Enteric Tuft Cells in Host-Parasite Interactions

Rajeev, Sruthi; Sosnowski, Olivia; Li, Shuhua; Allain, Thibault; Buret, André G.; McKay, Derek M.

doi:10.3390/pathogens10091163

Cited by 12 publications

(10 citation statements)

References 136 publications

(314 reference statements)

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“…However, in response to various parasitic infections, tuft cells are known to expand exponentially. For example, enteric non-pathogenic commensal protists, including Tritrichomonas spp., and pathogens such as nematodes (e.g., N. brasiliensis , Heligmosomoides polygyrus , and Trichinella spiralis ) and trematodes (e.g., Echinostoma caproni ) cause tuft cell activation and expansion, triggering mainly type 2 host immunity involving ILC2s ( 66 – 68 ).…”

Section: Mucosal Immunity To Commensal Intestinal Protozoamentioning

confidence: 99%

Intestinal immune responses to commensal and pathogenic protozoa

2022

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The physical barrier of the intestine and associated mucosal immunity maintains a delicate homeostatic balance between the host and the external environment by regulating immune responses to commensals, as well as functioning as the first line of defense against pathogenic microorganisms. Understanding the orchestration and characteristics of the intestinal mucosal immune response during commensal or pathological conditions may provide novel insights into the mechanisms underlying microbe-induced immunological tolerance, protection, and/or pathogenesis. Over the last decade, our knowledge about the interface between the host intestinal mucosa and the gut microbiome has been dominated by studies focused on bacterial communities, helminth parasites, and intestinal viruses. In contrast, specifically how commensal and pathogenic protozoa regulate intestinal immunity is less well studied. In this review, we provide an overview of mucosal immune responses induced by intestinal protozoa, with a major focus on the role of different cell types and immune mediators triggered by commensal (Blastocystis spp. and Tritrichomonas spp.) and pathogenic (Toxoplasma gondii, Giardia intestinalis, Cryptosporidium parvum) protozoa. We will discuss how these various protozoa modulate innate and adaptive immune responses induced in experimental models of infection that benefit or harm the host.

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Section: Mucosal Immunity To Commensal Intestinal Protozoamentioning

confidence: 99%

Intestinal immune responses to commensal and pathogenic protozoa

2022

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“…For example, in the area of epithelial cell biology, C57BL/6 and BALB/c mice show differences in tuft cell response at steady state and in response to a protozoa parasite, Trichomonas muris, but no significant difference was seen in tuft cell response following chronic infection with H. polygyrus at peak of parasite establishment (58). The dynamics of tuft cell hyperplasia in the different inbred strain of mice could vary wherein the BALB/c mice might have higher response than the C57BL/6 mice (59). Hence, the role of these sentinels in the pathogenesis and outcome to helminth infection should be examined in different inbred strains of mice.…”

Section: Genetic Variation In Resistance To Helminth Infectionmentioning

confidence: 99%

The Influence of Genetic and Environmental Factors and Their Interactions on Immune Response to Helminth Infections

2022

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Helminth infection currently affect over 2 billion people worldwide, with those with the most pathologies and morbidities, living in regions with unequal and disproportionate access to effective healthcare solutions. Host genetics and environmental factors play critical roles in modulating and regulating immune responses following exposure to various pathogens and insults. However, the interplay of environment and genetic factors in influencing who gets infected and the establishment, persistence, and clearance of helminth parasites remains unclear. Inbred strains of mice have long been used to investigate the role of host genetic factors on pathogenesis and resistance to helminth infection in a laboratory setting. This review will discuss the use of ecological and environmental mouse models to study helminth infections and how this could be used in combination with host genetic variation to explore the relative contribution of these factors in influencing immune response to helminth infections. Improved understanding of interactions between genetics and the environment to helminth immune responses would be important for efforts to identify and develop new prophylactic and therapeutic options for the management of helminth infections and their pathogenesis.

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“…differentiation and drive a more secretory epithelial phenotype to facilitate intestinal remodeling and worm expulsion (33,38). At the same time, T H 2 cells produce IL-4 and IL-5 to promote the population expansion of alternatively activated (M2) macrophages and the migration of eosinophils to the affected tissues (39).…”

Section: Schistosoma Mansonimentioning

confidence: 99%

“…Once activated, T H 2 cells produce IL-13, influencing goblet cells within infected epithelial barriers to increase mucus production and facilitate worm expulsion ( 36 , 37 ). Moreover, IL-13 from IL-25 activated ILC2 can regulate epithelial cell differentiation and drive a more secretory epithelial phenotype to facilitate intestinal remodeling and worm expulsion ( 33 , 38 ). At the same time, T H 2 cells produce IL-4 and IL-5 to promote the population expansion of alternatively activated (M2) macrophages and the migration of eosinophils to the affected tissues ( 39 ).…”

Section: Introductionmentioning

confidence: 99%

Communication is key: Innate immune cells regulate host protection to helminths

et al. 2022

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Parasitic helminth infections remain a significant global health issue and are responsible for devastating morbidity and economic hardships. During infection, helminths migrate through different host organs, which results in substantial tissue damage and the release of diverse effector molecules by both hematopoietic and non-hematopoietic cells. Thus, host protective responses to helminths must initiate mechanisms that help to promote worm clearance while simultaneously mitigating tissue injury. The specialized immunity that promotes these responses is termed type 2 inflammation and is initiated by the recruitment and activation of hematopoietic stem/progenitor cells, mast cells, basophils, eosinophils, dendritic cells, neutrophils, macrophages, myeloid-derived suppressor cells, and group 2 innate lymphoid cells. Recent work has also revealed the importance of neuron-derived signals in regulating type 2 inflammation and antihelminth immunity. These studies suggest that multiple body systems coordinate to promote optimal outcomes post-infection. In this review, we will describe the innate immune events that direct the scope and intensity of antihelminth immunity. Further, we will highlight the recent progress made in our understanding of the neuro-immune interactions that regulate these pathways and discuss the conceptual advances they promote.

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Enteric Tuft Cells in Host-Parasite Interactions

Cited by 12 publications

References 136 publications

Intestinal immune responses to commensal and pathogenic protozoa

Intestinal immune responses to commensal and pathogenic protozoa

The Influence of Genetic and Environmental Factors and Their Interactions on Immune Response to Helminth Infections

Communication is key: Innate immune cells regulate host protection to helminths

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