Enterocyte loss of polarity and gut wound healing rely upon the F-actin–severing function of villin

Ubelmann, Florent; Chamaillard, Mathias; El-Marjou, Fatima; Simon, Anthony; Netter, Jeanne; Vignjević, Danijela; Nichols, Buford L.; Quezada‐Calvillo, Roberto; Grandjean, Teddy; Louvard, Daniel; Revenu, Céline; Robine, Sylvie

doi:10.1073/pnas.1218446110

Cited by 72 publications

(74 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Both TGFβ1 and TFF3 have been reported to play important roles in protecting intestinal mucosa and prompting reconstruction of damaged mucosa[39]. Viliin, which is an actin-binding protein expressed in microvilli of the intestine, has also been proposed to be involved in colonic wound repair by remodeling of actin filaments in microvilli[40,41]. Moreover, the cysteine-rich domain of MUC3 has been shown to promote cell migration and improve wound healing of the colonic mucosa[42].…”

Section: Discussionmentioning

confidence: 99%

Oral administration of Bifidobacterium bifidum G9-1 alleviates rotavirus gastroenteritis through regulation of intestinal homeostasis by inducing mucosal protective factors

Kawahara¹,

Makizaki²,

Oikawa³

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

Human rotavirus (RV) infection is a leading cause of dehydrating diarrhea in infants and young children worldwide. Since therapeutic approaches to RV gastroenteritis are limited to alleviation of dehydration with oral rehydration solutions, more direct approaches to palliate symptoms of RV gastroenteritis are required. Treatments with probiotics have been increasingly recognized as alternative safe and low cost treatments for moderate infectious diarrhea. In this study, Bifidobacterium bifidum G9-1 (BBG9-1), which has been used as an intestinal drug for several decades, was shown to have a remarkable protective effect against RV gastroenteritis in a suckling mice model. As well as prophylactic oral administration of BBG9-1 from 2 days before RV infection, therapeutic oral administration of BBG9-1 from 1 day after RV infection significantly alleviated RV-induced diarrhea. Therapeutic administration of BBG9-1 reduced various types of damage in the small intestine, such as epithelial vacuolization and villous shortening, and significantly diminished the infectious RV titer in mixtures of cecal contents and feces. It was also shown that therapeutic administration of BBG9-1 significantly increased the number of acidic mucin-positive goblet cells and the gene expression of mucosal protective factors including MUC2, MUC3, MUC4, TGFβ1 and TFF3 in the small intestine. This led to alleviation of low gut permeability shown as decreased gene expression levels of occludin, claudin-1 and villin-1 after RV infection. Furthermore, in the small intestine, therapeutic administration of BBG9-1 significantly palliated the decreased gene expression of SGLT-1, which plays an important role in water absorption. In the large intestine, administered BBG9-1 was shown to replicate to assimilate undigested nutrients, resulting in normalization of the abnormally high osmotic pressure. These results suggested that water malabsorption caused by RV infection was alleviated in mice administered BBG9-1. Thus, the present study showed that oral administration of BBG9-1 palliated diarrhea partly through protection against RV-induced lesions by inducing mucosal protective factors. Oral administration of BBG9-1 is thought to be an efficient method for management of an RV epidemic for both prophylactic and therapeutic purposes.

show abstract

Section: Discussionmentioning

confidence: 99%

Oral administration of Bifidobacterium bifidum G9-1 alleviates rotavirus gastroenteritis through regulation of intestinal homeostasis by inducing mucosal protective factors

Kawahara¹,

Makizaki²,

Oikawa³

et al. 2017

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…Many opportunities exist to apply GLP-2 as a pre or postinfection therapeutic for infection, including GLP-2's effects on increasing mucin production, villus length, and tight junction protein expression to defend against parasitic invasion, as well as reducing nitro-oxidative stress, improving gut healing, and enhancing expression and activity of brush-border enzymes impacted by C parvum infection. Of particular interest, GLP-2 treatment of cultured GLP-2R-expressing cells has been shown to reduce F-actin abundance and alter its distribution within the cytoskeleton, a process associated with cellular proliferation [114] and required for enterocyte microvillus depolarization and remodeling during intestinal healing [115]. Therefore, there is the potential for GLP-2 pre-treatment to impair C parvum's ability to induce actin polymerization, which is required for envelopment by host epithelial cells [116].…”

Section: Potential Uses Of Glp-2 and Stimulators Of Glp-2 Secretion Imentioning

confidence: 99%

Glucagon-like peptide 2 and its beneficial effects on gut function and health in production animals

Connor

Evock‐Clover

Wall³

et al. 2016

Domestic Animal Endocrinology

View full text Add to dashboard Cite

Numerous endocrine cell subtypes exist within the intestinal mucosa and produce peptides contributing to the regulation of critical physiological processes including appetite, energy metabolism, gut function, and gut health. The mechanisms of action and the extent of the physiological effects of these enteric peptides are only beginning to be uncovered. One peptide in particular, glucagon-like peptide 2 (GLP-2) produced by enteroendocrine L cells, has been fairly well characterized in rodent and swine models in terms of its ability to improve nutrient absorption and healing of the gut after injury. In fact, a long-acting form of GLP-2 recently has been approved for the management and treatment of human conditions like inflammatory bowel disease and short bowel syndrome. However, novel functions of GLP-2 within the gut continue to be demonstrated, including its beneficial effects on intestinal barrier function and reducing intestinal inflammation. As knowledge continues to grow about GLP-2's effects on the gut and its mechanisms of release, the potential to use GLP-2 to improve gut function and health of food animals becomes increasingly more apparent. Thus, the purpose of this review is to summarize: (1) the current understanding of GLP-2's functions and mechanisms of action within the gut; (2) novel applications of GLP-2 (or stimulators of its release) to improve general health and production performance of food animals; and (3) recent findings, using dairy calves as a model, that suggest the therapeutic potential of GLP-2 to reduce the pathogenesis of intestinal protozoan infections.

show abstract

“…Mice lacking IEC PPARγ were generated by crossing the transgenic mouse expressing Cre recombinase under control of the villin1. Because villin 1 is found in epithelial cells of the large and small intestine (23), these mice lack PPARγ throughout the intestine. We have not investigated other areas of the bowel in our model.…”

Section: Discussionmentioning

confidence: 99%

Protection by Enteral Glutamine is Mediated by Intestinal Epithelial Cell Peroxisome Proliferator–Activated Receptor-γ During Intestinal Ischemia/Reperfusion

Peng

Ban

Wawrose

et al. 2015

Shock

View full text Add to dashboard Cite

We have demonstrated that enteral glutamine provides protection to the post ischemic gut and that PPARγ plays a role in this protection. Using Cre/lox technology to generate an intestinal-epithelial cell (IEC) specific PPARγ null mouse model, we now investigated the contribution of IEC PPARγ to glutamine’s local and distant organ protective effects. These mice exhibited absence of expression of PPARγ in the intestine but normal PPARγ expression in other tissues. Following one hour of intestinal ischemia under isoflurane anesthesia, wild type and null mice received enteral glutamine (60 mM) or vehicle followed by 6 hours of reperfusion or 7 days in survival experiments and compared to shams. Small intestine. liver, and lungs were analyzed for injury and inflammatory parameters. Glutamine provided significant protection against gut injury and inflammation with similar protection in the lung and liver. Changes in systemic TNFα reflected those seen in the injured organs. Importantly, mice lacking IEC PPARγ had worsened injury and inflammation and glutamine lost its protective effects in the gut and lung. The survival benefit found in glutamine treated wild type mice was not observed in null mice. Using an IEC-targeted loss-of-function approach, these studies provide the first in vivo confirmation in native small intestine and lung that PPARγ is responsible for the protective effects of enteral glutamine in reducing intestinal and lung injury and inflammation and improving survival. These data suggest that early enteral glutamine may be a potential therapeutic modality to reduce shock-induced gut dysfunction and subsequent distant organ injury.

show abstract

Enterocyte loss of polarity and gut wound healing rely upon the F-actin–severing function of villin

Cited by 72 publications

References 59 publications

Oral administration of Bifidobacterium bifidum G9-1 alleviates rotavirus gastroenteritis through regulation of intestinal homeostasis by inducing mucosal protective factors

Oral administration of Bifidobacterium bifidum G9-1 alleviates rotavirus gastroenteritis through regulation of intestinal homeostasis by inducing mucosal protective factors

Glucagon-like peptide 2 and its beneficial effects on gut function and health in production animals

Protection by Enteral Glutamine is Mediated by Intestinal Epithelial Cell Peroxisome Proliferator–Activated Receptor-γ During Intestinal Ischemia/Reperfusion

Contact Info

Product

Resources

About