The potential roles of interleukin-25 in infectious diseases

Wu, Jing; Zhang, Fang; Tao, Hongji; Nawaz, Waqas; Chen, Deyan; Wu, Zhiwei

doi:10.3389/fimmu.2022.986118

Cited by 7 publications

(7 citation statements)

References 121 publications

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“…IL‐25 belongs to the IL‐17 family, also known as IL‐17E, 11 and has been identified as an “alarmin” cytokine that responds to pathogenic infection 12,13 . After infection, IL‐25 is produced rapidly and promotes innate lymphoid cell proliferation 14 .…”

Section: Introductionmentioning

confidence: 99%

“…IL-25 belongs to the IL-17 family, also known as IL-17E, 11 and has been identified as an "alarmin" cytokine that responds to pathogenic infection. 12,13 After infection, IL-25 is produced rapidly and promotes innate lymphoid cell proliferation. 14 A previous study has reported that tuft cell expansion was modulated by IL-25 expression during parasitic and bacterial infections.…”

Section: Introductionmentioning

confidence: 99%

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Folate supports IL‐25‐induced tuft cell expansion following enteroviral infections

Lyu,

Wu,

et al. 2024

The FASEB Journal

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Intestinal tuft cells, a kind of epithelial immune cells, rapidly expand in response to pathogenic infections, which is associated with infection‐induced interleukin 25 (IL‐25) upregulation. However, the metabolic mechanism of IL‐25‐induced tuft cell expansion is largely unknown. Folate metabolism provides essential purine and methyl substrates for cell proliferation and differentiation. Thus, we aim to investigate the roles of folate metabolism playing in IL‐25‐induced tuft cell expansion by enteroviral infection and recombinant murine IL‐25 (rmIL‐25) protein‐stimulated mouse models. At present, enteroviruses, such as EV71, CVA16, CVB3, and CVB4, upregulated IL‐25 expression and induced tuft cell expansion in the intestinal tissues of mice. However, EV71 did not induce intestinal tuft cell expansion in IL‐25−/− mice. Interestingly, compared to the mock group, folate was enriched in the intestinal tissues of both the EV71‐infected group and the rmIL‐25 protein‐stimulated group. Moreover, folate metabolism supported IL‐25‐induced tuft cell expansion since both folate‐depletion and anti‐folate MTX‐treated mice had a disrupted tuft cell expansion in response to rmIL‐25 protein stimulation. In summary, our data suggested that folate metabolism supported intestinal tuft cell expansion in response to enterovirus‐induced IL‐25 expression, which provided a new insight into the mechanisms of tuft cell expansion from the perspective of folate metabolism.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Folate supports IL‐25‐induced tuft cell expansion following enteroviral infections

Lyu,

Wu,

et al. 2024

The FASEB Journal

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“…Studies show that apart from Th2 cells, a rare population of epithelial cells that are recognized as tuft cells is an important source of IL-25 in the intestinal environment [ 21 ]. Tuft cells are a group of rare secretory epithelial cells mainly distributed in the respiratory tract and gastrointestinal tract [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

“…IL-25 –/– mice infected by Trichuris showed intestinal inflammation associated with increased expression of interferon γ (IFN-γ) and IL-17 [ 65 ]. IL-25 reduces Th1 cytokines such as IL-1, IL-6, and TNF-α produced by most helminth infections [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

“…Though IL-25 is generally considered a protective cytokine during helminth infection, IL-25 may also be involved in the pathogenic process [ 21 ]. Disruption of IL-25 along with thymic stromal lymphopoietin (TSLP) and IL-33 signaling suppressed chronic and progressive pulmonary type 2 cytokine-driven inflammation and fibrosis; however, blockade of IL-25 alone failed to present any significant change [ 73 ].…”

Section: Introductionmentioning

confidence: 99%

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Interleukin 25 and its biological features and function in intestinal diseases

Jiang¹,

Wang²,

Zhang³

et al. 2022

cejoi

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Interleukin 25 (IL-25), also known as IL-17E, is a member of the IL-17 cytokine family and an important regulator of the type 2 immune response. Accumulating evidence suggests that IL-25 interacts with diverse immune as well as non-immune cells and plays a rather complicated role in different backgrounds of multiple organs. IL-25 has been studied in the physiology and pathology of the intestine to some extent. With epithelial cells being an important source in the intestine, IL-25 plays a key role in intestinal immune responses and is associated with inappropriate allergic reactions, autoimmune diseases, and cancer tumorigenesis. In this review, we discuss the emerging comprehension of the biology of IL-25, as well as its cellular sources, targets, and signaling transduction. In particular, we discuss how IL-25 participates in the development of intestinal diseases including helminth infection, inflammatory bowel diseases, food allergy and colorectal cancer, as well as its underlying role in future therapy.

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Trained immunity of intestinal tuft cells during infancy enhances host defense against enteroviral infections in mice

Chen,

Wu,

Zhang

et al. 2024

EMBO Mol Med

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Innate immune cells have been acknowledged as trainable in recent years. While intestinal tuft cells are recognized for their crucial roles in the host defense against intestinal pathogens, there remains uncertainty regarding their trainability. Enterovirus 71 (EV71), a prevalent enterovirus that primarily infects children but rarely infects adults. At present, there is a significant expansion of intestinal tuft cells in the EV71-infected mouse model, which is associated with EV71-induced interleukin-25 (IL-25) production. Further, we found that IL-25 pre-treatment at 2 weeks old mouse enabled tuft cells to acquire immune memory. This was evidenced by the rapid expansion and stronger response of IL-25-trained tuft cells in response to EV71 infection at 6 weeks old, surpassing the reactivity of naïve tuft cells in mice without IL-25-trained progress. Interestingly, IL-25-trained intestinal tuft cells exhibit anti-enteroviral effect via producing a higher level of IL-25. Mechanically, IL-25 treatment upregulates spermidine/spermine acetyl-transferase enzyme (SAT1) expression, mediates intracellular polyamine deficiency, further inhibits enterovirus replication. In summary, tuft cells can be trained by IL-25, which supports faster and higher level IL-25 production in response to EV71 infection and further exhibits anti-enteroviral effect via SAT1-mediated intracellular polyamine deficiency. Given that IL-25 can be induced by multiple gut microbes during human growth and development, including shifts in gut flora abundance, which may partially explain the different susceptibility to enteroviral infections between adults and children.

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The potential roles of interleukin-25 in infectious diseases

Cited by 7 publications

References 121 publications

Folate supports IL‐25‐induced tuft cell expansion following enteroviral infections

Folate supports IL‐25‐induced tuft cell expansion following enteroviral infections

Interleukin 25 and its biological features and function in intestinal diseases

Trained immunity of intestinal tuft cells during infancy enhances host defense against enteroviral infections in mice

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