scholarly journals Apoptosis, Necrosis, and Necroptosis in the Gut and Intestinal Homeostasis

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Anna Negroni ◽  
Salvatore Cucchiara ◽  
Laura Stronati
Keyword(s):  
Cell Death ◽  
Immune Responses ◽  
Intestinal Epithelial Cells ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
Commensal Microbiota ◽  
Adaptive Immune ◽  
Epithelial Cell Death

Intestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota. Moreover, IECs are strongly involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This review is focused on previous reports on different forms of cell death in intestinal epithelium.

scholarly journals IL-22–induced cell extrusion and IL-18–induced cell death prevent and cure rotavirus infection

2020 ◽  
Vol 5 (52) ◽  
pp. eabd2876
Author(s):  
Zhan Zhang ◽  
Jun Zou ◽  
Zhenda Shi ◽  
Benyue Zhang ◽  
Lucie Etienne-Mesmin ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Viral Infections ◽  
Intestinal Epithelial Cells ◽  
Intestinal Lumen ◽  
Intestinal Epithelial ◽  
And Migration ◽  
Rapid Drop ◽  
Cell Extrusion ◽  
Proliferation And Migration

Bacterial flagellin can elicit production of TLR5-mediated IL-22 and NLRC4-mediated IL-18 cytokines that act in concert to cure and prevent rotavirus (RV) infection. This study investigated the mechanism by which these cytokines act to impede RV. Although IL-18 and IL-22 induce each other’s expression, we found that IL-18 and IL-22 both impeded RV independently of one another and did so by distinct mechanisms that involved activation of their cognate receptors in intestinal epithelial cells (IEC). IL-22 drove IEC proliferation and migration toward villus tips, which resulted in increased extrusion of highly differentiated IEC that serve as the site of RV replication. In contrast, IL-18 induced cell death of RV-infected IEC thus directly interrupting the RV replication cycle, resulting in spewing of incompetent virus into the intestinal lumen and causing a rapid drop in the number of RV-infected IEC. Together, these actions resulted in rapid and complete expulsion of RV, even in hosts with severely compromised immune systems. These results suggest that a cocktail of IL-18 and IL-22 might be a means of treating viral infections that preferentially target short-lived epithelial cells.

scholarly journals Expression of TNFAIP3 in intestinal epithelial cells protects from DSS- but not TNBS-induced colitis

2012 ◽  
Vol 303 (2) ◽  
pp. G220-G227 ◽  
Author(s):  
Lesley Rhee ◽  
Stephen F. Murphy ◽  
Lauren E. Kolodziej ◽  
Wesley A. Grimm ◽  
Christopher R. Weber ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Sulfonic Acid ◽  
Feedback Loop ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Intestinal Lumen ◽  
Mucosal Inflammation ◽  
Trinitrobenzene Sulfonic Acid ◽  
Intestinal Epithelial ◽  
Wild Type

Intestinal epithelial cells (IEC) maintain gastrointestinal homeostasis by providing a physical and functional barrier between the intestinal lumen and underlying mucosal immune system. The activation of NF-κB and prevention of apoptosis in IEC are required to maintain the intestinal barrier and prevent colitis. How NF-κB activation in IEC prevents colitis is not fully understood. TNFα-induced protein 3 (TNFAIP3) is a NF-κB-induced gene that acts in a negative-feedback loop to inhibit NF-κB activation and also to inhibit apoptosis; therefore, we investigated whether TNFAIP3 expression in the intestinal epithelium impacts susceptibility of mice to colitis. Transgenic mice expressing TNFAIP3 in IEC (villin-TNFAIP3 Tg mice) were exposed to dextran sodium sulfate (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS), and the severity and characteristics of mucosal inflammation and barrier function were compared with wild-type mice. Villin-TNFAIP3 Tg mice were protected from DSS-induced colitis and displayed reduced production of NF-κB-dependent inflammatory cytokines. Villin-TNFAIP3 Tg mice were also protected from DSS-induced increases in intestinal permeability and induction of IEC death. Villin-TNFAIP3 Tg mice were not protected from colitis induced by TNBS. These results indicate that TNFAIP3 expression in IEC prevents colitis involving DSS-induced IEC death, but not colitis driven by T cell-mediated inflammation. As TNFAIP3 inhibits NF-κB activation and IEC death, expression of TNFAIP3 in IEC may provide an avenue to inhibit IEC NF-κB activation without inducing IEC death and inflammation.

scholarly journals A20 and ABIN-1 team up against intestinal epithelial cell death

2018 ◽  
Vol 215 (7) ◽  
pp. 1771-1773
Author(s):  
Ken Cadwell
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Mouse Model ◽  
Intestinal Epithelium ◽  
Intestinal Epithelial Cell ◽  
Inflammatory Diseases ◽  
Intestinal Epithelial ◽  
Binding Partner ◽  
Epithelial Cell Death

A20 and its binding partner ABIN-1 are genetically linked to inflammatory diseases. In this issue of JEM, Kattah et al. (https://doi.org/10.1084/jem.20180198) demonstrate that simultaneous deletion in a mouse model leads to instantaneous cell death in the intestinal epithelium and mortality.

scholarly journals Luminal-Applied Flagellin Is Internalized by Polarized Intestinal Epithelial Cells and Elicits Immune Responses via the TLR5 Dependent Mechanism

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e24869 ◽  
Author(s):  
Tonyia Eaves-Pyles ◽  
Heng-Fu Bu ◽  
Xiao-di Tan ◽  
Yingzi Cong ◽  
Jignesh Patel ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Dependent Mechanism

scholarly journals Butyrophilin-like 2 regulates site-specific adaptations of intestinal γδ intraepithelial lymphocytes

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Casandra Panea ◽  
Ruoyu Zhang ◽  
Jeffrey VanValkenburgh ◽  
Min Ni ◽  
Christina Adler ◽  
...  
Keyword(s):  
Immune Responses ◽  
Intraepithelial Lymphocytes ◽  
Homeostatic Proliferation ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Site Specific ◽  
Adaptive Immune ◽  
Intestinal Segments ◽  
Repertoire Diversity

AbstractTissue-resident γδ intraepithelial lymphocytes (IELs) orchestrate innate and adaptive immune responses to maintain intestinal epithelial barrier integrity. Epithelia-specific butyrophilin-like (Btnl) molecules induce perinatal development of distinct Vγ TCR+ IELs, however, the mechanisms that control γδ IEL maintenance within discrete intestinal segments are unclear. Here, we show that Btnl2 suppressed homeostatic proliferation of γδ IELs preferentially in the ileum. High throughput transcriptomic characterization of site-specific Btnl2-KO γδ IELs reveals that Btnl2 regulated the antimicrobial response module of ileal γδ IELs. Btnl2 deficiency shapes the TCR specificities and TCRγ/δ repertoire diversity of ileal γδ IELs. During DSS-induced colitis, Btnl2-KO mice exhibit increased inflammation and delayed mucosal repair in the colon. Collectively, these data suggest that Btnl2 fine-tunes γδ IEL frequencies and TCR specificities in response to site-specific homeostatic and inflammatory cues. Hence, Btnl-mediated targeting of γδ IEL development and maintenance may help dissect their immunological functions in intestinal diseases with segment-specific manifestations.

Combining PD-L1 Inhibitors with Immunogenic Cell Death Triggered by Chemo-Photothermal therapy via a Thermosensitive Liposome System to Stimulate Tumor-specific Immunological Response

Nanoscale ◽  
2021 ◽  
Author(s):  
Jie Yu ◽  
Xidong He ◽  
Zigui Wang ◽  
Yu Peng Wang ◽  
Sha Liu ◽  
...  
Keyword(s):  
Cell Death ◽  
Immune Responses ◽  
Photothermal Therapy ◽  
Immunological Response ◽  
Immune Checkpoint Blockade ◽  
Immunogenic Cell Death ◽  
Adaptive Immune Responses ◽  
Adaptive Immune ◽  
Thermosensitive Liposome ◽  
Liposome System

Immune checkpoint blockade (ICB) therapy in combination with immunogenic death (ICD) triggered by photothermal therapy (PTT) and oxaliplatin (OXA) treatment was expected to elicit both innate and adaptive immune responses...

scholarly journals Arctigenin fromFructus Arctii(Seed of Burdock) Reinforces Intestinal Barrier Function in Caco-2 Cell Monolayers

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Hee Soon Shin ◽  
Sun Young Jung ◽  
Su Yeon Back ◽  
Jeong-Ryong Do ◽  
Dong-Hwa Shon
Keyword(s):  
Barrier Function ◽  
Active Component ◽  
Inflammatory Diseases ◽  
Intestinal Barrier ◽  
Transepithelial Electrical Resistance ◽  
Intestinal Barrier Function ◽  
Intestinal Epithelial ◽  
Traditional Herbal Medicine ◽  
Cell Monolayers ◽  
Basolateral Side

Fructus Arctiiis used as a traditional herbal medicine to treat inflammatory diseases in oriental countries. This study aimed to investigate effect ofF. Arctiiextract on intestinal barrier function in human intestinal epithelial Caco-2 cells and to reveal the active component ofF. Arctii. We measured transepithelial electrical resistance (TEER) value (as an index of barrier function) and ovalbumin (OVA) permeation (as an index of permeability) to observe the changes of intestinal barrier function. The treatment ofF. Arctiiincreased TEER value and decreased OVA influx on Caco-2 cell monolayers. Furthermore, we found that arctigenin as an active component ofF. Arctiiincreased TEER value and reduced permeability of OVA from apical to the basolateral side but not arctiin. In the present study, we revealed thatF. Arctiicould enhance intestinal barrier function, and its active component was an arctigenin on the functionality. We expect that the arctigenin fromF. Arctiicould contribute to prevention of inflammatory, allergic, and infectious diseases by reinforcing intestinal barrier function.

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