The role of NOD2 in intestinal immune response and microbiota modulation: A therapeutic target in inflammatory bowel disease

Liu, Ziyue; Zhang, Yaqin; Jin, Tao; Yi, Chengxue; Ocansey, Dickson Kofi Wiredu; Mao, Fei

doi:10.1016/j.intimp.2022.109466

Cited by 17 publications

(12 citation statements)

References 113 publications

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“… 99 Specifically, mice with gut‐specific Atg5 knockout display an altered gut microbiota composition and structure, characterized by an upsurge of proinflammatory bacteria and a decrease in alpha diversity. 100 , 101 Mice specifically lacking Atg7 in colonic epithelial cells also exhibit comparable outcomes. 102 Additionally, mice carrying the Atg16l1 T300A/T300A mutation exhibit an altered gut microbiota composition, characterized by a notable increase in the prevalence of bacteria linked to IBD, such as Ruminococcaceae .…”

Section: Autophagy In Autoimmune and Inflammatory Diseasesmentioning

confidence: 99%

“…Dysfunctional autophagy has been associated with dysbiosis of the gut microbiota, which heightens the susceptibility to developing IBD 99 . Specifically, mice with gut‐specific Atg5 knockout display an altered gut microbiota composition and structure, characterized by an upsurge of proinflammatory bacteria and a decrease in alpha diversity 100,101 . Mice specifically lacking Atg7 in colonic epithelial cells also exhibit comparable outcomes 102 .…”

Section: Autophagy In Autoimmune and Inflammatory Diseasesmentioning

confidence: 99%

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Modulation of the immunity and inflammation by autophagy

Gan

Zhang

et al. 2023

MedComm

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Autophagy, a highly conserved cellular self‐degradation pathway, has emerged with novel roles in the realms of immunity and inflammation. Genome‐wide association studies have unveiled a correlation between genetic variations in autophagy‐related genes and heightened susceptibility to autoimmune and inflammatory diseases. Subsequently, substantial progress has been made in unraveling the intricate involvement of autophagy in immunity and inflammation through functional studies. The autophagy pathway plays a crucial role in both innate and adaptive immunity, encompassing various key functions such as pathogen clearance, antigen processing and presentation, cytokine production, and lymphocyte differentiation and survival. Recent research has identified novel approaches in which the autophagy pathway and its associated proteins modulate the immune response, including noncanonical autophagy. This review provides an overview of the latest advancements in understanding the regulation of immunity and inflammation through autophagy. It summarizes the genetic associations between variants in autophagy‐related genes and a range of autoimmune and inflammatory diseases, while also examining studies utilizing transgenic animal models to uncover the in vivo functions of autophagy. Furthermore, the review delves into the mechanisms by which autophagy dysregulation contributes to the development of three common autoimmune and inflammatory diseases and highlights the potential for autophagy‐targeted therapies.

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Section: Autophagy In Autoimmune and Inflammatory Diseasesmentioning

confidence: 99%

Section: Autophagy In Autoimmune and Inflammatory Diseasesmentioning

confidence: 99%

Modulation of the immunity and inflammation by autophagy

Gan

Zhang

et al. 2023

MedComm

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“…NOD2 (Nucleotide-Binding Oligomerization Domain-Containing Protein 2) encodes a protein involved in the regulation of the immune system and the maintenance of the intestinal barrier function [ 46 , 47 , 48 ]. NOD2 is an intracellular receptor that recognizes muramyl dipeptide motifs, a component of the bacterial cell wall, and upon activation elicits responses to eradicate invading pathogens including activation of NFκB inflammatory signaling.…”

Section: Autophagy-related CD Susceptibility Genesmentioning

confidence: 99%

Autophagy in Crohn’s Disease: Converging on Dysfunctional Innate Immunity

Alula

Theiss

2023

Cells

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Crohn’s disease (CD) is a chronic inflammatory bowel disease marked by relapsing, transmural intestinal inflammation driven by innate and adaptive immune responses. Autophagy is a multi-step process that plays a critical role in maintaining cellular homeostasis by degrading intracellular components, such as damaged organelles and invading bacteria. Dysregulation of autophagy in CD is revealed by the identification of several susceptibility genes, including ATG16L1, IRGM, NOD2, LRRK2, ULK1, ATG4, and TCF4, that are involved in autophagy. In this review, the role of altered autophagy in the mucosal innate immune response in the context of CD is discussed, with a specific focus on dendritic cells, macrophages, Paneth cells, and goblet cells. Selective autophagy, such as xenophagy, ERphagy, and mitophagy, that play crucial roles in maintaining intestinal homeostasis in these innate immune cells, are discussed. As our understanding of autophagy in CD pathogenesis evolves, the development of autophagy-targeted therapeutics may benefit subsets of patients harboring impaired autophagy.

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“…• NOD2: se ha asociado a un incremento del riesgo para EC de tres veces más con respecto a la población general, si hay variantes heterocigotas, 38 veces más si variantes homocigotas y 44 veces más si variantes en heterocigosis compuesta (20,21) . Está asociado a mayor agresividad en EC, mayor riesgo de enfermedad estenosante y necesidad de intervención quirúrgica temprana (22) . • ABCB1: algunos polimorfismos se han asociado a incremento en el riesgo para CU (23) .…”

Section: Introductionunclassified

Fenotipificación y genotipificación en pacientes con enfermedad inflamatoria intestinal en un centro de referencia de Colombia

Parra Izquierdo,

Hani,

Romero-Sánchez

et al. 2024

Rev Gastroenterol Peru

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Introducción: Se ha tratado de identificar los factores genéticos relacionados con susceptibilidad para enfermedad inflamatoria intestinal (EII), y los hallazgos actuales se inclinan por un modelo de patología complejo, sin un patrón hereditario claro. Objetivo: Realizar caracterización fenotípica y genotípica de pacientes con EII en población colombiana y describir su posible asociación con predisposición. Materiales y métodos: Serie de casos, 16 pacientes con EII por criterios clínicos y anatomopatológicos, inicio de síntomas gastrointestinales después de los 18 años. Todos tuvieron asesoramiento genético pre-test y se realizaron árboles genealógicos de mínimo tres generaciones. También, genotipificación, por medio de un panel de genes múltiples que incluía genes relacionados con EII y algunos trastornos autoinmunitarios. Finalmente, se realizó análisis genómico de variantes. Resultados: 9 mujeres y 7 hombres, con edad media de diagnóstico de EII 35 años, y 32 años para aparición de síntomas gastrointestinales. 11/16(68,75%) requirieron terapia biológica. 10/16 (62,5%) presentaron refractariedad a terapia estándar. 3/16 (18,75%) tenían antecedentes familiares positivos de EII. 100% casos presentaron al menos un single nucleotide polymorphism relacionado con riesgo de EII en más de un gen. Los genes más relacionados con colitis ulcerosa (CU), fueron CD48, CD6, y TYK2 para CU, y CD6 e ITGAM para la enfermedad de Crohn. El gen más frecuente fue CD6. Se observó en 3/16 (18,75%) presencia de hasta 5 genes, 4 en 3/16 (18,75%), y tres en 5/16 (31,25%). Conclusión: En EII hay presencia de variantes genéticas con predisposición asociada, pero sin patogenicidad confirmada, y cuya sumatoria parece contribuir en su fisiopatología

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The role of NOD2 in intestinal immune response and microbiota modulation: A therapeutic target in inflammatory bowel disease

Cited by 17 publications

References 113 publications

Modulation of the immunity and inflammation by autophagy

Modulation of the immunity and inflammation by autophagy

Autophagy in Crohn’s Disease: Converging on Dysfunctional Innate Immunity

Fenotipificación y genotipificación en pacientes con enfermedad inflamatoria intestinal en un centro de referencia de Colombia

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