Purpose: A steady increase in Clostridioides difficile enteritis (CDE) has been reported recently. CDE is associated with intestinal dysbiosis, and vitamin D receptors are known to play an important role in this microbial imbalance as immunological regulators. We investigated the difference in vitamin D levels between children with CDE and those with other acute infectious enteritis. Methods: This retrospective study was conducted on children below 18 years of age who visited the Gil hospital, underwent investigation to assess vitamin D levels, and had confirmed gastrointestinal infection between January 2015 and December 2018. Patients were divided into two groups: the "CDE group" (n=18) and the "other infectious enteritis group" (n=88); their clinical characteristics, other laboratory results, and vitamin D levels were analyzed. Results: There was no difference in gender, age, and seasonal distributions between the CDE and other infectious enteritis groups. Other laboratory results were not significantly different between two groups, excluding serum albumin level (4.52±0.45 g/dL vs. 4.31±0.28 g/dL, p=0.011). The mean 25-hydroxy vitamin D level in the CDE group was higher than that in the control group (18.75±8.11 ng/mL vs. 14.50±6.79 ng/mL, p=0.021). Conclusion: Vitamin D levels in the CDE group were lower than normal but higher than the other infectious enteritis group. These results suggested that CDE has a different mechanism or susceptibility associated with vitamin D in children, and even marginal changes in vitamin D levels can act as a risk factor for infection.
Tuberculosis is a highly contagious disease caused by Mycobacterium tuberculosis. It affects about 10 million people each year and is still one of the leading causes of death worldwide. About 2 to 3 billion people (equivalent to 1 in 3 people in the world) are infected with latent tuberculosis. Moreover, as the number of multidrug-resistant, extensively drug-resistant, and totally drug-resistant strains of M. tuberculosis continues to increase, there is an urgent need to develop new anti-tuberculosis drugs that are different from existing drugs to combat antibiotic-resistant M. tuberculosis. Against this background, we aimed to develop new anti-tuberculosis drugs using probiotics. Here, we report the anti-tuberculosis effect of Pediococcus acidilactici PMC202 isolated from young radish kimchi, a traditional Korean fermented food. Under coculture conditions, PMC202 inhibited the growth of M. tuberculosis. In addition, PMC202 inhibited the growth of drug-sensitive and -resistant M. tuberculosis- infected macrophages at a concentration that did not show cytotoxicity and showed a synergistic effect with isoniazid. In a 2-week, repeated oral administration toxicity study using mice, PMC202 did not cause weight change or specific clinical symptoms. Furthermore, the results of 16S rRNA-based metagenomics analysis confirmed that dysbiosis was not induced in bronchoalveolar lavage fluid after oral administration of PMC202. The anti-tuberculosis effect of PMC202 was found to be related to the reduction of nitric oxide. Our findings indicate that PMC202 could be used as an anti-tuberculosis drug candidate with the potential to replace current chemical-based drugs. However, more extensive toxicity, mechanism of action, and animal efficacy studies with clinical trials are needed.
Kim, Hyo-Eun;Kim, Jongjin;Maeng, Sejung;Oh, Bumjo;Hwang, Ki-Tae;Kim, Bong-Soo
Journal of Microbiology and Biotechnology
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제31권12호
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pp.1643-1655
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2021
Recent studies have reported dysbiosis of the microbiome in breast tissue collected from patients with breast cancer and the association between the microbiota and disease progression. However, the role of the microbiota in breast tissue remains unclear, possibly due to the complexity of breast cancer and various factors, including racial and geographical differences, influencing microbiota in breast tissue. Here, to determine the potential role of microbiota in breast tumor tissue, we analyzed 141 tissue samples based on three different tissue types (tumor, adjacent normal, and lymph node tissues) from the same patients with breast cancer in Korea. The microbiota was not simply distinguishable based on tissue types. However, the microbiota could be divided into two cluster types, even within the same tissue type, and the clinicopathologic factors were differently correlated in the two cluster types. Risk of regional recurrence was also significantly different between the microbiota cluster types (p = 0.014). In predicted function analysis, the pentose and glucuronate interconversions were significantly different between the cluster types (q < 0.001), and Enterococcus was the main genus contributing to these differences (q < 0.01). Results showed that the microbiota of breast tissue could interact with the host and influence the risk of regional recurrence. Although further studies would be recommended to validate our results, this study could expand our understanding on the breast tissue microbiota, and the results might be applied to develop novel prediction methods and treatments for patients with breast cancer.
Despite evidence that bacteria-sensing Toll-like receptors (TLRs) are activated in salivary gland tissues of Sjogren syndrome (SS) patients, the role of oral bacteria in SS etiopathogenesis is unclear. We previously reported that two SS-associated oral bacteria, Prevotella melaninogenica (Pm) and Rothia mucilagenosa (Rm), oppositely regulate the expression of major histocompatibility complex class I (MHC I) in human salivary gland (HSG) cells. Here, we elucidated the mechanisms underlying the differential regulation of MHC I expression by these bacteria. The ability of Pm and Rm to activate TLR2, TLR4, and TLR9 was examined using TLR reporter cells. HSG cells were stimulated by the TLR ligands, Pm, and Rm. The levels of MHC I expression, bacterial invasion, and viability of HSG cells were examined by flow cytometry. The hypoxic status of HSG cells was examined using Hypoxia Green. HSG cells upregulated MHC I expression in response to TLR2, TLR4, and TLR9 activation. Both Pm and Rm activated TLR2 and TLR9 but not TLR4. Rm-induced downregulation of MHC I strongly correlated with bacterial invasion and cell death. Rm-induced cell death was not rescued by inhibitors of the diverse cell death pathways but was associated with hypoxia. In conclusion, Pm upregulated MHC I likely through TLR2 and TLR9 activation, while Rm-induced hypoxia-associated cell death and the downregulation of MHC I, despite its ability to activate TLR2 and TLR9. These findings may provide new insight into how oral dysbiosis can contribute to salivary gland tissue damage in SS.
Ruiz-Gutierrez, Alondra del Carmen;Rodriguez-Montano, Ruth;Pita-Lopez, Maria Luisa;Zamora-Perez, Ana Lourdes;Guerrero-Velazquez, Celia
Journal of Periodontal and Implant Science
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제51권4호
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pp.254-263
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2021
Purpose: Periodontitis is associated with a dysbiosis of periodontopathic bacteria, which stimulate the interleukin (IL)-23/IL-17 axis that plays an essential role in the immunopathogenesis of this disease, leading to alveolar bone destruction through receptor activator of nuclear factor κB ligand (RANKL). IL-23 receptor mRNA (IL-23R) has been identified in periodontitis, and IL-17 receptor A mRNA (IL-17RA) and its protein have not yet been evaluated in patients with periodontitis. In this study was measure IL-23R and IL-17RA in gingival tissue (GT) from patients with generalized chronic periodontitis (GCP) and generalized aggressive periodontitis (GAP) and to explore correlations with clinical parameters. Methods: We included 16 healthy subjects (HS), 18 patients with GCP, and 14 with GAP. GT samples were collected during periodontal surgery. Both IL-23R and IL-17RA were detected by enzyme-linked immunosorbent assay. Results: The results were analyzed with Mann-Whitney U test and Spearman' rank correlation coefficients using SPSS version 25.0. We found lower IL-23R levels in patients with GCP and GAP than in HS. Contrarily, we observed higher IL-17RA levels in GCP and GAP patients than in HS. Moreover, we found negative correlations between IL-23R in GT and probing depth and clinical attachment loss (CAL). Likewise, a positive correlation of IL-17RA in GT with CAL was found. Conclusions: The results of these findings suggest that the reverse behavior between IL-23R and IL-17RA in periodontitis patients may also be involved with the activation of RANKL, which promotes alveolar bone loss.
[Purpose] Recent studies have shown that COVID-19 is often associated with altered gut microbiota composition and reflects disease severity. Furthermore, various reports suggest that the interaction between COVID-19 and host-microbiota homeostasis is mediated through the modulation of microRNAs (miRNAs). Thus, in this review, we aim to summarize the association between human microbiota and miRNAs in COVID-19 pathogenesis. [Methods] We searched for the existing literature using the keywords such "COVID-19 or microbiota," "microbiota or microRNA," and "COVID-19 or probiotics" in PubMed until March 31, 2021. Subsequently, we thoroughly reviewed the articles related to microbiota and miRNAs in COVID-19 to generate a comprehensive picture depicting the association between human microbiota and microRNAs in the pathogenesis of COVID-19. [Results] There exists strong experimental evidence suggesting that the composition and diversity of human microbiota are altered in COVID-19 patients, implicating a bidirectional association between the respiratory and gastrointestinal tracts. In addition, SARS-CoV-2 encoded miRNAs and host cellular microRNAs modulated by human microbiota can interfere with viral replication and regulate host gene expression involved in the initiation and progression of COVID-19. These findings suggest that the manipulation of human microbiota with probiotics may play a significant role against SARS-CoV-2 infection by enhancing the host immune system and lowering the inflammatory status. [Conclusion] The human microbiota-miRNA axis can be used as a therapeutic approach for COVID-19. Hence, further studies are needed to investigate the exact molecular mechanisms underlying the regulation of miRNA expression in human microbiota and how these miRNA profiles mediate viral infection through host-microbe interactions.
Preterm birth (PTB) is defined as giving birth prior to the 37th week of pregnancy and is a major cause of infant mortality. Studies have indicated that the vaginal microbiota's composition and its dysbiosis, particularly during pregnancy, may play a major role in PTB. While previous research work concentrated on well-studied microorganisms such as Lactobacillus, Prevotella, Gardnerella, various other microbes, and their significance in the vaginal microbiota's stability remain unknown. Moreover, current studies have focused primarily on the relative abundances of the microbes found, without considering their interactions with other members of the vaginal microbiota. In this work, we developed a novel computational approach and performed taxonomic classification of vaginal microbiota samples stratified longitudinally (Term/PTB) to observe compositional disparities and find underexamined microbes that may be contributing to PTB. Furthermore, we carried out a correlational analysis to build a microbial co-interaction network and investigated the functional implications of the genes present in both Term and PTB samples. The co-occurrence network revealed that Lactobacillus acts in solidarity to maintain the stability of the vaginal microbiota and did not have strong co-interactions with any of the other microbes. Similarly, microbes with strong interactions with Atopobium, a well-known marker microbe of PTB, were also observed. Additionally, several genes such as PTXA, FANCM, GPX, and DUSP were found to be playing an important role in the occurrence of PTB. This study provides a novel conceptual framework revealing distinct vaginal microbiota signatures that could be potential therapeutic targets for the prevention of PTB.
Seo Gu Han;Hyuk Cheol Kwon;Do Hyun Kim;Seong Joon Hong;Sung Gu Han
한국축산식품학회지
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제43권5호
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pp.751-766
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2023
Helicobacter pylori is a bacterium that naturally thrives in acidic environments and has the potential to induce various gastrointestinal disorders in humans. The antibiotic therapy utilized for treating H. pylori can lead to undesired side effects, such as dysbiosis in the gut microbiota. The objective of our study was to explore the potential antibacterial effects of nisin and lactic acid (LA) in yogurt against H. pylori. Additionally, we investigated the anti-inflammatory effects of nisin and LA in human gastric (AGS) cells infected with H. pylori. Nisin and LA combination showed the strongest inhibitory activity, with confirmed synergy at 0.375 fractional inhibitory concentration index. Also, post-fermented yogurt with incorporation of nisin exhibited antibacterial effect against H. pylori. The combination of nisin and LA resulted in a significant reduction of mRNA levels of bacterial toxins of H. pylori and pro-inflammatory cytokines in AGS cells infected with H. pylori. Furthermore, this also increased bacterial membrane damage, which led to DNA and protein leakage in H. pylori. Overall, the combination of nisin and LA shows promise as an alternative therapy for H. pylori infection. Additionally, the incorporation of nisin into foods containing LA presents a potential application. Further studies, including animal research, are needed to validate these findings and explore clinical applications.
Background: Periodontitis is a chronic inflammatory condition associated with dysbiosis of the oral microbiota. The aim of the present clinical study was to explore the adjunctive effect of ozonized water irrigation in the circuits of ultrasonic scalers for the full-mouth decontamination of patients with periodontitis Stage I or II. Methods: The study was a randomized, single-blinded, parallel-group clinical trial. The test group (n=25) was treated with ultrasonic scalers irrigated with ozonized water, whereas the control group (n=25) received normal tap water irrigation within the ultrasonic scalers used during the professional mechanical debridement. Full mouth plaque score, bleeding score, probing pocket depth, and the gingival index were evaluated at baseline, two, and 4 weeks after treatment. The pain perceived and dental anxiety were also assessed after treatment by means of the visual analog scale (VAS). Results: All periodontal parameters resulted in significant improvement for both study groups. The effect of the treatment group on the gingival index was significant, in particular, patients in the test group experienced a greater reduction in this score. No significant differences could be observed with regards to the average probing depth, full mouth plaque index and bleeding score. Patients treated with ozonized water running in the circuits of ultrasonic scalers displayed also lower scores for pain and dental anxiety. Conclusion: The present study showed a significant clinical effect on gingival inflammation attributable to adjunctive ozone irrigation during nonsurgical periodontal therapy. Further studies, including patients with severe periodontitis and greater sample sizes, are recommended to test the clinical effect of ozonized water in the circuits of ultrasonic scalers.
Objectives: The incidence of inflammatory bowel disease (IBD) is increasing globally, and excessive added sugar consumption has been identified as one of the contributing factors. In the context of IBD, it is essential to explore functional sweeteners that can improve metabolic health and minimize the risk of IBD-related symptoms. This review article aims to shed light on the effects of natural mono- and di-saccharides as alternative sweeteners, specifically focusing on potential benefits for IBD. Methods: A comprehensive literature review was performed using PubMed and Google Scholar databases with articles published after the year 2000. The search terms 'IBD', 'added sugar', 'sweeteners', 'mono-saccharide', and 'di-saccharide' were combined to retrieve relevant articles. A total of 21 manuscripts, aligning with the objectives of the study, were selected. Papers focusing on artificial or high-intensity sweeteners were excluded to ensure relevant literature selection. Results: Multiple studies have emphasized the association between the high consumption of added sugars such as simple sugars and the increased risk of developing IBD. This is suggested to be attributed to the induction of pro-inflammatory cytokine productions and dysbiosis of the gut microbiota. Consequently, there is a growing demand for safe and functional sweeteners, in particular mono- and di-saccharides, that can serve as alternatives for IBD patients. Those functional sweeteners regulate inflammation, oxidative stress, and Intestinal barrier protection, and restore microbiome profiles in various IBD models including cells, animals, and humans. Conclusions: Understanding these mechanisms resolves the link between how sugar consumption and IBD, and highlights the beneficial effects of natural alternative sweeteners on IBD when they were administered by itself or as a replacement for simple sugar. Further, exploration of this relationship leads us to recognize the necessity of natural alternative sweeteners in dietary planning. This knowledge could potentially lead to more effective dietary strategies for individuals with IBD.
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