Inhibitor of Differentiation-2 Protein Ameliorates DSS-Induced Ulcerative Colitis by Inhibiting NF-κB Activation in Neutrophils

Ren, Jie; Yan, Dong; Wang, Yichun; Zhang, Jiaojiao; Li, Min; Xiong, Wancheng; Jing, Xueqian; Li, Puze; Zhao, Weidong; Xiong, Xin; Wu, Minna; Zhong, Genshen

doi:10.3389/fimmu.2021.760999

Cited by 10 publications

(3 citation statements)

References 62 publications

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“…In addition, a low-fat diet significantly reduced patients' levels of expressed inflammatory markers and attenuated the dysregulation of their gut microbiota. Studies based on IBD animal models have shown that proteolytic diets induce remission associated with decreased abundance of pathogens such as E. coli and Clostridium perfringens , increased abundance of Clostridium hiranonis , a secondary bile acid producer, and elevated levels of chicholic acid and deoxycholic acid[ 110 ].…”

Section: Aiec In Ucmentioning

confidence: 99%

Role of adherent invasive Escherichia coli in pathogenesis of inflammatory bowel disease

Duan¹,

Dai²,

Wu³

2022

World J Clin Cases

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Gut microbiota imbalances play an important role in inflammatory bowel disease (IBD), but no single pathogenic microorganism critical to IBD that is specific to the IBD terminal ileum mucosa or can invade intestinal epithelial cells has been found. Invasive Escherichia coli ( E. coli) adhesion to macrophages is considered to be closely related to the pathogenesis of inflammatory bowel disease. Further study of the specific biological characteristics of adherent invasive E. coli (AIEC) may contribute to a further understanding of IBD pathogenesis. This review explores the relationship between AIEC and the intestinal immune system, discusses the prevalence and relevance of AIEC in Crohn's disease and ulcerative colitis patients, and describes the relationship between AIEC and the disease site, activity, and postoperative recurrence. Finally, we highlight potential therapeutic strategies to attenuate AIEC colonization in the intestinal mucosa, including the use of phage therapy, antibiotics, and anti-adhesion molecules. These strategies may open up new avenues for the prevention and treatment of IBD in the future.

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Section: Aiec In Ucmentioning

confidence: 99%

Role of adherent invasive Escherichia coli in pathogenesis of inflammatory bowel disease

Duan¹,

Dai²,

Wu³

2022

World J Clin Cases

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“…This results in the main pathological feature of UC: chronic ulcerative damage to the colonic mucosa. Previous studies have confirmed the uncontrolled accumulation and persistence of PMNs in damaged mucosal lamina propria [11]. A vicious cycle is formed, in which infiltrating PMNs damage the mucosa, which in turn leads to further PMN infiltration.…”

Section: Introductionmentioning

confidence: 77%

Effects of the N-butanol Extract of Pulsatilla Decoction on Neutrophils in a Mouse Model of Ulcerative Colitis

Wang,

Wu,

Sun

et al. 2024

Preprint

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Ulcerative colitis (UC) is a chronic inflammatory disease, the incidence of which is increasing worldwide. However, the etiology and pathogenesis of UC remains unclear. The n-butanol extract of pulsatilla decoction (BEPD) of the traditional Chinese medicine herbal formula has been shown to be effective in treating UC. We aimed to explore the molecular mechanism underlying the effects of BEPD on UC, in particular its effects on neutrophil extracellular trap (NET) formation by neutrophils. High-performance liquid chromatography was used to determine the principal compounds of BEPD. UC was induced in mice using dextran sodium sulfate, and mice were treated with 20, 40, or 80 mg/kg BEPD daily for seven days. Colonic inflammation was determined by assessing the disease activity index, histopathology, colonic mucosal damage index, colonic mucosal permeability, and pro- and anti-inflammatory cytokine levels. The infiltration and activation status of neutrophils in the colon were determined by analyzing the levels of chemokine (C-X-C motif) ligand (CXCL)1 and CXCL2, reactive oxygen species, Ly6G, and numerous NET proteins. Our results showed that BEPD improved the disease activity index, histopathology, and colonic mucosal damage index scores of mice with UC, and restored colonic mucosal permeability compared with untreated mice. The expression levels of the pro-inflammatory cytokines interleukin-1β, interleukin-6, and tumor necrosis factor-α in colon tissues were significantly decreased, while the expression levels of anti-inflammatory cytokines in colon tissues were significantly increased, exceeding those of control mice. In addition, BEPD reduce the expression of the neutrophil chemokines CXCL1 and CXCL2 in the colon tissue of mice with UC, reduced neutrophil infiltration, reduced reactive oxygen species levels, and significantly reduced the expression of NET proteins. BEPD also significantly reduced NET formation. The results of this study suggest that BEPD exerts therapeutic effects in a murine model of UC by inhibiting neutrophil infiltration and activation in the colon, as well as by inhibiting the expression of key proteins involved in NET formation and reducing NET formation, thereby alleviating local tissue damage and disease manifestations.

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“…At days 22 and 28, peripheral blood (PB) was collected from the mouse tail, and the absolute CD19 + NALM-6 numbers were determined using the flow cytometry with the 123count™ eBeads (Thermo Fisher, Cat#: 01–1234-42) as described in our previous study. 23 At day 35 after NALM-6 inoculation, the peripheral blood was collected from the mice, and the CD4 + and CD8 + subsets of T cells were counted with the 123count™ eBeads.…”

Section: Cytokine Assaymentioning

confidence: 99%

scRNA-seq reveals ATPIF1 activity in control of T cell antitumor activity

Zhong

Wang

et al. 2022

OncoImmunology

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ATP synthase inhibitory factor 1 (ATPIF1) is a mitochondrial protein with an activity in inhibition of F 1 F o -ATP synthase. ATPIF1 activity remains unknown in the control of immune activity of T cells. In this study, we identified ATPIF1 activity in the induction of CD8 + T cell function in tumor models through genetic approaches. ATPIF1 gene inactivation impaired the immune activities of CD8 + T cells leading to quick tumor growth (B16 melanoma and Lewis lung cancer) in ATPIF1-KO mice. The KO T cells exhibited a reduced activity in proliferation and IFN-γ secretion with metabolic reprogramming of increased glycolysis and decreased oxidative phosphorylation (OXPHOS) after activation. T cell exhaustion was increased in the tumor infiltrating leukocytes (TILs) of KO mice as revealed by the single-cell RNA sequencing (scRNA-seq) and confirmed by flow cytometry. In contrast, ATPIF1 overexpression in T cells increased expression of IFN-γ and Granzyme B, subset of central memory T cells in CAR-T cells, and survival rate of NALM-6 tumor-bearing mice. These data demonstrate that ATPIF1 deficiency led to tumor immune deficiency through induction of T cell exhaustion. ATPIF1 overexpression enhanced the T cell tumor immunity. Therefore, ATPIF1 is a potential molecular target in the modulation of antitumor immunity of CD8 + T cells in cancer immunotherapy. Induction of ATPIF1 activity may promote CAR-T activity in cancer therapy.

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Inhibitor of Differentiation-2 Protein Ameliorates DSS-Induced Ulcerative Colitis by Inhibiting NF-κB Activation in Neutrophils

Cited by 10 publications

References 62 publications

Role of adherent invasive Escherichia coli in pathogenesis of inflammatory bowel disease

Role of adherent invasive Escherichia coli in pathogenesis of inflammatory bowel disease

Effects of the N-butanol Extract of Pulsatilla Decoction on Neutrophils in a Mouse Model of Ulcerative Colitis

scRNA-seq reveals ATPIF1 activity in control of T cell antitumor activity

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