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 4 publications

(7 citation statements)

References 121 publications

(81 reference statements)

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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

Self Cite

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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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Mendelian randomization analyses of genetically predicted circulating levels of cytokines with risk of Inflammatory bowel disease

liu,

Li,

Gao

et al. 2023

Preprint

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Objective The literature has previously reported the associations between inflammatory bowel disease (IBD) and certain inflammatory cytokines, such as CRP, IL-1, and TNFα. To additionally evaluate the causal relationships between 41 inflammatory cytokines and IBD, a Mendelian randomization (MR) study was conducted. Methods The two-sample MR investigation utilized data from three large publicly available genome-wide association studies (GWAS) on IBD, ulcerative colitis (UC), and Crohn's disease (CD) genetic variants. Additionally, inflammatory cytokine data from a GWAS meta-analysis, including 8,293 healthy individuals, were incorporated into the study. Causal relationships between exposures and outcomes were predominantly determined utilizing inverse variance-weighted methods. To evaluate the heterogeneity, pleiotropy, and stability of these genetic variants, the MR-Egger intercept test, Cochran's Q test, and leave-one-out sensitivity analysis were conducted. Results The findings revealed that IL13 was linked to an elevated risk of IBD, UC, and CD, while MIF demonstrated a correlation with an elevated risk of CD. Conversely, TNF-related apoptosis-inducing ligand (TRAIL) was linked to a decreased risk of IBD and UC. Additionally, reverse MR analyses revealed that IBD was correlated with elevated levels of Monokine Induced by Gamma Interferon (MIG) and Stromal Cell-Derived Factor-1α (SDF1A), while UC showed an association with elevated levels of MIG and IL10. The CD was linked to elevated levels of stem cell factor (SCF) and decreased levels of TNF-β. Conclusion In the MR study, three upstream regulatory factors and five downstream regulatory factors were identified for IBD and its subtypes, providing avenues for developing new therapies for IBD.

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The potential roles of interleukin-25 in infectious diseases

Cited by 4 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

Mendelian randomization analyses of genetically predicted circulating levels of cytokines with risk of Inflammatory bowel disease

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