Neonatal colonization of mice with LGG promotes intestinal development and decreases susceptibility to colitis in adulthood

Yan, Fang; Liu, L; Cao, Hailong; Moore, Daniel J.; Washington, Mary Kay; Wang, B; Peek, Richard M.; Acra, Sari; Polk, D. Brent

doi:10.1038/mi.2016.43

Cited by 86 publications

(99 citation statements)

References 63 publications

(75 reference statements)

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“…3F). Our previous studies found that no LGG was detected in feces of mice maintained in our animal facility using this qPCR method (29). In the current experiment, mice with and without colitis received the same amounts of LGG and exhibited the same amounts of LGG in feces 24 h after gavage, indicating that there is no significant difference in the amount of LGG in these two groups of mice.…”

Section: Resultssupporting

confidence: 49%

Production of a Functional Factor, p40, by Lactobacillus rhamnosus GG Is Promoted by Intestinal Epithelial Cell-Secreted Extracellular Vesicles

et al. 2019

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The symbiotic relationship between the gut microbiome and the host provides a nutrient-rich environment for gut microbes and has beneficial effects on host health. Although the composition of the gut microbiome is known to be influenced by both host genetics and environmental factors, host effects on the activities and functions of the gut microbial communities remain poorly understood. Intestinal epithelial cells exert front-line responses to gut microbes and contribute to maintaining a healthy intestinal homeostasis. Here, seeking to elucidate whether intestinal epithelial cells modulate Lactobacillus rhamnosus GG (LGG) functions, we examined the production of p40, an LGG-derived secretory protein that protects intestinal epithelial cells against inflammation. We found that growth medium conditioned with colonic epithelial cell-derived components promotes p40 protein synthesis and secretion by LGG and enhances LGG-stimulated protective responses in intestinal epithelial cells. Furthermore, when LGG was cultured with the colonic luminal contents from healthy mice, p40 production was upregulated but was attenuated with luminal contents from mice with intestinal inflammation. Importantly, the colonic epithelial cell-derived components potentiated LGG-produced p40 levels in a mouse model of colitis and enhanced LGG-mediated amelioration of intestinal inflammation in this model. Notably, we found that colonic epithelial cell-secreted extracellular vesicles participate in communicating with LGG and that heat shock protein 90 (HSP90) in these vesicles might mediate the promotion of p40 production. These results reveal a previously unrecognized mechanism by which the anti-inflammatory effect of LGG is reinforced by intestinal epithelial cells and thereby maintains intestinal health.

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Section: Resultssupporting

confidence: 49%

Production of a Functional Factor, p40, by Lactobacillus rhamnosus GG Is Promoted by Intestinal Epithelial Cell-Secreted Extracellular Vesicles

et al. 2019

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“…15 Furthermore, the neonatal colonization of mice with Lactobacillus rhamnosus GG decreases susceptibility to colitis in the adult by inducing higher levels of IgA. 87 RA, generated from dietary vitamin A, is required for a protective weaning reaction, 15 and riboflavin metabolites are required during the neonatal period to generate MAIT cells 44,45 Thus, a combination of bacteria and food supplement may be designed to favor healthy imprinting and decrease the incidence of inflammatory pathologies later in life.…”

Section: Preventing and Reversing Pathological Imprintingmentioning

confidence: 99%

Imprinting of the immune system by the microbiota early in life

2020

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The ontogeny and maturation of the immune system is modulated by the microbiota. During fetal life, the mother's microbiota produces compounds that are transferred to the fetus and offspring, and enhance the generation of innate immune cells. After birth, the colonizing microbiota induces the development of intestinal lymphoid tissues and maturation of myeloid and lymphoid cells, and imprints the immune system with a reactivity level that persists long after weaning into adulthood. When the cross-talk between host and microbiota is perturbed early in life, a pathological imprinting may develop that is characterized by excessive immune reactivity in adulthood, which translates into increased susceptibility to inflammatory pathologies. In this review, we discuss the recent data that demonstrate the existence of a time window of opportunity early in life during which mice and human have to be exposed to microbiota in order to develop a balanced immune system. We also discuss the factors involved in imprinting, such as the microbiota, immune cells and stromal cells, as well as the nature of imprinting.Mucosal Immunology (2020) 13:183-189; https://doi.

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“…Dysregulation of the Wnt signaling pathway has been shown to be closely related to multiple tumorigenesis . Previous studies have demonstrated that Lactobacillus can effectively prevent pathogen invasion and protect the integrity of the intestinal mucosal barrier . However, the probiotic role of Lactobacillus mainly focuses on the induction of a low pH value, antimicrobial peptide secretion, and tight junction maintenance …”

Section: Introductionmentioning

confidence: 99%

Lactobacillus Protects Against S. Typhimurium–Induced Intestinal Inflammation by Determining the Fate of Epithelial Proliferation and Differentiation

Xiao

Xie

et al. 2020

Molecular Nutrition Food Res

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Scope The influence of the intestinal microbiota, such as Lactobacillus, on the intestinal mucosa, particularly intestinal stem cells, remains incompletely understood. In this study, mice and intestinal organoids are used to explore the regulatory effect of Lactobacillus on the proliferation and differentiation of intestinal epithelial cells. Methods and results This study demonstrates that S. typhimurium causes intestinal epithelial damage and affected growth of intestinal organoids. S. typhimurium also colonizes the intestine and then causes pathological changes to the intestinal epithelium, intestinal inflammation, and even death. However, L. acidophilus alleviates damage to intestinal organoids, increases the survival ratio of mice infected with S. typhimurium, and reduces tumor necrosis factor‐α (TNF‐α) secretion. Moreover, L. acidophilus affects the differentiation of epithelial cells through inhibition of the excessive expansion of goblet cells and Paneth cells induced by S. typhimurium to avoid over‐exhaustion. Finally, it is also demonstrated that L. acidophilus ameliorates overactivation of Wnt/β‐catenin pathway by Salmonella, depending on the contact with toll‐like receptor 2 (TLR2), to affect the proliferation of the intestinal epithelium. Conclusions This study demonstrates that L. acidophilus protects the intestinal mucosa against S. typhimurium infection through not only the inhibition of pathogen invasion but also determination of the fate of the intestinal epithelium.

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Neonatal colonization of mice with LGG promotes intestinal development and decreases susceptibility to colitis in adulthood

Cited by 86 publications

References 63 publications

Production of a Functional Factor, p40, by Lactobacillus rhamnosus GG Is Promoted by Intestinal Epithelial Cell-Secreted Extracellular Vesicles

Production of a Functional Factor, p40, by Lactobacillus rhamnosus GG Is Promoted by Intestinal Epithelial Cell-Secreted Extracellular Vesicles

Imprinting of the immune system by the microbiota early in life

Lactobacillus Protects Against S. Typhimurium–Induced Intestinal Inflammation by Determining the Fate of Epithelial Proliferation and Differentiation

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