Journal of microbiology and biotechnology最新文献

This study was performed to investigate the use of plant-based lactic acid bacteria (LAB) to reduce microbiological hazards in kimchi. Cell-free supernatants (CFS) from four LAB strains isolated from kimchi were tested for antimicrobial activity against five foodborne pathogens and two soft-rot pathogens. Each CFS showed antimicrobial activity against both foodborne and soft-rot pathogens. Washing salted kimchi cabbages inoculated with B. cereus with 5% CFS inhibited B. cereus to a greater extent than NaClO. The CFS from WiKim 83 and WiKim 87 exhibits inhibition rates of 25.09% and 24.21%, respectively, compared to the 19.19% rate of NaClO. Additionally, the CFS from WiKim 116 and WiKim 117 showed inhibition rates of 18.74% and 20.03%, respectively. Direct treatment of kimchi cabbage with soft-rot pathogens and CFS for five days inhibited the pathogens with similar efficacy to that of NaClO. To elucidate the antimicrobial activity mechanisms, pH neutralization, heat treatment, and organic acid analyses were performed. pH neutralization reduced the antimicrobial activity, whereas heat treatment did not, indicating that lactic, acetic, citric, and phenyllactic acids contribute to the thermal stability and antimicrobial properties of CFS. This study suggests that the four kimchi-derived LAB, which maintain a low pH through organic acid production, could be viable food preservatives capable of reducing biological hazards in kimchi.

Chronic exposure to particulate matter (PM)_2.5 causes brain damage through intestinal imbalance. This study was estimated to confirm the regulatory activity of green tea against chronic PM_2.5 exposure-induced abnormal gut-brain axis (GBA) in BALB/c mice. The green tea, as an aqueous extract of matcha (EM), ameliorated the colon length, short chain fatty acid contents, antioxidant biomarkers, myeloperoxidase (MPO) activity, and serum inflammatory cytokines. EM regulated the gut microbiota related to tryptophan intake and hormone metabolism. EM showed regulatory effect of intestinal tight junction (TJ) protein, inflammatory response, and apoptotic biomarkers. In addition, EM improved PM_2.5-induced tryptophan-related hormonal metabolic dysfunction in intestinal tissue and serum. Through the ameliorating effect on GBA function, the consumption of EM presented the protective effect against inflammatory effect, apoptosis, synaptic damage, and hormonal activity in cerebral tissue, and suppressed abnormal change of brain lipid metabolites. In particular, EM intake showed relatively excellent improvement effects on indicators including Bacteroides, Ruminococcus, Murinobaculaceae, Allopreyotella, cyclooxygenase-2 (COX-2), acetylcholinesterase (AChE), 11,12-dihydroxyeicosatrienoic acid (DHET), and intestinal acetate from the PM group. These findings indicate that the dietary intake of EM might provide a regulatory effect against PM_2.5-exposed GBA dysfunction via the intestinal microbiota and hormonal changes.

The microbial community inhabiting the human gut resembles a bustling metropolis, wherein beneficial bacteria play pivotal roles in regulating our bodily functions. These microorganisms adeptly break down resilient dietary fibers to fuel our energy, synthesize essential vitamins crucial for our well-being, and maintain the delicate balance of our immune system. Recent research indicates a potential correlation between alterations in the composition and activities of these gut microbes and the development of coronary artery disease (CAD). Consequently, scientists are delving into the intriguing realm of manipulating these gut inhabitants to potentially mitigate disease risks. Various promising strategies have emerged in this endeavor. Studies have evidenced that probiotics can mitigate inflammation and enhance the endothelial health of our blood vessels. Notably, strains such as Lactobacilli and Bifidobacteria have garnered substantial attention in both laboratory settings and clinical trials. Conversely, prebiotics exhibit anti-inflammatory properties and hold potential in managing conditions like hypertension and hypercholesterolemia. Synbiotics, which synergistically combine probiotics and prebiotics, show promise in regulating glucose metabolism and abnormal lipid profiles. However, uncertainties persist regarding postbiotics, while antibiotics are deemed unsuitable due to their potential adverse effects. On the other hand, TMAO blockers, such as 3,3-dimethyl-1-butanol, demonstrate encouraging outcomes in laboratory experiments owing to their anti-inflammatory and tissue-protective properties. Moreover, fecal transplantation, despite yielding mixed results, warrants further exploration and refinement. In this comprehensive review, we delve into the intricate interplay between the gut microbiota and CAD, shedding light on the multifaceted approaches researchers are employing to leverage this understanding for therapeutic advancements.

The scientific community actively pursuits novel compounds with biological activities. In this context, our study utilized the predicted data mining approach (PDMA), which can efficiently screen out biotransformable precursor candidates to produce new bioactive compounds. The PDMA was applied to Bacillus megaterium tyrosinase (BmTYR) to form new bioactive hydroxyl compounds from isoxsuprine hydrochloride (isoxsuprine). The results show that isoxsuprine could be biotransformed by BmTYR to form a new compound, 3''-hydroxyisoxsuprine. 3''-Hydroxyisoxsuprine exhibited 40-fold and 10-fold higher potent antioxidant and anti-inflammation activities than the precursor, isoxsuprine. The 3''-hydroxyisoxsuprine effectively mitigates the hyperimmune response in RAW 264.7 macrophages by inhibiting the upregulation of pro-inflammatory cytokine (IL-1β and IL-6) and inflammatory enzyme COX-2 gene expression triggered by LPS stimulation. This study illustrates that PDMA is an effective strategy for screening known natural and chemical compounds and for generating new bioactive compounds through biotransformation. Our newly produced compound has potential future applications in pharmacology and biotechnology.

Osteoporosis arises from the disturbance of bone homeostasis, a process regulated by osteoblasts and osteoclasts. The treatment and prevention of bone metabolic disorders resulting from an imbalance in bone homeostasis require the use of agents that effectively promote both bone formation and anti-resorptive effects. Therefore, an investigation was carried out to determine the potential of the edible mushroom Auricularia auricula-judae in modulating bone remodeling by inhibiting RANKL-induced osteoclastogenesis and enhancing BMP-2-stimulated osteoblast differentiation. Moreover, this study assessed the mode of action of the Auricularia auricula-judae extracts. The staining of tartrate-resistant acid phosphatase (TRAP), a marker for osteoclast activity, demonstrated that Auricularia auricula-judae water extract (AAJWE) inhibited the formation of multinucleated osteoclasts while exhibiting no cytotoxic effects. The study demonstrated that AAJWE reduced RANKL-induced osteoclast differentiation by inhibiting c-Fos/NFATc1 through the inhibition of ERK and JNK phosphorylation during the RANKL-induced osteoclast differentiation. Moreover, AAJWE exhibited a dose-dependent induction of ALP expression in the presence of BMP-2 during osteoblast differentiation. The AAJWE strengthened BMP-2-induced osteogenesis through the activation of Runx2 and Smad phosphorylation. Therefore, AAJWE emerges as a promising candidate for both prevention and therapy owing to its biphasic effect, which aids in the preservation of bone homeostasis.

Gastrointestinal disorders are widespread globally, with inflammatory diseases being particularly prominent. This study aimed to investigate the effect of Kjellmaniella crassifolia hot water extract (KCH) on lipopolysaccharide (LPS)-induced inflammation in human intestinal epithelial (Caco-2) cells and loperamide-induced constipation in BALB/c mice. The study's findings revealed that KCH dose-dependently increased the cell viability and reduced the NO production by decreasing the iNOS and COX-2 expression in LPS-stimulated Caco-2 cells. Also, KCH downregulated the mRNA expression of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α) by regulating the activation of MAPK and NF-κB signaling pathways in LPS-stimulated Caco-2 cells. In addition, KCH increased the expression levels of tight junction proteins, occludin, ZO-1, and claudin-1 in a dose-dependent manner. Furthermore, in vivo study outcomes demonstrated that KCH improved intestinal transit, increased fecal moisture content, and reduced fecal impaction in constipated mice. KCH decreased the mRNA expression of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and TNF-α), thereby increasing the expression levels of intestinal tight junction proteins (occludin, ZO-1, and claudin-1) in the small intestine tissues of the experimental mice. These proteins may help regulate intestinal motility and improve stool passage, thus reducing constipation. These findings suggest that KCH could be a promising functional food ingredient for managing intestinal inflammation, inflammation-related disorders, constipation, and the pathophysiology of constipation.

Current cancer burden caused by persistent infection with human papillomaviruse genotype 16 (HPV16) cannot be ignored. The related mechanisms of oncoproteins E6 and E7 from HPV16 on keratinocyte malignant transformation need to be further elucidated. GSE3292 dataset analysis revealed the upregulation of ETS transcription factor 3 (ELF3) and cyclin E2 (CCNE2). To verify whether there is an interaction between ELF3 and CCNE2, E74 like ELF3 and CCNE2 expression profiles as well as their putative binding sites were analyzed using bioinformatics. Retroviruses encoding HPV16 E6 and E7 genes were used to induce immortalization of human foreskin keratinocytes (HFKs) in vitro. Dual luciferase reporters assay was used to verify the binding of ELF3 and CCNE2. The effect of ELF3 on the immortalized cells was investigated using CCK-8 assay, cell cycle analysis and western blot. ELF3 and CCNE2 presented overexpression patterns in head and neck squamous cell carcinoma. HPV16 E6/E7-expressing HFKs showed enhanced viability, accelerated cell cycle as well as upregulated ELF3 and CCNE2. ELF3 overexpression enhanced the activity of CCNE2 promoter. ELF3 silencing reduced viability, induced cell cycle arrest and suppressed expressions of CCNE2, E6 and E7 in HPV16 E6/E7-expressing HFKs. Downregulation of ELF3 played an inhibiting role in the malignant transformation of HPV16 E6/E7-immortalized HFKs by decreasing CCNE2 expression.

Neuroinflammation and microglial activation play critical roles in neurodegenerative diseases such as Alzheimer's and Parkinson's disease. Modulating microglial activation may help prevent the progression of these disorders. This study aimed to investigate the effects and mechanisms of Melissa officinalis ethanol extract on lipopolysaccharide (LPS)-induced microglial activation in BV2 cells. Cell viability and nitric oxide (NO) production were assessed using MTT assay and Griess reagent, while inflammatory cytokine levels were measured by qPCR. Key inflammatory pathways, including MAPK, TLR4, and antioxidant biomarkers, were analyzed through western blot and immunofluorescence. Rosmarinic acid content in M. officinalis was determined using high-performance liquid chromatography (HPLC). The results demonstrated that M. officinalis ethanol extract significantly inhibited LPS-induced NO production and reduced inflammatory cytokine expression. Additionally, it downregulated inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TLR4, NF-κB, and MAPK signaling pathways (p38, JNK, ERK), while increasing the expression of antioxidant markers, including Nrf2, HO-1, catalase, and SOD2. In conclusion, M. officinalis ethanol extract exerts neuroprotective effects by modulating inflammation and enhancing antioxidant defenses, suggesting its potential in the prevention and treatment of inflammation-related neurodegenerative diseases.

Phaeodactylum tricornutum, a unicellular diatom, is considered a potential feedstock for the production of biofuel and a promising producer for high-value products eicosapentaenoic acid and fucoxanthin. However, a high-efficient cultivating strategy to achieve commercial production of triacylglycerol (TAG) from the diatom is an urgent demand. In this study, we optimized the content and ratio of nitrate and tryptone in the medium to enhance biomass and TAG accumulation simultaneously. Growth with tryptone as the sole nitrogen gave rise to the lowest cell density but the highest TAG content in P. tricornutum relative to nitrate, nitrite, ammonium or urea cultures. In 500 μM NaNO₃ cultures, the growth of P. tricornutum increased with the increasing concentration (from 294 to 7056 μM nitrogen) of supplemented tryptone, however supplementation of high tryptone (≥882 μM nitrogen) decreased the neutral lipid content. Elevating nitrogen concentration from 294 to 882 μM via tryptone addition in 250 μM nitrate culture increased cell densities from day 6 to 10 and neutral lipid content on day 10. In particular, supplementing 588 μM nitrogen of tryptone in the 250 μM nitrate culture gave rise to the highest neutral lipid content on days 8 and 10 (increased by 109% and 62% relative to 500 μM nitrate-sole) with a comparable growth to that in 500 μM nitrate-sole culture from day 2 to 8. In conclusion, we optimized nitrate/tryptone ratio and found that a suitable tryptone addition to a relatively low nitrate culture was favourable to the biomass and TAG accumulation simultaneously in P. tricornutum.

Angiogenesis and lymphangiogenesis are some of the routes that cause metastasis. Vascular Endothelial Growth Factors (VEGFs) stimulate angiogenesis and lymphangiogenesis through VEGF receptors. Especially, VEGF-D and its receptor, VEGFR-3, play a pivotal role in regulating cellular processes such as survival, proliferation, and migration, thereby influencing lymphangiogenesis. The aim of this research is to clarify the molecular characteristics of VEGF-D and VEGFR-3 proteins and identify the key residues that are essential for the interaction between VEGF-D and VEGFR-3. Experiments, including size exclusion chromatography and GST pull-down assay analysis, reveal that specific residues, particularly D103 and Q110, are essential for VEGF-D/VEGFR-3 binding. Mutations in these residues induce structural alterations, resulting in reduced binding affinity and impaired activation of VEGFR-3. Moreover, this study suggests that a synthesized peptide, designed based on key residues of VEGF-D involved in binding to VEGFR-3, may act as a metastasis suppressor by competitively inhibiting the interaction between VEGF-D and VEGFR-3. Understanding these molecular interactions is expected to have significant potential to develop therapeutic peptides that can inhibit cancer cell-induced lymphangiogenesis and resolve metastasis via lymphangiogenesis across various cancer types.