IntestiCult™ Organoid Growth Medium (Mouse)

Cell culture medium for establishment and maintenance of mouse intestinal organoids

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IntestiCult™ Organoid Growth Medium (Mouse)

Cell culture medium for establishment and maintenance of mouse intestinal organoids

1 Kit
Catalog #06005
276 USD

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IntestiCult™ Organoid Growth Medium (Mouse) is a defined, serum-free cell culture medium for efficient establishment and long-term maintenance of mouse intestinal organoids.These organoids, or “mini-guts”, provide a convenient in vitro organotypic culture system for studying both the small and large intestinal epithelium and associated stem cell dynamics. Organoids grown in IntestiCult™ feature a polarized epithelium that contains all of the known cell types of the adult intestinal epithelium. Individual intestinal crypts rapidly form organoids when cultured in IntestiCult™ Organoid Growth Medium (Mouse). Applications of these cultures include studying the development and function of the normal and tumorigenic intestinal epithelium, modeling intestinal disease, and investigating stem cell properties and regenerative therapy approaches. Organoid culture enables convenient in vitro characterization of a system with strong physiological relevance to the adult intestine.
• Convenient, in vitro system that recapitulates the identity and organization of the adult intestinal epithelium, including intra- and intercellular signaling, self-propagating stem cell niche and functional transport into and out of the lumen
• Serum-free and defined medium formulation that delivers consistent results
• Enables generation of intestinal organoids in less than one week
• Simple format and easy-to-use protocol
  • IntestiCult™ OGM (Mouse) Basal Medium, 90 mL
  • IntestiCult™ OGM (Mouse) Supplement 1, 5 mL
  • IntestiCult™ OGM (Mouse) Supplement 2, 5 mL
Specialized Media
Cell Type:
Intestinal Cells
Cell Culture; Differentiation; Expansion; Maintenance; Organoid Culture
Area of Interest:
Cancer Research; Disease Modeling; Drug Discovery and Toxicity Testing; Epithelial Cell Biology; Stem Cell Biology
Serum-Free; Defined

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Data and Publications


Scientific reports 2017 MAY

Organoid-based epithelial to mesenchymal transition (OEMT) model: from an intestinal fibrosis perspective.

Hahn S et al.


The current in vitro or in vivo intestinal fibrosis models have many limitations. Recent advancements in the isolation and culturing of organoids has led to development of various three-dimensional (3D) intestinal disease models with in vivo physiology. In this study, we generated an organoid-based epithelial to mesenchymal transition (OEMT) model, which could be used as a novel intestinal fibrosis model. Intestinal epithelial organoids (IEOs) were isolated and cultured from the small intestines of normal mice. IEOs were treated with transforming growth factor- $$1 (TGF-$$1) or Tumor necrosis factor-$$ (TNF-$$) to evaluate their phenotypic change. Raw 264.7 cells (macrophage) stimulated with lipopolysaccharide were co-cultured with IEOs in growth media with or without TGF-$$1. TGF-$$1 alone slightly induced epithelial to mesenchymal transition (EMT) in the IEOs but mainly disrupted them. Macrophage released cytokines synergistically induced mesenchymal phenotypic changes in TGF-$$1 stimulated intestinal organoids. TNF-$$ and TGF-$$1 synergistically induced proliferation of mesenchymal cells as well as EMT in the IEOs. We generated a novel OEMT model based on our finding that TNF-$$ and TGF-$$ synergistically induce type 2 EMT in IEOs. This 3D EMT model with in vivo physiology could be used to study EMT associated intestinal fibrosis.
American journal of physiology. Gastrointestinal and liver physiology 2017 JUL

Absence of the NOD2 protein renders epithelia more susceptible to barrier dysfunction due to mitochondrial dysfunction.

Saxena A et al.


Irregular mitochondria structure and reduced ATP in some patients with IBD suggest that metabolic stress contributes to disease. Loss-of-function mutation in the nucleotide-binding oligomerization domain (NOD)-2 gene is a major susceptibility trait for IBD. Hence, we assessed if loss of NOD2 further impairs the epithelial barrier function instigated by disruption of mitochondrial ATP synthesis via the hydrogen ionophore dinitrophenol (DNP). NOD2 protein (virtually undetectable in epithelia under basal conditions) was increased in T84 (human colon cell line) cells treated with noninvasive Escherichia coli + DNP (16 h). Increased intracellular bacteria in wild-type (WT) and NOD2 knockdown (KD) cells and colonoids from NOD2(-/-) mice were mediated by reactive oxygen species (ROS) and the MAPK ERK1/2 pathways as determined by cotreatment with the antioxidant mitoTEMPO and the ERK inhibitor U0126: ROS was upstream of ERK1/2 activation. Despite increased E. coli in DNP-treated NOD2 KD compared with WT cells, there were no differences in the internalization of fluorescent inert beads or dead E. coli particles. This suggests that lack of killing in the NOD2 KD cells was responsible for the increased numbers of viable intracellular bacteria; a conclusion supported by evidence of reduced autophagy in NOD2 KD T84 epithelia. Thus, in a two-hit hypothesis, decreased barrier function due to dysfunctional mitochondrial is amplified by lack of NOD2 in transporting enterocytes: subsequently, greater numbers of bacteria entering the mucosa would be a significant inflammatory threat especially since individuals with NOD2 mutations have compromised macrophage and Paneth cell responses to bacteria.NEW & NOTEWORTHY Increased internalization of bacteria by epithelia with dysfunctional mitochondria (reduced ATP) is potentiated if the cells lack nucleotide-binding oligomerization domain 2 (NOD2), mutations in which are inflammatory bowel disease-susceptibility traits. Uptake of bacteria was dependent on reactive oxygen species and MAP-kinase activity, and the increased viable intracellular bacteria in NOD2(-/-) cells likely reflect a reduced ability to recognize and kill bacteria. Thus a significant barrier defect occurs with NOD2 deficiency in conjunction with metabolic stress that could contribute to inflammation.
Scientific reports 2017 JUL

Epithelial cell specific Raptor is required for initiation of type 2 mucosal immunity in small intestine.

Aladegbami B et al.


Intestinal tuft cells are one of 4 secretory cell linages in the small intestine and the source of IL-25, a critical initiator of the type 2 immune response to parasite infection. When Raptor, a critical scaffold protein for mammalian target of rapamycin complex 1 (mTORC1), was acutely deleted in intestinal epithelium via Tamoxifen injection in Tritrichomonas muris (Tm) infected mice, tuft cells, IL-25 in epithelium and IL-13 in the mesenchyme were significantly reduced, but Tm burden was not affected. When Tm infected mice were treated with rapamycin, DCLK1 and IL-25 expression in enterocytes and IL-13 expression in mesenchyme were diminished. After massive small bowel resection, tuft cells and Tm were diminished due to the diet used postoperatively. The elimination of Tm and subsequent re-infection of mice with Tm led to type 2 immune response only in WT, but Tm colonization in both WT and Raptor deficient mice. When intestinal organoids were stimulated with IL-4, tuft cells and IL-25 were induced in both WT and Raptor deficient organoids. In summary, our study reveals that enterocyte specific Raptor is required for initiating a type 2 immune response which appears to function through the regulation of mTORC1 activity.
Radiation research 2017 AUG

Growth Differentiation Factor 11 does not Mitigate the Lethal Effects of Total-Abdominal Irradiation.

Duhachek-Muggy S et al.


Total-body exposure to radiation causes widespread tissue injury. Damage to the hematopoietic and intestinal stem cell compartments is particularly lethal and mitigators of this damage are critical in providing effective treatment. Parabiosis radiation experiments, in which the vasculatures of two rodents are anastomosed prior to irradiation of one of the animals, have shown that there is a circulating factor that protects mice from radiation-induced intestinal death. Recently reported studies have suggested that growth differentiation factor 11 (GDF11) is responsible for the rejuvenation of stem cells observed in parabiosis experiments involving aging mice. In this study, we investigated the efficacy of GDF11 as a potential mitigator of radiation-induced damage to intestinal stem cells. In ex vivo cultures of intestinal organoids, the number of cells expressing the stem cell marker Lgr5 was increased after irradiation and GDF11 supplementation. Further ex vivo studies to assess stem cell function, measured by the ability to grow new crypt-like structures, did not show increased stem cell activity in response to GDF11 treatment. In addition, GDF11 was unable to improve survival of mice subjected to total-abdominal irradiation. These data demonstrate that GDF11 does not mitigate radiation damage to intestinal stem cells.
Frontiers in immunology 2017

Cell Polarization and Epigenetic Status Shape the Heterogeneous Response to Type III Interferons in Intestinal Epithelial Cells.

Bhushal S et al.


Type I and type III interferons (IFNs) are crucial components of the first-line antiviral host response. While specific receptors for both IFN types exist, intracellular signaling shares the same Jak-STAT pathway. Due to its receptor expression, IFN-$$ responsiveness is restricted mainly to epithelial cells. Here, we display IFN-stimulated gene induction at the single cell level to comparatively analyze the activities of both IFN types in intestinal epithelial cells and mini-gut organoids. Initially, we noticed that the response to both types of IFNs at low concentrations is based on a single cell decision-making determining the total cell intrinsic antiviral activity. We identified histone deacetylase (HDAC) activity as a crucial restriction factor controlling the cell frequency of IFN-stimulated gene (ISG) induction upon IFN-$$ but not IFN-$$ stimulation. Consistently, HDAC blockade confers antiviral activity to an elsewise non-responding subpopulation. Second, in contrast to the type I IFN system, polarization of intestinal epithelial cells strongly enhances their ability to respond to IFN-$$ signaling and raises the kinetics of gene induction. Finally, we show that ISG induction in mini-gut organoids by low amounts of IFN is characterized by a scattered heterogeneous responsiveness of the epithelial cells and HDAC activity fine-tunes exclusively IFN-$$ activity. This study provides a comprehensive description of the differential response to type I and type III IFNs and demonstrates that cell polarization in gut epithelial cells specifically increases IFN-$$ activity.
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