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Parasite Versus Host: Pathology and Disease
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
To cite just one example, mice and other rodents are susceptible to infection with the intestinal nematode Heligmosomoides polygyrus. When the microbiota of infected and uninfected, control mice were compared, it was found to differ significantly (Figure 5.21). Indicators of colitis severity were also elevated in infected mice. Finally, it was demonstrated that mice infected with the nematode displayed higher levels of Treg activation and IL-10 production: components of the host immune response to helminths discussed in Chapter 4. These data suggest that the reduced inflammatory response observed in helminth infections alters the microbiota of the host in a manner that may increase the likelihood of infection with opportunistic pathogens. Similar results have also been observed in humans. When people in Malaysia who were infected with Trichuris trichiura were compared to uninfected individuals, significant differences were observed in the microbiota (see also Figure 6.3).
Mucosal responses to helminth infections
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
William Gause, Richard Grencis
Another species used to model hookworm infection is Heligmosomoides polygyrus bakeri, a natural parasite of rodents, including mice, which resides in the small intestine. In this case, infection occurs by ingestion of the L3 larval stage, and no systemic migration occurs. A single infection usually results in a long-lived infection in most inbred strains of mouse, although strong resistance to infection can be generated experimentally by clearing a primary infection with anthelmintic drugs (see Section 27.8) prior to challenge with a secondary infection. Helminth models are therefore available that allow investigation of mucosal responses to parasites that live in different niches within the intestine.
Host Defense and Parasite Evasion
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2015
Eric S. Loker, Bruce V. Hofkin
Brugia malayi provides a useful example. This filarial worm, a causative agent of lymphatic filariasis, secretes an analog of the mammalian cytokine macrophage migration inhibitory factor (MIF). This molecule seems to mimic the effects of the host cytokine, helping to prevent the pro-inflammatory activation of macrophages. B. malayi also produces a TGFβ analog, which may promote Treg development, as has been found for mammalian TGFβ. A different nematode, Heligmosomoides polygyrus, a common intestinal parasite of rodents, also produces a TGFβ analog. When CD4+ T cells are exposed to this parasite molecule in vitro, they up-regulate their expression of FoxP3, an important marker for Treg cells. Thus it appears that the nematode may induce Treg development, suggesting an important role in immunosuppression and parasite survival.
Immunomodulatory effects of chronic trichinellosis on Toxoplasma gondii RH virulent strain in experimental rats
Published in Pathogens and Global Health, 2023
Abeer E. Saad, Dalia S. Ashour, Eman Rashad
On the other hand, our results showed improved histopathological changes in the liver and brain of the co-infected rats with a marked reduction in the extent of inflammatory infiltrates. A similar improvement in tissue pathology was reported by Abdel Hamed et al. [38] who showed that pre-infection with T. spiralis attenuated T. gondii-induced inflammation and intestinal damage. Also, Marshall et al. [20] investigated coinfection with T. gondii and Schistosoma mansoni (S. mansoni). They found that intestinal pathology in double-infected animals was less severe than in those animals infected with either parasite alone. Mostly because type 2 responses associated with chronic helminth infections would alleviate IFN-γ-mediated pathology. Correspondingly, Khan et al. [39] observed that neither the characteristically strong Th2 response to Heligmosomoides polygyrus (H. polygrus) nor the increased IFN-γ levels and the severe intestinal pathology mediated by T. gondii were observed in H. polygrus and T. gondii dually infected mice.
Identifying novel candidates and configurations for human helminth vaccines
Published in Expert Review of Vaccines, 2021
A second mechanistic approach with a strong immunological foundation has been to target the suite of factors that helminths release to modify their environment and down-modulate the host immune system. Indeed, many of the first experimental vaccines in different helminth models utilized released molecules (termed excretory/secretory or ES products) and achieved high levels of protection [39]. However, these are generally complex mixtures and in very few cases have individual ES proteins been shown to induce protective immunity. Most probably, the redundancy of parasite products is responsible for lack of efficacy, returning the discussion to the need for multicomponent vaccines. In a study on a murine model system, Heligmosomoides polygyrus, immunization with ES products elicited sterile immunity to challenge infection; from the mixture, a combination of 3 proteins (VAL-1/2/3) were sufficient to drive immunity [40]. Interestingly these are members of the same gene family as N. americanus ASP-2, which was an earlier human vaccine candidate, and a number of homologs tested as vaccines for veterinary nematodes [41]. It remains to be determined if there is functional homology between members of this gene family in the different host-parasite combinations, but their prominence as effective immunogens does indicate a key role in parasite modulation of the host [41].
Worm expulsion is independent of alterations in composition of the colonic bacteria that occur during experimental Hymenolepis diminuta-infection in mice
Published in Gut Microbes, 2020
Adam Shute, Arthur Wang, Timothy S. Jayme, Marc Strous, Kathy D. McCoy, Andre G. Buret, Derek M. McKay
It is intuitive to accept that helminths residing in the intestine would affect bacteria in this niche; a postulate reinforced by culture-independent sequencing of the small-subunit ribosomal RNA gene (16S) revealing order/family level shifts in bacterial abundance and diversity in helminth-infected humans, rodents and other mammals.2 Acknowledging parasite-host specificity, infection with helminth parasites often results in contraction of Bacteroidetes and expansion of Firmicutes in the hosts’ colon.3 While reports using 16S rRNA sequence analysis describe alterations in the gut microbiome of helminth-infected individuals, the functional consequences of such shifts on the helminth-bacteria relationship and enteric homeostasis remain incompletely understood. Ova hatching and establishment of the whipworm Trichuris muris in the mouse require the presence of commensal bacteria.4 Similarly, it appears that gut bacteria are essential for the nematode Heligmosomoides polygyrus to thrive.5 The protection against airway inflammation evoked by H. polygyrus was attributed to the short-chain fatty acid (SCFA) acetate, produced by the gut microbiota.6