11 research outputs found

    Effect of curcumin on Helicobacter pylori biofilm formation

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    Helicobacter pylori is a leading etiologic agent causing peptic ulcer and gastric cancer. The alternative lifestyle as a biofilm facilitates H. pylori to survive in adverse environments. Here, we investigated effect of curcumin on H. pylori biofilm formation both qualitatively by pellicle assay and quantitatively by crystal violet staining. Three-dimensional structure of biofilm was imaged by scanning electron microscopy. The effect of curcumin on H. pylori adherence to HEp-2 cells was also investigated. Subinhibitory concentrations of curcumin inhibited the biofilm in dose dependent manner. However, H.pylori could restore ability to form biofilm during extended time of incubation. Scanning electron microscopy revealed less amorphous extracellular polymeric matrix, slow of morphological conversion to coccoid form with cell damage after curcumin treatment. Curcumin significantly decreased the abilityof H. pylori to adhere to the HEp-2 cells. Our findings demonstrated advantages of curcumin to inhibit biofilm formation by H. pylori, making it as a potential complimentary medicine for curing of H. pyloribiofilmrelated infections

    The effects of Kaempferia parviflora on anti-internalization activity of Helicobacter pylori to HEp-2 cells

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    Helicobacter pylori, an etiological agent of active chronic gastritis and peptic ulcer disease, is now considered to be an invasive enteropathogen. Anti-adhesion and anti-internalization are new strategies for prevention and treatment of bacterial infection including the alternative of medicinal plants. In this study, four parts of Kaempferia parviflora’s extracts composing of volatile oil, hexane, ethyl acetate and methanol were examined for their antibacterial and anti-internalization activities of H. pylori against HEp-2 cells. All extracts except volatile oil showed significant antibacterial activity and had a minimum inhibitory concentration (MIC) ranging from 32 - 64 ìg/ml. The most active extract of ethyl acetateexhibited significant anti-internalization activity which corresponded to dose and time of treatment. Moreover, K. parviflora’s ethyl acetate extract could significantly inhibit the invasion of both H. pylori virulent strains (cagA+) and non-virulent strains (cagA-) in HEp-2 cells. Thus, K. parviflora is one of the effective herbs for potential prevention and treatment of H. pylori infection

    Kaempferia parviflora Extracellular Vesicle Loaded with Clarithromycin for the Treatment of Helicobacter pylori Infection

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    Variya Nemidkanam,1 Wijit Banlunara,2 Nuntaree Chaichanawongsaroj3 1Department of Clinical Chemistry, Graduate Program in Clinical Biochemistry and Molecular Medicine, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10330, Thailand; 2Department of Pathology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok, 10330, Thailand; 3Department of Transfusion Medicine and Clinical Microbiology, Research Unit of Innovative Diagnosis of Antimicrobial Resistance, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10330, ThailandCorrespondence: Nuntaree Chaichanawongsaroj, Department of Transfusion Medicine and Clinical Microbiology, Research Unit of Innovative Diagnosis of Antimicrobial Resistance, Faculty of Allied Health Sciences, Chulalongkorn University, Bangkok, 10330, Thailand, Tel +66 838199988, Email [email protected]: Kaempferia parviflora extracellular vesicles (KPEVs) have been reported as promising nanovesicles for drug delivery. This study aimed to load clarithromycin (CLA) into KPEVs (KPEVS-CLA) and determine the physical properties, drug-releasing efficiency, gastric cell uptake, anti-H. pylori activities, and anti-inflammatory responses in comparison with free CLA and KPEVs.Methods: The size and surface charge of KPEVs-CLA were evaluated using dynamic light scattering and visualized using a transmission electron microscope. The encapsulation efficiency (EE%), loading capacity (LC%), and drug release of KPEVs-CLA were examined using HPLC. Anti-H. pylori growth and anti-adhesion were evaluated. IL-8 gene expression, NF-κB signaling proteins, and anti-inflammatory profiles were examined using qRT-PCR, Western blotting, and Bio-Plex immunoassay, respectively. Anti-chemotaxis was then examined using a Transwell assay.Results: KPEVs-CLA were intact and showed a negative surface charge similar to that of KPEVs. However, slightly enlarged KPEVs were observed. CLA was successfully loaded into KPEVs with EE of 93.45% ± 2.43%, LC of 9.3% ± 3.02%. CLA release in the PBS and gastric mimic buffer with Fickian diffusion (n ≤ 0.43) according to Korsmeyer-Peppas kinetic model (R2=0.98). KPEVs-CLA was localized in the gastric cells’ cytoplasm and perinuclear region. Anti-H. pylori growth and anti-H. pylori adhesion of KPEVs-CLA were compared with those of free CLA with no cytotoxicity to adenocarcinoma gastric cells. KPEVs-CLA significantly reduced IL-8, G-CSF, MIP-1α, and MIP-1β levels. Moreover, KPEVs-CLA showed a superior effect over CLA in reducing G-CSF, MIP-1α, and NF-κB phosphorylation and monocyte chemotactic activities.Conclusion: KPEVs serve as potential carriers of CLA. They exhibited a higher efficiency in inhibiting gastric cell inflammation mediated by H. pylori infection than free CLA. The establishment of KPEVs-CLA as a nanodrug delivery model for H. pylori treatment could be applied to other plant extracellular vesicles or loaded with other cancer drugs for gastric cancer treatment.Keywords: extracellular vesicle, clarithromycin, Kaempferia parviflora, Helicobacter pylori, inflammatio

    Strongyloidiasis in Oceania

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    Strongyloidiasis is a potentially fatal disease caused by species of Strongyloides (Nematoda). In Oceania, two species infect humans: S. stercoralis and S. kellyi. S. stercoralis is widespread throughout Oceania and causes serious disease in any age group. S. kellyi is localised to Papua New Guinea and causes serious disease in infants. Infective larvae enter the body through the skin and migrate through the tissues. Adult females live in the mucosa of the proximal small intestine. The life cycle of S. stercoralis includes autoinfection, unusual in parasitic worms, whereby some of the offspring of the parasitic adults become infective in the lower intestine and complete the life cycle in the same person. This ensures that the infection persists, and the population of the worms can increase out of control, usually when the person is immunodefi cient or immunosuppressed. The worms can be eliminated by oral ivermectin, and the person is probably cured if their serology is negative 6 months after treatment. This chapter contains details of the life cycles, transmission, clinical manifestations, diagnostic tests and how to interpret them, most effective treatment options, how to ensure that treatment has been effective and what to consider when developing effective prevention and control strategies
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