Inflammatory bowel disease results from alterations in the immune system and intestinal microbiota. The role of intestinal epithelial cells (IECs) in maintaining gut homeostasis is well known and its perturbation often causes gastrointestinal disorders including IBD. The epithelial specific adaptor protein (AP)-1B is involved in the establishment of the polarity of IECs. Deficiency of the AP-1B μ subunit (Ap1m2-/-) leads to the development of chronic colitis in mice. However, how this deficiency affects the gut microbes and its potential functions remains elusive. To gain insights into the gut microbiome of Ap1m2-/- mice having the colitis phenotype, we undertook shotgun metagenomic sequencing analysis of knockout mice. We found important links to the microbial features involved in altering various physiological pathways, including carbohydrate metabolism, nutrient transportation, oxidative stress, and bacterial pathogenesis (cell motility). In addition, an increased abundance of sulfur-reducing and lactate-producing bacteria has been observed which may aggravate the colitis condition.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7093000PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0228358PLOS

Publication Analysis

Top Keywords

knockout mice
8
association colitis
4
colitis gut-microbiota
4
gut-microbiota dysbiosis
4
dysbiosis clathrin
4
clathrin adapter
4
adapter ap-1b
4
ap-1b knockout
4
mice
4
mice inflammatory
4

Similar Publications

IL-35 modulates Tfh2 and Tfr cell balance to alleviate allergic rhinitis.

Inflamm Res

January 2025

Department of Otolaryngology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, China.

Background: Allergic rhinitis (AR) represents a persistent inflammatory condition affecting the upper respiratory tract, characterized by abnormal initiation of the immunoglobulin E (IgE)-mediated cascade. Follicular helper T (Tfh) cells and regulatory T (Tfr) cells are pivotal in orchestrating the development of IgE production in AR patients. IL-35, an anti-inflammatory cytokine, secreted by various cellular subpopulations.

View Article and Find Full Text PDF

Palmitate potentiates the SMAD3-PAI-1 pathway by reducing nuclear GDF15 levels.

Cell Mol Life Sci

January 2025

Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Sciences, Unitat de Farmacologia, Universitat de Barcelona, Av. Joan XXIII 27-31, 08028, Barcelona, Spain.

Nuclear growth differentiation factor 15 (GDF15) reduces the binding of the mothers' against decapentaplegic homolog (SMAD) complex to its DNA-binding elements. However, the stimuli that control this process are unknown. Here, we examined whether saturated fatty acids (FA), particularly palmitate, regulate nuclear GDF15 levels and the activation of the SMAD3 pathway in human skeletal myotubes and mouse skeletal muscle, where most insulin-stimulated glucose use occurs in the whole organism.

View Article and Find Full Text PDF

() is a causative gene for genetic hydrocephalus found in hemorrhagic hydrocephalus () mice. The knockout (KO) rat has subcortical heterotopia with frequent brain hemorrhage as seen in mice. In this study, we report aberrant alpha-smooth muscle actin (α-SMA) expression in the wall of lateral ventricle of the KO rats.

View Article and Find Full Text PDF

Purpose: Cardiomyocyte death is a major cytopathologic response in acute myocardial infarction (AMI) and involves complex inflammatory interactions. Although existing reports indicating that mixed lineage kinase domain-like protein (MLKL) is involved in macrophage necroptosis and inflammasome activation, the downstream mechanism of MLKL in necroptosis remain poorly characterized in AMI.

Methods: MLKL knockout mice (MLKL), RIPK3 knockout mice (RIPK3), and macrophage-specific MLKL conditional knockout mice (MLKL) were established.

View Article and Find Full Text PDF

Background And Aims: Oncogenic KRAS mutations are present in approximately 90% of pancreatic ductal adenocarcinoma (PDAC). However, Kras mutation alone is insufficient to transform precancerous cells into metastatic PDAC. This study investigates how KRAS-mutated epithelial cells acquire the capacity to escape senescence or even immune clearance, thereby progressing to advanced PDAC.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!