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Secreted effectors of the innate mucosal barrier
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Michael A. McGuckin, Andre J. Ouellette, Gary D. Wu
The intestinal epithelial barrier, along with specialized cells responsible for the secretion of mucus, antimicrobial peptides, and enteric hormones, is constantly renewed every 4–5 days. The primary function of the intestinal tract is the digestion and absorption of nutrients, electrolytes, and water. In the small intestine, the crypt compartment contains undifferentiated, proliferating progenitor cells, while the villi are populated by nonproliferating cells with specialized functions. Stem cells located in the base of the small intestinal crypt give rise to four differentiated cell types that populate the villus—absorptive enterocytes, enteroendocrine cells, tuft cells, and goblet cells—and a single differentiated cell type at the base of the crypt, Paneth cells. In specific regions of the intestine, namely in the terminal ileum, progenitor cells differentiate into specialized M cells that overlay Peyer's patches and play a role in internalizing luminal antigens for presentation to lymphocytes. Although villi are absent in the colon, similar compartmentalization exists with proliferating cells located in the lower two-thirds of the crypt and differentiated cells found higher in the crypt and at the epithelial surface. Molecular mechanisms that regulate intestinal epithelial homeostasis include defining the stem cell niche, regulating epithelial cell proliferation in the intestinal crypt, and epithelial cell differentiation and lineage allocation (Figure 4.2).
Cell Proliferation In Colon Carcinogenesis
Published in Herman Autrup, Gary M. Williams, Experimental Colon Carcinogenesis, 2019
The proliferative zone in the mucosa of the large intestine covers the basal three quarters of the crypts. Epithelial cells migrate toward the gut lumen and are extruded from the mucosal surface between crypts. These large intestinal crypts are more closely spaced than either stomach or small intestine and the surface of the mucosa is flat. The surface area of the colonic mucosa between crypts is larger than the surface area of the crypt columns, supporting the assumption that the major function of the surface lining cells is absorption, while the major activity of the crypt columns is cell replacement.
Bacteria Causing Gastrointestinal Infections
Published in K. Balamurugan, U. Prithika, Pocket Guide to Bacterial Infections, 2019
B. Vinoth, M. Krishna Raja, B. Agieshkumar
The LT is structurally and functionally similar to the cholera toxin and is destroyed by heat and acid. It is a combination of A subunit and pentameric ring of 5B subunits. The B subunit binds to GM1 gangliosides of enterocytes and the A subunit causes G protein coupled activation of adenylate cyclase inside the enterocytes, leading to increased production of cyclic adenosine monophosphate (cAMP). These result in increased chloride secretion via cystic fibrosis transmembrane conductance regulator (CFTR) from the intestinal crypt cells of the small intestine resulting in voluminous diarrhea. The ST is not destroyed by heating even at 100°C, and their action is mediated through activation of guanylate kinase resulting in an increase of cyclic guanosine monophosphate (cGMP), leading to increased intestinal secretion from both small and large intestines.
A single cell survey of the microbial impacts on the mouse small intestinal epithelium
Published in Gut Microbes, 2022
Derek K.L. Tsang, Ryan J. Wang, Oliver De Sa, Arshad Ayyaz, Elisabeth G. Foerster, Giuliano Bayer, Shawn Goyal, Daniel Trcka, Bibaswan Ghoshal, Jeffrey L. Wrana, Stephen E. Girardin, Dana J. Philpott
The cellular architecture of the intestinal epithelium has been well characterized to be impacted by the microbiota in a community and species-dependent manner.29,30,39 By scRNAseq, we captured all epithelial cell lineages in both the GF and SPF mice, illustrating that no epithelial cell lineage is directly dependent on the presence of microbes. While we observed trends in the differences of epithelial cell subsets captured between GF and SPF samples (Supp Figure 1 F), it is impossible to infer physiological differences in abundance as our crypt enrichment process may impact the proportion of villus-associated cells captured under different conditions. However, in line with previous studies, we observed a microbiota-dependent increase in PC numbers within the intestinal crypt.29,30 Interestingly, we did not observe differences in GC, ISC, or TA cell abundances. Trajectory inference analysis demonstrated that the differentiation pathway of ISCs to terminal ECs or secretory lineages occurs independently of microbes. With the increase in PCs and similar differentiation trajectories, our data suggest microbiota stimulate an increase in PCs from ISCs through a pathway that is intrinsic to the epithelium.
Modulation of the Canonical Wnt Signaling Pathway by Dietary Polyphenols, an Opportunity for Colorectal Cancer Chemoprevention and Treatment
Published in Nutrition and Cancer, 2022
Hernan Villota, Sarah Röthlisberger, Johanna Pedroza-Díaz
Aberrant activation of the Wnt/β-catenin signaling pathway is frequently observed in CRC. In the colon, a monolayer of epithelial cells forms intestinal crypts. The intestinal stem cells (ISCs) at the base of the crypt allow the renewal of differentiated cells. The activity of the Wnt/β-catenin pathway is highest at the base of the crypt, and therefore, the suppression of Wnt signaling leads to both suspended proliferation and ISC deficiency, resulting in ablation of the intestinal epithelium (15). For example, transgenic expression of the Wnt inhibitor Dickkopf1 (Dkk1) results in the loss of crypts in the intestine (16). On the contrary, the number of ISCs is increased by the potentiation of Wnt signaling (17). This shows that the Wnt signaling plays a crucial role in colon homeostasis, in terms of ISC self-renewal and proliferation.
Oral administration of hydroxylated-graphene quantum dots induces intestinal injury accompanying the loss of intestinal stem cells and proliferative progenitor cells
Published in Nanotoxicology, 2019
Lan Yu, Xin Tian, Dexuan Gao, Yue Lang, Xiang-Xiang Zhang, Chen Yang, Meng-Meng Gu, Jianming Shi, Ping-Kun Zhou, Zeng-Fu Shang
The intestinal crypts can be cultured ex vivo to form intestinal organoids that simulate the native intestinal epithelium. We established a 3 D intestinal ‘mini-gut’ model to further analyze the toxic effects of OH-GQDs on the ISC population. The overall organoid formation efficiency was reduced from 93.83 ± 6.20% in the normal crypts to 46.17 ± 5.10% in the crypts isolated from 10 μg/ml OH-GQD-treated mice 24 h post-harvest. In addition, the organoid formation efficiency decreased to 54 ± 6.01% in the control group during the 7-day ex vivo culture, and to 52.3 ± 8.31%, 37.42 ± 2.42% and 16.33 ± 0.51% in the 0.1, 1, 10 μg/ml OH-GQD-treated groups respectively (Figure 7(A,B)). Furthermore, OH-GQD also significantly reduced the size of the surviving intestinal organoids (Figure 7(C,D)).