Background Eradication of Helicobacter pylori infection is the most direct and effective way for preventing gastric cancer. Lactic acid bacteria are considered as alternative therapeutic agents against H. pylori infection. Methods Effects of Lactobacillus rhamnosus JB3 (LR‐JB3) on the virulence gene expression of H. pylori and infection‐induced cellular responses of AGS cells were investigated by co‐cultivating infected AGS cells with different multiplicity of infections (MOIs) of LR‐JB3. Results LR‐JB3, specifically at a MOI of 25, suppressed the association ability of H. pylori and its induced IL‐8 levels, as well as the mRNA levels of vacA, sabA, and fucT of H. pylori, infection‐induced Lewis (Le)x antigen and Toll‐like receptor 4 (TLR4) expressions in AGS cells. However, the apoptosis mediated by infection was inhibited by LR‐JB3 in a dose‐dependent manner. In addition, autoinducer (AI)‐2 was observed to have increased the association ability and fucT expression of H. pylori, and Lex antigen and TLR4 expression of AGS cells. Interestingly, an unknown bioactive cue was hypothesized to have been secreted from LR‐JB3 at a MOI of 25 to act as an antagonist of AI‐2. Conclusions LR‐JB3 possesses various means to interfere with H. pylori pathogenesis and infection‐induced cellular responses of AGS cells to fight against infection.
Helicobacter pylori is a Gram-negative pathogen that can increase the risk of stomach cancer in infected patients. H. pylori exploits lipid rafts to infect host cells. Infection triggers clustering of Lewis x antigen (Lex) and integrins in lipid rafts to facilitate H. pylori adherence to the gastric epithelium. H. pylori infection can be treated with probiotics containing lactic acid bacteria that offer numerous benefits to the host while lacking the side effects associated with antibiotic therapy. Previously, we showed that the cell-free supernatant (CFS) derived from Lactobacillus rhamnosus JB3 (LR-JB3) at a multiplicity of infection (MOI) of 25 attenuated the pathogenicity of H. pylori. In this study, we established a mucin model to simulate the gastric environment and to further understand the influence of mucin on the pathogenesis of H. pylori. Porcine stomach mucin dramatically upregulated H. pylori virulence gene expression, including that of babA, sabA, fucT, vacA, hp0499, cagA, and cagL, as well as the adhesion and invasion ability of H. pylori and induced increased levels of IL-8 in infected-AGS cells. The CFS derived from LR-JB3 at a MOI of 25 reduced the expression of H. pylori sabA, fucT, and hp0499 in mucin, as well as that of the Lex antigen and the α5β1 integrin in AGS cells during co-cultivation. These inhibitory effects of LR-JB3 also suppressed lipid raft clustering and attenuated Lewis antigen-dependent adherence, type IV secretion system-mediated cell contact, and lipid raft-mediated entry of VacA to host cells. In conclusion, LR-JB3 could affect H. pylori infection through mediating lipid raft formation of the host cells. The currently unknown cues secreted from LR-JB3 are valuable not only for treating H. pylori infection, but also for treating diseases that are also mediated by lipid raft signaling, such as cancer and aging-associated and neurodegenerative conditions.
Background and aim: Staphylococcus aureus is a significant public health concern due to its ability to develop antibiotic resistance. Biofilm formation or the enhancement of bacterial cell membrane permeability contributes to antibiotic resistance ability. Herbal therapy presents a promising strategy to overcome antibiotic resistance challenges. This study aims to investigate the potential of herbal extracts to reverse antibiotic resistance in S. aureus. Experimental Procedure: In this study, both Wild-type and Kanamycin-adapted (Km-adapted) S. aureus strains were pre-treated with herbal extracts derived from Zingiber zerumbet (ZZ), Eucalyptus globulus (EG), Andrographis paniculata (AP), Clerodendrum inerme(CI), Combretum quadrangular (CQ), and Plectranthus amboinicus (PA) at subinhibitory concentrations. The effects of these extracts on biofilm formation, bacterial cell surface hydrophobicity, cell permeability, and kanamycin sensitivity on pre-treated S. aureus were evaluated. Results: Our results demonstrated that S. aureus formed thick biofilms that were less sensitive to Km treatment, particularly in Km-adapted strains. However, extracts from ZZ, EG, and AP effectively reduced biofilm formation in both wild-type and Km-adapted strains and decreased bacterial cell surface hydrophobicity. Additionally, all herbal extracts increased the permeability of S. aureus cells, resulting in enhanced antibiotic sensitivity. Conclusion: Herbal therapy has the potential to reverse antibiotic resistance and reduce the necessary antibiotic dosage for treating S. aureus-related infections.
Background Whitefly Bemisia tabaci Gennadius (Hemiptera: Aleyrodidae) is a plant-damaging insect in tropical and subtropical regions that causes agricultural damage worldwide, including in Viet Nam. The abuse of pesticides derived from chemicals has resulted in the evolution of insect-resistant strains, polluting the environment and threatening human health. Using entomopathogenic fungi (EPF) for biological control is an alternative strategy in integrated pest management. Hence, an attempt was conducted to isolate, characterize and evaluate the efficacy of EPF, Purpureocillium lilacinum against whitefly B. tabaci under laboratory and field conditions. Results Purpureocillium lilacinum PL1 (PL1) was isolated from the whitefly B. tabaci cadavers and subsequently identified using morphological study and internal transcribed spacer sequencing. Purpureocillium lilacinum PL1 had effectively grown and sporulated at temperatures ranging from 25 to 35 °C and throughout a broad pH range, which is particularly advantageous against the harsh tropical monsoon climate. Bioassay study indicated that 1 × 107 conidia/ml of P. lilacinum PL1 had a high lethality against the whitefly B. tabaci nymphs in vitro with efficiency was 88.24% after 7 days of treatment. The median lethal concentration (LC50) of P. lilacinum PL1 to B. tabaci after 7 days of treatment was 1.24 × 105 conidia/ml. In field conditions, 1 × 107 conidia/ml of P. lilacinum PL1 lowered the population of B. tabaci nymphs with efficacy was 78.86% after 2 batches, 7 days after treatments. Conclusion The findings indicated that P. lilacinum PL1 was effective in the biological control of B. tabaci nymphs, which could be a potential alternative to chemical pesticides for pest management.
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