RESUMO
A Gram-negative, facultative anaerobic, non-motile and rod-shaped bacterium, designated 10c7w1T, was isolated from a human gastrointestinal tract. Colonies on agar plates were small, circular, smooth and beige. The optimal growth conditions were determined to be 37â°C, pH 7.0-7.5 and 0â% (w/v) NaCl. Comparative analysis of complete 16S rRNA gene sequences revealed that strain 10c7w1T showed the highest sequence similarity of 95.8â% to Ottowia beijingensis MCCC 1A01410T, followed by Ottowia thiooxydans (95.2â%) JCM 11629T. The average amino acid identity values between 10c7w1T and O. beijingensis MCCC 1A01410T and O. thiooxydans JCM 11629T were above 60â% (71.4 and 69.5â%). The average nucleotide identity values between strain 10c7w1T and O. beijingensis MCCC 1A01410T and O. thiooxydans JCM 11629T were 76.9 and 72.5â%, respectively. The dominant fatty acids (≥10â%) were straight chain ones, with summed feature 3 (C16â:â1 ω7c/C16â:â1 ω6c), summed feature 8 (C18â:â1 ω7c/C18â:â1 ω6c) and C16â:â00 being the most abundant. Q-8 was the only respiratory quinone. The major polar lipids of strain 10c7w1T were phosphatidylethanolamine, diphosphatidylglycerol and unknown lipids. The DNA G+C content of strain 10c7w1T was 63.6âmol%. On the basis of phylogenetic, phenotypic and chemotaxonomic data, strain 10c7w1T is considered to represent a novel species within the genus Ottowia, for which the name Ottowia cancrivicina sp. nov. is proposed. The type strain is 10c7w1T (=MCCC 1H01399T=KCTC 92200T).
Assuntos
Técnicas de Tipagem Bacteriana , Composição de Bases , DNA Bacteriano , Ácidos Graxos , Filogenia , RNA Ribossômico 16S , Análise de Sequência de DNA , Estômago , RNA Ribossômico 16S/genética , Ácidos Graxos/química , Humanos , DNA Bacteriano/genética , Estômago/microbiologia , Hibridização de Ácido Nucleico , Ubiquinona , Fosfolipídeos/químicaRESUMO
Helicobacter pylori (H. pylori) is one of the most important pathogenic bacteria associated with various gastrointestinal diseases. At present, its apoptotic or antiapoptotic mechanism on gastric epithelial cells remains unknown and needs further illustrated. In this study, acute infection model (H. pylori and GES-1 cells were co-cultured for 24 h at a multiplicity of infection MOI of 100:1) and chronic infection model (GES-1 cells were infected repeatedly every 24 h at a multiplicity of infection MOI of 100:1 for approximately 8 weeks) were established, respectively. the chronic H. pylori infected GES-1 cells underwent a typically morphological change and Western Blot results showed that there was slight decrease in expression of E-cadherin, and obvious increase in expression of Vimentin. Apoptosis of these two models were analyzed by flow cytometry compared with the control cells, meanwhile, apoptosis associated markers (Bcl-xL, Bcl-2, Bax, etc) were detected by Western blot, additional in clinical H. pylori-positive gastric cancer tissues. Results showed that compared with the control cells, acute infection of H. pylori significantly accelerated the apoptosis of GES-1, increased the expression of Bax and Cleaved caspase-3, down-regulated expression of Bcl-xL and Bcl-2. Moreover, an opposite result was found in chronic infection of model and clinical gastric cancer tissues, and enhanced expression of NF-κB p65. Taken together, these findings suggest that H. pylori infection plays differential effects on apoptosis of gastric epithelial cells.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , Apoptose , Células Epiteliais , Mucosa Gástrica , HumanosRESUMO
Helicobacter pylori, a Gram-negative microaerobic bacteria belonging to the phylum Proteobacteria, can colonize in the stomach and duodenum, and cause a series of gastrointestinal diseases such as gastritis, gastric ulcer and even gastric cancer. At present, the high diversity of the microorganisms in the stomach has been confirmed with culture-independent methods; some researchers have also studied the stomach microbiota composition at different stages of H. pylori carcinogenesis. Here, we mainly review the possible role of H. pylori-mediated microbiota changes in the occurrence and development of gastric cancer to provide new ideas for preventing H. pylori infection and regulating microecological imbalance.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , Microbiota , Neoplasias Gástricas , Humanos , Helicobacter pylori/genética , Neoplasias Gástricas/microbiologia , Infecções por Helicobacter/microbiologia , HomeostaseRESUMO
Helicobacter pylori (H. pylori) infection plays a pivotal role in the development of gastric cancer (GC). However, the association between aberrant microRNAs (miRNAs/miRs) expression and H. pyloriinduced GC remains poorly understood. The present study reported that repeated infection of H. pylori caused the oncogenicity of GES1 cells in BALB/c Nude mice. miRNA sequencing revealed that both miR7 and miR153 were significantly decreased in the cytotoxinassociated gene A (CagA) positive GC tissues and this was further confirmed in a chronic infection model of GES1/HP cells. Further biological function experiments and in vivo experiments validated that miR7 and miR153 can promote apoptosis and autophagy, inhibit proliferation and inflammatory response in GES1/HP cells. All the associations between miR7/miR153 and their potential targets were revealed via bioinformatics prediction and dualluciferase reporter assay. Particularly, downregulation of both miR7 and miR153 obtained an improved sensitivity and specificity in diagnosing H. pylori (CagA+)induced GC. The present study identified that the combination of miR7 and miR153 may be regarded as novel therapeutic targets in H. pylori CagA (+)associated GC.
Assuntos
Infecções por Helicobacter , Helicobacter pylori , MicroRNAs , Neoplasias Gástricas , Animais , Camundongos , Antígenos de Bactérias/genética , Proteínas de Bactérias/genética , Carcinogênese/genética , Regulação para Baixo , Infecções por Helicobacter/complicações , Infecções por Helicobacter/genética , Helicobacter pylori/genética , Camundongos Nus , MicroRNAs/genética , MicroRNAs/metabolismo , Neoplasias Gástricas/metabolismo , HumanosRESUMO
Bloodstream infections remain a leading cause of death worldwide, despite advances in critical care and understanding of the pathophysiology and treatment strategies. No specific biomarkers or therapy are available for these conditions. Neutrophils play a critical role in controlling infection and it is suggested that their migration and antimicrobial activity are impaired during sepsis which contribute to the dysregulation of immune responses. Recent studies further demonstrated that interruption or reversal of the impaired migration and antimicrobial function of neutrophils improves the outcome of sepsis in animal models. In this review, we provide an overview of the associated diagnostic biomarkers involved neutrophils in sepsis, and discuss the potential of neutrophils as a target to specifically predict the outcome of sepsis.