Journal of Microbiology

Journal Article

Lactobacillus gasseri BNR17 and Limosilactobacillus fermentum ABF21069 Ameliorate High Sucrose-Induced Obesity and Fatty Liver via Exopolysaccharide Production and β-oxidation.: Yu Mi Jo, Yoon Ji Son, Seul-Ah Kim, Gyu Min Lee, Chang Won Ahn, Han-Oh Park, Ji-Hyun Yun; J. Microbiol. 2024;62(10):907-918. Published online October 17, 2024; DOI: https://doi.org/10.1007/s12275-024-00173-6

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Abstract: Obesity and metabolic dysfunction-associated fatty liver disease (MAFLD) are prevalent metabolic disorders with substantial global health implications that are often inadequately addressed by current treatments and may have side effects. Probiotics have emerged as promising therapeutic agents owing to their beneficial effects on gut health and metabolism. This study investigated the synergistic effects of a probiotic combination of BNR17 and ABF21069 on obesity and MAFLD in C57BL/6 mice fed a high-sucrose diet. The probiotic combination significantly reduced body weight and fat accumulation compared with the high-sucrose diet. It also alleviated elevated serum leptin levels induced by a high-sucrose diet. Histological analysis revealed a significant reduction in white adipose tissue and fatty liver in the mice treated with the probiotic combination. Furthermore, increased expression of genes related to β-oxidation, thermogenesis, and lipolysis suggested enhanced metabolic activity. The probiotic groups, particularly the BNR17 group, showed an increase in fecal exopolysaccharides, along with a tendency toward a lower expression of intestinal sugar transport genes, indicating reduced sugar absorption. Additionally, inflammatory markers in the liver tissue exhibited lower expression in the ABF21069 group than in the HSD group. Despite each strain in the combination group having distinct characteristics and functions, their combined effect demonstrated synergy in mitigating obesity and MAFLD, likely through the modulation of fecal exopolysaccharides content and improvement in lipid metabolism. These findings underscore the potential of probiotic supplementation as a promising assistant therapy for managing obesity and MAFLD and provide valuable insights into its therapeutic mechanisms in metabolic disorders.

Review

Metabolic Interaction Between Host and the Gut Microbiota During High‑Fat Diet‑Induced Colorectal Cancer: Chaeeun Lee, Seungrin Lee, Woongjae Yoo; J. Microbiol. 2024;62(3):153-165. Published online April 16, 2024; DOI: https://doi.org/10.1007/s12275-024-00123-2

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Abstract: Colorectal cancer (CRC) is the second-highest cause of cancer-associated mortality among both men and women worldwide. One of the risk factors for CRC is obesity, which is correlated with a high-fat diet prevalent in Western dietary habits. The association between an obesogenic high-fat diet and CRC has been established for several decades; however, the mechanisms by which a high-fat diet increases the risk of CRC remain unclear. Recent studies indicate that gut microbiota strongly infuence the pathogenesis of both high-fat diet-induced obesity and CRC. The gut microbiota is composed of hundreds of bacterial species, some of which are implicated in CRC. In particular, the expansion of facultative anaerobic Enterobacteriaceae, which is considered a microbial signature of intestinal microbiota functional imbalance (dysbiosis), is associated with both high-fat diet-induced obesity and CRC. Here, we review the interaction between the gut microbiome and its metabolic byproducts in the context of colorectal cancer (CRC) during high-fat diet-induced obesity. In addition, we will cover how a high-fat diet can drive the expansion of genotoxin-producing Escherichia coli by altering intestinal epithelial cell metabolism during gut infammation conditions.

Journal Articles

The efficacy of a 2,4-diaminoquinazoline compound as an intranasal vaccine adjuvant to protect against influenza A virus infection in vivo: Kyungseob Noh , Eun Ju Jeong , Timothy An , Jin Soo Shin , Hyejin Kim , Soo Bong Han , Meehyein Kim; J. Microbiol. 2022;60(5):550-559. Published online April 18, 2022; DOI: https://doi.org/10.1007/s12275-022-1661-7

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4 Citations

Abstract: Adjuvants are substances added to vaccines to enhance antigen- specific immune responses or to protect antigens from rapid elimination. As pattern recognition receptors, Toll-like receptors 7 (TLR7) and 8 (TLR8) activate the innate immune system by sensing endosomal single-stranded RNA of RNA viruses. Here, we investigated if a 2,4-diaminoquinazolinebased TLR7/8 agonist, (S)-3-((2-amino-8-fluoroquinazolin- 4-yl)amino)hexan-1-ol (named compound 31), could be used as an adjuvant to enhance the serological and mucosal immunity of an inactivated influenza A virus vaccine. The compound induced the production of proinflammatory cytokines in macrophages. In a dose-response analysis, intranasal administration of 1 μg compound 31 together with an inactivated vaccine (0.5 μg) to mice not only enhanced virus-specific IgG and IgA production but also neutralized influenza A virus with statistical significance. Notably, in a virus-challenge model, the combination of the vaccine and compound 31 alleviated viral infection-mediated loss of body weight and increased survival rates by 40% compared with vaccine only-treated mice. We suggest that compound 31 is a promising lead compound for developing mucosal vaccine adjuvants to protect against respiratory RNA viruses such as influenza viruses and potentially coronaviruses.

The type II histidine triad protein HtpsC facilitates invasion of epithelial cells by highly virulent Streptococcus suis serotype 2: Yunjun Lu , Shu Li , Xiaodong Shen , Yan Zhao , Dongming Zhou , Dan Hu , Xushen Cai , Lixia Lu , Xiaohui Xiong , Ming Li , Min Cao; J. Microbiol. 2021;59(10):949-957. Published online September 7, 2021; DOI: https://doi.org/10.1007/s12275-021-1129-1

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Abstract: Streptococcus suis serotype 2 (S. suis 2) is an important zoonotic pathogen that presents a significant threat both to pigs and to workers in the pork industry. The initial steps of S. suis 2 pathogenesis are unclear. In this study, we found that the type II histidine triad protein HtpsC from the highly virulent Chinese isolate 05ZYH33 is structurally similar to internalin A (InlA) from Listeria monocytogenes, which plays an important role in mediating listerial invasion of epithelial cells. To determine if HtpsC and InlA function similarly, an isogenic htpsC mutant (ΔhtpsC) was generated in S. suis by homologous recombination. The htpsC deletion strain exhibited a diminished ability to adhere to and invade epithelial cells from different sources. Double immunofluorescence microscopy also revealed reduced survival of the ΔhtpsC mutant after cocultivation with epithelium. Adhesion to epithelium and invasion by the wild type strain was inhibited by a monoclonal antibody against E-cadherin. In contrast, the htpsC-deficient mutant was unaffected by the same treatment, suggesting that E-cadherin is the host-cell receptor that interacts with HtpsC and facilitates bacterial internalization. Based on these results, we propose that HtpsC is involved in the process by which S. suis 2 penetrates host epithelial cells, and that this protein is an important virulence factor associated with cell adhesion and invasion.

Review

Rediscovery of antimicrobial peptides as therapeutic agents: Minkyung Ryu , Jaeyeong Park , Ji-Hyun Yeom , Minju Joo , Kangseok Lee; J. Microbiol. 2021;59(2):113-123. Published online February 1, 2021; DOI: https://doi.org/10.1007/s12275-021-0649-z

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22 Citations

Abstract: In recent years, the occurrence of antibiotic-resistant pathogens is increasing rapidly. There is growing concern as the development of antibiotics is slower than the increase in the resistance of pathogenic bacteria. Antimicrobial peptides (AMPs) are promising alternatives to antibiotics. Despite their name, which implies their antimicrobial activity, AMPs have recently been rediscovered as compounds having antifungal, antiviral, anticancer, antioxidant, and insecticidal effects. Moreover, many AMPs are relatively safe from toxic side effects and the generation of resistant microorganisms due to their target specificity and complexity of the mechanisms underlying their action. In this review, we summarize the history, classification, and mechanisms of action of AMPs, and provide descriptions of AMPs undergoing clinical trials. We also discuss the obstacles associated with the development of AMPs as therapeutic agents and recent strategies formulated to circumvent these obstacles.

Journal Articles

WasC, a WASP family protein, is involved in cell adhesion and migration through regulation of F-actin polymerization in Dictyostelium: Pyeonghwa Jeon , Taeck Joong Jeon; J. Microbiol. 2020;58(8):696-702. Published online June 10, 2020; DOI: https://doi.org/10.1007/s12275-020-0138-9

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5 Citations

Abstract: The actin cytoskeleton is involved in the regulation of cell morphology and migration. Wiskott-Aldrich Syndrome proteins (WASPs) play an important role in controlling actin polymerization by activating the Arp2/3 complex. The present study investigated the roles of WasC, one of the 3 WASPs in Dictyostelium, in cellular processes. Cells lacking WasC displayed strong cell adhesion and approximately 1.5-fold increase in F-actin levels as compared to the wild-type cells. Loss of wasC caused defects in phagocytosis and decreased the migration speed in chemoattractant-mediated cell migration but did not affect directionality. WasC was localized to the protruding region in migrating cells and, transiently and rapidly translocated to the cell cortex in response to chemoattractant stimulation, in an F-actin dependent manner. Our
results
suggest that WasC is involved in cell adhesion and migration by regulating F-actin polymerization at the leading edge of migrating cells, probably as a negative regulator. The increased strength of adhesion in wasC null cells is likely to decrease the migration speed but not the directionality.

Diet-induced obese mice exhibit altered immune responses to early Salmonella Typhimurium oral infection: Ricardo Ernesto Ramírez-Orozco , Elena Franco Robles , Victoriano Pérez Vázquez , Joel Ramírez Emiliano , Marco Antonio Hernández Luna , Sergio López Briones; J. Microbiol. 2018;56(9):673-682. Published online August 23, 2018; DOI: https://doi.org/10.1007/s12275-018-8083-6

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9 Citations

Abstract: Obesity is a chronic disease associated with different metabolic diseases as well as alterations in immune cell function. It is characterized by a chronic systemic low grade inflammation. There are several studies demonstrating the influence of obesity on the impaired immune response to infection. However, it is not completely clear whether the obese environment influences the development or maintenance of the immune response against infections. The aim of this study was to determine how obesity induced by a high-fat diet affects the immune response to an early oral Salmonella infection. Four groups of mice were kept in separate cages. Two of these designated as controls, fed with a normal diet; whereas other two groups were fed with a high fat diet for 10 weeks. Some mice were used for Salmonella oral infection. After 7 days of oral infection with S. Thypimurium the proportions of spleen cell subsets expressing activation markers in normal diet and HFD obese mice were stained with monoclonal antibodies and analyzed by flow cytometry. Also, mRNA levels of different cytokines were quantified by RT-PCR. It was found that obesity affects the function of the immune system against an early oral Salmonella infection, decreasing NK cells, altering the expression of activation molecules as well as cytokines mRNA levels. Interestingly, the expression some activation molecules on T lymphocytes was reestablished after Salmonella infection, but not the CD25 expression. Immune alterations could lead to immunosuppression or increased susceptibility to infections in HFD obese mice.

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