Neutrophil–Epithelial Crosstalk During Intestinal Inflammation

Kang, Le; Fang, Xue; Song, Yi-Hang; He, Zixuan; Wang, Zhijie; Wang, Shuling; Li, Zhao‐Shen; Bai, Yu

doi:10.1016/j.jcmgh.2022.09.002

Cited by 23 publications

(10 citation statements)

References 108 publications

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“…Several studies demonstrate the effect of neutrophils on other components of the intestinal mucosa in IBD, such as other immune cells and epithelial cells and other non-immune cells. However, less is known about the reciprocal effect on neutrophils of these other cells, particularly intra-epithelial cell components as stroma and epithelial cells, although some studies point to the importance of neutrophil–epithelial cell communication for essential neutrophil functions such as recruitment, transepithelial migration, cell death, and clearance (Reviewed in [ 63 ]).…”

Section: Discussionmentioning

confidence: 99%

“…The intestinal epithelium constitutes a physical barrier that isolates subepithelial tissues from luminal contents, providing a fundamental support for intestinal homeostasis. Neutrophils are associated with bystander tissue damage, but also play a role in epithelial restitution [ 63 ].…”

Section: Ibd Pathophysiologymentioning

confidence: 99%

“…Neutrophils are also, themselves, regulated by the effects of intestinal epithelial cells during intestinal inflammation, a topic recently reviewed in [ 63 ].…”

Section: Ibd Pathophysiologymentioning

confidence: 99%

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Pathophysiology of Inflammatory Bowel Disease: Innate Immune System

Saéz

Herrero‐Fernández

Gómez-Bris

et al. 2023

IJMS

172

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Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), is a heterogeneous state of chronic intestinal inflammation with no exact known cause. Intestinal innate immunity is enacted by neutrophils, monocytes, macrophages, and dendritic cells (DCs), and innate lymphoid cells and NK cells, characterized by their capacity to produce a rapid and nonspecific reaction as a first-line response. Innate immune cells (IIC) defend against pathogens and excessive entry of intestinal microorganisms, while preserving immune tolerance to resident intestinal microbiota. Changes to this equilibrium are linked to intestinal inflammation in the gut and IBD. IICs mediate host defense responses, inflammation, and tissue healing by producing cytokines and chemokines, activating the complement cascade and phagocytosis, or presenting antigens to activate the adaptive immune response. IICs exert important functions that promote or ameliorate the cellular and molecular mechanisms that underlie and sustain IBD. A comprehensive understanding of the mechanisms underlying these clinical manifestations will be important for developing therapies targeting the innate immune system in IBD patients. This review examines the complex roles of and interactions among IICs, and their interactions with other immune and non-immune cells in homeostasis and pathological conditions.

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Section: Discussionmentioning

confidence: 99%

Section: Ibd Pathophysiologymentioning

confidence: 99%

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Pathophysiology of Inflammatory Bowel Disease: Innate Immune System

Saéz

Herrero‐Fernández

Gómez-Bris

et al. 2023

IJMS

172

View full text Add to dashboard Cite

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“…Neutrophil cryptitis and crypt abscesses are key pathogenic events in UC [ 80 ]. Impairment of the function of the intestinal barrier can predispose the immune cells in the lamina propria to enteric bacteria, which can promote neutrophil accumulation and consequently induce inflammation [ 81 ]. Herein, we discovered that treatment with Nec-1 or GSK-872 effectively attenuates gut inflammation.…”

Section: Discussionmentioning

confidence: 99%

Macrophage Tim-3 maintains intestinal homeostasis in DSS-induced colitis by suppressing neutrophil necroptosis

Wang,

Zhou,

Peng

et al. 2024

Redox Biology

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“…Most importantly, aberrant neutrophil-endothelial interactions are implicated in a wide range of inflammatory diseases that relate to neutrophil influx and tissue damage ( 62 – 64 ). Similarly, neutrophil-epithelial crosstalk is involved in the maintenance of the epithelial-lined organs where uncontrolled neutrophil processes contribute to pathogenesis of diseases ( 65 – 68 ).…”

Section: Neutrophil Biology: the Basicsmentioning

confidence: 99%

A metabolic perspective of the neutrophil life cycle: new avenues in immunometabolism

Thind,

Uhlig,

Glogauer

et al. 2024

Front. Immunol.

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Neutrophils are the most abundant innate immune cells. Multiple mechanisms allow them to engage a wide range of metabolic pathways for biosynthesis and bioenergetics for mediating biological processes such as development in the bone marrow and antimicrobial activity such as ROS production and NET formation, inflammation and tissue repair. We first discuss recent work on neutrophil development and functions and the metabolic processes to regulate granulopoiesis, neutrophil migration and trafficking as well as effector functions. We then discuss metabolic syndromes with impaired neutrophil functions that are influenced by genetic and environmental factors of nutrient availability and usage. Here, we particularly focus on the role of specific macronutrients, such as glucose, fatty acids, and protein, as well as micronutrients such as vitamin B3, in regulating neutrophil biology and how this regulation impacts host health. A special section of this review primarily discusses that the ways nutrient deficiencies could impact neutrophil biology and increase infection susceptibility. We emphasize biochemical approaches to explore neutrophil metabolism in relation to development and functions. Lastly, we discuss opportunities and challenges to neutrophil-centered therapeutic approaches in immune-driven diseases and highlight unanswered questions to guide future discoveries.

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Neutrophil–Epithelial Crosstalk During Intestinal Inflammation

Cited by 23 publications

References 108 publications

Pathophysiology of Inflammatory Bowel Disease: Innate Immune System

Pathophysiology of Inflammatory Bowel Disease: Innate Immune System

Macrophage Tim-3 maintains intestinal homeostasis in DSS-induced colitis by suppressing neutrophil necroptosis

A metabolic perspective of the neutrophil life cycle: new avenues in immunometabolism

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