compare the immune response induced in primary and secondary infections to elucidate the factors determining the different outcome of the infection in each type of infection. The results obtained indicate that susceptibility is determined by the lack of IL-25 expression in response to primary infection. In contrast, infection in an environment with elevated levels of IL-25, as occurs in challenge infection, results in a Th2 phenotype impairing parasite survival. This was confirmed by treatment of naïve mice with exogenous IL-25 and subsequent infection. Changes induced in goblet cell populations and mucin glycosylation could be implicated in resistance to infection.

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Section: Discussioncontrasting

confidence: 67%

Interleukin-25 Induces Resistance Against Intestinal Trematodes

Muñoz-Antolí

Cortés

Santano

et al. 2016

Sci Rep

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“…), mice and rat intestine with Echinostoma caproni (Cortés et al . ), rat airway and small intestine with Nippostrongylus brasiliensis (Tsubokawa et al . ), lamb gut with Haemonchus contortus or Teladorsagia circumcincta (Hoang, Williams & Simpson ; Simpson et al .…”

Section: Discussionmentioning

confidence: 99%

Protective responses of intestinal mucous cells in a range of fish–helminth systems

Bosi

Giari

DePasquale

et al. 2016

Journal of Fish Diseases

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Histopathological, immunofluorescence and ultrastructural studies were conducted on the intestines of four fish species infected with different taxa of enteric helminths. Brown trout (Salmo trutta trutta), eel (Anguilla anguilla) and tench (Tinca tinca) obtained from Lake Piediluco (central Italy) were examined. Brown trout and eel were infected with two species of acanthocephalans, and tench was parasitized with a tapeworm species. In addition to the above site, specimens of chub (Squalius cephalus) and brown trout infected with an acanthocephalan were examined from the River Brenta (north Italy). Moreover, eels were examined from a brackish water, Comacchio lagoons (north Italy), where one digenean species was the predominant enteric worm. All the helminths species induced a similar response, the hyperplasia of the intestinal mucous cells, particularly of those secreting acid mucins. Local endocrine signals seemed to affect the production and secretion of mucus in the parasitized fish, as worms often were surrounded by an adherent mucus layer or blanket. This is the first quantitative report of enteric worm effects on the density of various mucous cell types and on the mucus composition in intestine of infected/uninfected conspecifics. We provide a global comparison between the several fish-helminth systems examined

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“…Stimulated electrogenic ion transport creates a driving force for water movement that can lubricate the epithelial surface and may assist in the expulsion of intestinal helminths: 82 water is important in the physical properties of mucus. 83,84 Intestinal goblet cell hyperplasia is perhaps the most prominent gut characteristic of infection with gastrointestinal parasitic helminths 3,85 and increases in mucin production, type (e.g., Muc5a) and glycosylation can be critical components of the epithelial barrier that aids the expulsion of helminths, such as the nematode N. brasiliensis [86][87][88][89] and the trematode, Echinostoma caproni; 90 indeed, helminths in their own defense may release proteases to degrade mucus. 91 The advent of mucin-gene knockout mice positions the field to unequivocally test the role of mucus in the expulsion of a range of parasitic helminths.…”

Section: Helminth and Host-derived Factors Impact On Intestinal Barrimentioning

confidence: 99%

Helminths and intestinal barrier function

2017

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Approximately one-sixth of the worlds' population is infected with helminths and this class of parasite takes a major toll on domestic livestock. The majority of species of parasitic helminth that infect mammals live in the gut (the only niche for tapeworms) where they contact the hosts' epithelial cells. Here, the helminth-intestinal epithelial interface is reviewed in terms of the impact on, and regulation of epithelial barrier function, both intrinsic (epithelial permeability) and extrinsic (mucin, bacterial peptides, commensal bacteria) elements of the barrier. The data available on direct effects of helminths on epithelial permeability are scant, fragmentary and pales in comparison with knowledge of mobilization of immune reactions and effector cells in response to helminth parasites and how these impact intestinal barrier function. The interaction of helminth-host and helminthhost-bacteria is an important determinant of gut form and function and precisely defining these interactions will radically alter our understanding of normal gut physiology and pathophysiological reactions, revealing new approaches to infection with parasitic helminths, bacterial pathogens and idiopathic auto-inflammatory disease.

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Echinostoma caproni (Trematoda): differential in vivo mucin expression and glycosylation in high‐ and low‐compatible hosts

Cited by 20 publications

References 47 publications

Interleukin-25 Induces Resistance Against Intestinal Trematodes

Interleukin-25 Induces Resistance Against Intestinal Trematodes

Protective responses of intestinal mucous cells in a range of fish–helminth systems

Helminths and intestinal barrier function

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