Polyphosphate, Derived from Lactobacillus brevis, Modulates the Intestinal Microbiome and Attenuates Acute Pancreatitis

Takauji, Shuhei; Konishi, Hiroaki; Fujiya, Mikihiro; Ueno, Nobuhiro; Tanaka, Hiroki; Sato, Hiroki; Isozaki, Shotaro; Moriichi, Kentaro; Mizukami, Yusuke; Okumura, Toshikatsu

doi:10.1007/s10620-020-06747-9

Cited by 20 publications

(18 citation statements)

References 43 publications

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“…In an in vitro trial, AR281 suppressed the differentiation of OCPs into osteoclasts via the TRAF6//NF-κB/NFATc1 pathway. Several strains of L. brevis have anti-inflammatory properties [36][37][38], but studies on the effects of L. brevis on ovx-induced osteoporosis are still limited.…”

Section: Discussionmentioning

confidence: 99%

Anti-Osteoporotic Effect of Lactobacillus brevis AR281 in an Ovariectomized Mouse Model Mediated by Inhibition of Osteoclast Differentiation

Hang

Sun

et al. 2022

Biology

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Osteoporosis is a global disease characterized by weakened bone microarchitecture, leading to osteoporotic fractures. Estrogen replacement therapy is the traditional treatment for osteoporosis but carries with it an increased risk of cardiac events. In search of a safe and effective treatment, we used Lactobacillus brevis AR281, which has anti-inflammatory properties, to conduct a 7-week experiment, investigating its inhibitory effects on osteoporosis in an ovariectomized (ovx) mouse model. The results demonstrated that AR281 significantly improved bone microarchitecture and biomechanical strength in ovx mice by attenuating bone resorption. AR281 significantly decreased the critical osteoclast activator, the ratio of the receptor activator for nuclear factor kappa B (NF-κB) ligand (RANKL) to osteoprotegerin, and pro-inflammatory osteoclastogenic mediators, such as IL-1, IL-6, and IL-17, which can increase the RANKL expression. Moreover, AR281 modulated intestinal microbiota in ovx mice increased the abundance of Akkermansia, which is responsible for the improvement of gut epithelial barrier integrity. In an in vitro trial, AR281 suppressed the number of osteoclasts differentiated from the osteoclast precursor RAW264.7 cells caused by RANKL through the tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6)/NF-κB/nuclear factor of activated T cells c1 (NFATc1) pathway. Therefore, AR281 may be a natural alternative for combating osteoporosis.

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Section: Discussionmentioning

confidence: 99%

Anti-Osteoporotic Effect of Lactobacillus brevis AR281 in an Ovariectomized Mouse Model Mediated by Inhibition of Osteoclast Differentiation

Hang

Sun

et al. 2022

Biology

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“…Jakub W. R. et al showed that probiotics can reverse the gut barrier failure in the late phase of AP, but only if administered before the onset of AP [28]. Similarly, Shuhei T. et al documented in an animal model that the oral administration of Lactobacillus brevis-derived polyphosphate for 24 days before the induction of AP by caerulein, attenuated inflammation in mice [29]. K. Minaga et al attributed the preventive effect of polyphosphate on AP to the suppression of pancreatic chemokine production, particularly C-C motif chemokine ligand 2 (CCL2), but also to the increased expression of the tight junction (TJ) proteins zonula occludens (ZO)-1 and occludin in the colon, a part of the intestinal TJ that regulates paracellular permeability [30].…”

Section: Acute Pancreatitismentioning

confidence: 98%

Microbiota in Pancreatic Diseases: A Review of the Literature

Schepis

Lucia

Nista

et al. 2021

JCM

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The gut microbiota is a critical element in the balance between human health and disease. Its impairment, defined as dysbiosis, is associated with gastroenterological and systemic diseases. Pancreatic secretions are involved in the composition and changes of the gut microbiota, and the gut microbiota may colonize the pancreatic parenchyma and be associated with the occurrence of diseases. The gut microbiota and the pancreas influence each other, resulting in a “gut microbiota-pancreas axis”. Moreover, the gut microbiota may be involved in pancreatic diseases, both through direct bacterial colonization and an indirect effect of small molecules and toxins derived from dysbiosis. Pancreatic diseases such as acute pancreatitis, chronic pancreatitis, autoimmune pancreatitis, and pancreatic cancer are common gastroenterological diseases associated with high morbidity and mortality. The involvement of the microbiota in pancreatic diseases is increasingly recognized. Therefore, modifying the intestinal bacterial flora could have important therapeutic implications on these pathologies. The aim of this study is to review the literature to evaluate the alterations of the gut microbiota in pancreatic diseases, and the role of the microbiota in the treatment of these diseases.

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“…Evidence is emerging that postbiotics have multiple health benefits and are considered to be the next horizon in microbial therapeutics and functional foods ( 224 ). In a cerulein-induced AP mouse, oral administration of probiotic Lactobacillus brevis SBL88-derived polyphosphate for 24 days prior to induction of AP mitigated the severity of AP, which was not only associated with modulation of the intestinal microbiome but also enhancement of the gut barrier integrity ( 225 ). A postbiotic, heat-killed Lactococcus chungangensis CAU 1447, could facilitate wound healing in type I diabetic mice; however, the authors did not investigate its effect on T1DM ( 226 ).…”

Section: Gut Microbiome-target Therapiesmentioning

confidence: 99%

Gut Dysbiosis in Pancreatic Diseases: A Causative Factor and a Novel Therapeutic Target

et al. 2022

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Pancreatic-related disorders such as pancreatitis, pancreatic cancer, and type 1 diabetes mellitus (T1DM) impose a substantial challenge to human health and wellbeing. Even though our understanding of the initiation and progression of pancreatic diseases has broadened over time, no effective therapeutics is yet available for these disorders. Mounting evidence suggests that gut dysbiosis is closely related to human health and disease, and pancreatic diseases are no exception. Now much effort is under way to explore the correlation and eventually potential causation between the gut microbiome and the course of pancreatic diseases, as well as to develop novel preventive and/or therapeutic strategies of targeted microbiome modulation by probiotics, prebiotics, synbiotics, postbiotics, and fecal microbiota transplantation (FMT) for these multifactorial disorders. Attempts to dissect the intestinal microbial landscape and its metabolic profile might enable deep insight into a holistic picture of these complex conditions. This article aims to review the subtle yet intimate nexus loop between the gut microbiome and pancreatic diseases, with a particular focus on current evidence supporting the feasibility of preventing and controlling pancreatic diseases via microbiome-based therapeutics and therapies.

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Polyphosphate, Derived from Lactobacillus brevis, Modulates the Intestinal Microbiome and Attenuates Acute Pancreatitis

Cited by 20 publications

References 43 publications

Anti-Osteoporotic Effect of Lactobacillus brevis AR281 in an Ovariectomized Mouse Model Mediated by Inhibition of Osteoclast Differentiation

Anti-Osteoporotic Effect of Lactobacillus brevis AR281 in an Ovariectomized Mouse Model Mediated by Inhibition of Osteoclast Differentiation

Microbiota in Pancreatic Diseases: A Review of the Literature

Gut Dysbiosis in Pancreatic Diseases: A Causative Factor and a Novel Therapeutic Target

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