• Journal of Ginseng Research
• /
• v.47 no.2
• /
• pp.255-264
• /
• 2023

Background: Red ginseng (RG) alleviates psychiatric disorders. Fermented red ginseng (fRG) alleviates stress-induced gut inflammation. Gut dysbiosis causes psychiatric disorders with gut inflammation. To understand the gut microbiota-mediated action mechanism of RG and fRG against anxiety/depression (AD), we investigated the effects of RG, fRG, ginsenoside Rd, and 20(S)-β-D-glucopyranosyl protopanaxadiol (CK) on gut microbiota dysbiosis-induced AD and colitis in mice. Methods: Mice with AD and colitis were prepared by exposing to immobilization stress (IS) or transplanting the feces of patients with ulcerative colitis and depression (UCDF). AD-like behaviors were measured in the elevated plus maze, light/dark transition, forced swimming, and tail suspension tests. Results: Oral gavage of UCDF increased AD-like behaviors and induced neuroinflammation, gastrointestinal inflammation, and gut microbiota fluctuation in mice. Oral administration of fRG or RG treatment reduced UCDF-induced AD-like behaviors, hippocampal and hypothalamic IL-6 expression, and blood corticosterone level, whereas UCDF-suppressed hippocampal BDNF⁺NeuN⁺ cell population and dopamine and hypothalamic serotonin levels increased. Furthermore, their treatments suppressed UCDF-induced colonic inflammation and partially restored UCDF-induced gut microbiota fluctuation. Oral administration of fRG, RG, Rd, or CK also decreased IS-induced AD-like behaviors, blood IL-6 and corticosterone and colonic IL-6 and TNF-α levels, and gut dysbiosis, while IS-suppressed hypothalamic dopamine and serotonin levels increased. Conclusion: Oral gavage of UCDF caused AD, neuroinflammation, and gastrointestinal inflammation in mice. fRG mitigated AD and colitis in UCDF-exposed mice by the regulation of the microbiota-gut-brain axis and IS-exposed mice by the regulation of the hypothalamic-pituitary-adrenal axis.

• BMB Reports
• /
• v.49 no.5
• /
• pp.263-269
• /
• 2016

The intestine represents the largest and most elaborate immune system organ, in which dynamic and reciprocal interplay among numerous immune and epithelial cells, commensal microbiota, and external antigens contributes to establishing both homeostatic and pathologic conditions. The mechanisms that sustain gut homeostasis are pivotal in maintaining gut health in the harsh environment of the gut lumen. Intestinal epithelial cells are critical players in creating the mucosal platform for interplay between host immune cells and luminal stress inducers. Thus, knowledge of the epithelial interface between immune cells and the luminal environment is a prerequisite for a better understanding of gut homeostasis and pathophysiologies such as inflammation. In this review, we explore the importance of the epithelium in limiting or promoting gut inflammation (e.g., inflammatory bowel disease). We also introduce recent findings on how small RNAs such as microRNAs orchestrate pathophysiologic gene regulation.

• Journal of the Korean Wood Science and Technology
• /
• v.51 no.5
• /
• pp.358-380
• /
• 2023

The intestinal microbiota plays a crucial role in determining human health, rendering it a major focus of scientific investigation. Rather than eliminating all microbes, promoting the proliferation of beneficial microorganisms within the gut has been recognized as a more effective approach to improving health. Unfavorable conditions potentially alter gut microbial populations, including a reduction in microbial diversity. However, intentionally enhancing the abundance of beneficial gut microbes can restore a state of optimal health. Polysaccharides are widely acknowledged for their potential to improve the gut microbiota. This review emphasizes the findings of recent studies examining the effects of forest product-derived polysaccharides on enhancing the gut microbiota and alleviating inflammation, diabetes symptoms, and obesity. The findings of several studies reviewed in this paper strongly suggest that forest products serve as an excellent dietary source for improving the gut microbiota and potentially offer valuable dietary interventions for chronic health problems, such as inflammation, diabetes, and obesity.

• Nutrition Research and Practice
• /
• v.15 no.4
• /
• pp.411-430
• /
• 2021

Irritable bowel syndrome (IBS) is a frequently diagnosed gastrointestinal (GI) disorder characterized by recurrent abdominal pain, bloating, and changes in the stool form or frequency without any structural changes and overt inflammation. It is not a life-threatening condition but causes a considerable level of discomfort and distress. Among the many pathophysiologic factors, such as altered GI motility, visceral hypersensitivity, and low-grade mucosal inflammation, as well as other immunologic, psychologic, and genetic factors, gut microbiota imbalance (dysbiosis), which is frequently found in IBS, has been highlighted as an etiology of IBS. Dysbiosis may affect gut mucosal homeostasis, immune function, metabolic regulation, and even visceral motor function. As diet is shown to play a fundamental role in the gut microbiota profile, this review discusses the influence of diet on IBS occurring through the modulation of gut microbiota. Based on previous studies, it appears that dietary modulation of the gut microbiota may be effective for the alleviation of IBS symptoms and, also an effective IBS management strategy based on the underlying mechanism; especially because, IBS currently has no specific treatment owing to its uncertain etiology.

• Journal of Microbiology and Biotechnology
• /
• v.33 no.9
• /
• pp.1111-1118
• /
• 2023

As a long-term condition that affects the airways and lungs, chronic obstructive pulmonary disease (COPD) is characterized by inflammation, emphysema, breathlessness, chronic cough, and sputum production. Currently, the bronchodilators and anti-inflammatory drugs prescribed for COPD are mostly off-target, warranting new disease management strategies. Accumulating research has revealed the gut-lung axis to be a bidirectional communication system. Cigarette smoke, a major exacerbating factor in COPD and lung inflammation, affects gut microbiota composition and diversity, causing gut microbiota dysbiosis, a condition that has recently been described in COPD patients and animal models. For this review, we focused on the gut-lung axis, which is influenced by gut microbial metabolites, bacterial translocation, and immune cell modulation. Further, we have summarized the findings of preclinical and clinical studies on the association between gut microbiota and COPD to provide a basis for using gut microbiota in therapeutic strategies against COPD. Our review also proposes that further research on probiotics, prebiotics, short-chain fatty acids, and fecal microbiota transplantation could assist therapeutic approaches targeting the gut microbiota to alleviate COPD.

• Animal Bioscience
• /
• v.34 no.7
• /
• pp.1221-1234
• /
• 2021

Objective: Weaning is an important stage in the life of young mammals, which is associated with intestinal inflammation, gut microbiota disorders, and even death. β-Carotene displays anti-inflammatory and antioxidant activities, which can prevent the development of inflammatory diseases. However, whether β-carotene can affect intestinal microbiota remains unclear. Methods: Twenty-four piglets were distributed into four groups: the normal suckling group (Con), the weaning group (WG), the weaning+β-carotene (40 mg/kg) group (LCBC), and the weaning+β-carotene (80 mg/kg) group (HCBC). The serum, jejunum, colon, and faeces were collected separately from each group. The effects of β-carotene on the phenotype, overall structure, and composition of gut microbiota were assessed in weaning piglets. Results: The results showed that β-carotene improved the growth performance, intestinal morphology and relieved inflammation. Furthermore, β-carotene significantly decreased the species from phyla Bacteroidetes and the genus Prevotella, and Blautia, and increased the species from the phyla Firmicutes and the genera p-75-a5, and Parabacteroides compared to the WG group. Spearman's correlation analysis showed that Prevotella and Blautia were positively correlated, and Parabacteroides and Synergistes were negatively correlated with the levels of interleukin-1β (IL-1β), IL-6, and tumour necrosis factor-α (TNF-α), while p-75-a5 showed negative correlation with IL-6 in serum samples from piglets. Conclusion: These findings indicate that β-carotene could alleviate weaning-induced intestinal inflammation by modulating gut microbiota in piglets. Prevotella may be a potential target of β-carotene in alleviating the weaning-induced intestinal inflammation in piglets.

• Journal of Digestive Cancer Research
• /
• v.10 no.1
• /
• pp.31-38
• /
• 2022

Ulcerative colitis (UC) exhibits chronic intestinal inflammatory conditions with cycles of relapse and remission. The incidence is rapidly growing in Asian countries including South Korea possibly due to changes in lifestyles. Although the etiology of inflammatory bowel disease is inconclusive, gut microbiota composition is considered a critical factor involved in the pathogenesis of UC. The overgrowth of pathogenic bacteria evokes hyper-immune responses in gut epithelium causing tissue inflammation and damage. Also, failure to regulate gut epithelium integrity due to chronic inflammation and mucus depletion accelerates bacterial translocation aggravating immune dysregulation. Gut microbiota composition responds to the diet in a very rapid manner. Epidemiological studies have indicated that the risk of UC is associated with low plant foods/high animal foods consumption. Several bacterial strains consistently found depleted in UC patients use plant food-originated dietary fiber producing short chain fatty acids to maintain epithelial integrity. These bacteria also use mucus layer mucin to keep gut microbiota diversity. These studies partly explain the association between dietary modification of gut microbiota in UC development. Further human intervention trials are required to allow the use of specific bacterial strains in the management of UC.

• Journal of Microbiology and Biotechnology
• /
• v.29 no.1
• /
• pp.30-36
• /
• 2019

Numerous studies have reported that enteric neurons involved in controlling neurotransmitter secretion and motility in the gut critically contribute to the progression of gut inflammation. Clostridium difficile toxins, which cause severe colonic inflammation, are also known to affect enteric neurons. Our previous study showed that C. difficile toxin A directly induces neural cell toxicities, such as viability loss and apoptosis. In the current study, we attempted to identify a potent inhibitor of toxin A-induced neural cell toxicity that may aid in managing toxin A-induced gut inflammation. In our recent study, we found that the Korea dung beetle-derived antimicrobial peptide CopA3 completely blocked neural cell apoptosis caused by okadaic acid or 6-OHDA. Here, we examined whether the antimicrobial peptide CopA3 inhibited toxin A-induced neural cell damage. In neuroblastoma SH-SY5Y cells, CopA3 treatment protected against both apoptosis and viability loss caused by toxin A. CopA3 also completely inhibited activation of the pro-apoptotic factor, caspase-3. Additionally, CopA3 rescued toxin A-induced downregulation of neural cell proliferation. However, CopA3 had no effect on signaling through ROS/p38 $MAPK/p27^{kip1}$, suggesting that CopA3 inhibits toxin A-induced neural cell toxicity independent of this well-characterized toxin A pathway. Our data further suggest that ability of CopA3 to rescue toxin A-induced neural cell damage may also ameliorate the gut inflammation caused by toxin A.

• Pediatric Gastroenterology, Hepatology & Nutrition
• /
• v.27 no.3
• /
• pp.137-145
• /
• 2024

Stunting, a condition characterized by impaired growth and development in children, remains a major public health concern worldwide. Over the past decade, emerging evidence has shed light on the potential role of gut microbiota modulation in stunting. Gut microbiota dysbiosis has been linked to impaired nutrient absorption, chronic inflammation, altered short-chain fatty acid production, and perturbed hormonal and signaling pathways, all of which may hinder optimal growth in children. This review aims to provide a comprehensive analysis of existing research exploring the bidirectional relationship between stunting and the gut microbiota. Although stunting can alter the gut microbial community, microbiota dysbiosis may exacerbate it, forming a vicious cycle that sustains the condition. The need for effective preventive and therapeutic strategies targeting the gut microbiota to combat stunting is also discussed. Nutritional interventions, probiotics, and prebiotics are among the most promising approaches to modulate the gut microbiota and potentially ameliorate stunting outcomes. Ultimately, a better understanding of the gut microbiota-stunting nexus is vital for guiding evidence-based interventions that can improve the growth and development trajectory of children worldwide, making substantial strides toward reducing the burden of stunting in vulnerable populations.

• Journal of Microbiology and Biotechnology
• /
• v.27 no.6
• /
• pp.1163-1170
• /
• 2017

Clostridium difficile releases two exotoxins, toxin A and toxin B, which disrupt the epithelial cell barrier in the gut to increase mucosal permeability and trigger inflammation with severe diarrhea. Many studies have suggested that enteric nerves are also directly involved in the progression of this toxin-mediated inflammation and diarrhea. C. difficile toxin A is known to enhance neurotransmitter secretion, increase gut motility, and suppress sympathetic neurotransmission in the guinea pig colitis model. Although previous studies have examined the pathophysiological role of enteric nerves in gut inflammation, the direct effect of toxins on neuronal cells and the molecular mechanisms underlying toxin-induced neuronal stress remained to be unveiled. Here, we examined the toxicity of C. difficile toxin A against neuronal cells (SH-SY5Y). We found that toxin A treatment time- and dose-dependently decreased cell viability and triggered apoptosis accompanied by caspase-3 activation in this cell line. These effects were found to depend on the up-regulation of reactive oxygen species (ROS) and the subsequent activation of p38 MAPK and induction of $p21^{Cip1/Waf1}$. Moreover, the N-acetyl-$\text\tiny L$-cysteine (NAC)-induced down-regulation of ROS could recover the viability loss and apoptosis of toxin A-treated neuronal cells. These results collectively suggest that C. difficile toxin A is toxic for neuronal cells, and that this is associated with rapid ROS generation and subsequent p38 MAPK activation and $p21^{Cip1/Waf1}$ up-regulation. Moreover, our data suggest that NAC could inhibit the toxicity of C. difficile toxin A toward enteric neurons.