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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.

Eggerthella lenta is an emerging and uncommon human pathogen that has been under recognized due to the limitations of phenotypic identification. Here we describe two cases of bacteremia caused by E. lenta and summarize the results of antimicrobial susceptibility testing according to some previous literatures, which illustrate the importance of identification and treatment of unusual organisms. The most reliable antibiotic treatment options to E. lenta appear to be metronidazole, amoxicillin-clavulanate, carbapenems, vancomycin, cefoxitin, chloramphenicol and clindamycin.

This article has been retracted: please see Future Science Group policy on retractions ( https://www.futuremedicine.com/authorguide/editorialpolicies ). The following article has been retracted from Future Microbiology as it did not meet the ethical standards of the Journal, owing to a lack of informed consent obtained from the patients, prior to publication: Mei Sun, Dong Guo, Jing Zhang, Jian Zhang, Hai-Feng Teng, Jun Xia, Peng Liu, Quan-Xu Ge, Ming-Yi Wang, 'Anal swab as a potentially optimal specimen for SARS-CoV-2 detection to evaluate hospital discharge of COVID-19 patients' appearing in the August issue of Future Microbiol. 15(12), 1101–1107 (2020). The authors and editors of Future Microbiology regret any negative consequences this publication might have caused in the scientific and medical communities.

Aim: To characterize the roles of VvhA in host's acquired immune response to Vibrio vulnificus infection. Materials & methods: The recombinant VvhA fusion protein was used to immunize mice and the anti-VvhA polyclonal antibody was produced in vivo for prophylactic and therapeutic efficacy assay. The roles of VvhA in T helper (Th) cells differentiation were analyzed by vvhA-deleted mutant during the early phase of infection, while the ratio of Th2 and T follicular helper (Tfh) cells were examined in VvhA immunization. Results: Anti-VvhA antibody exhibited neutralization activity against V. vulnificus. Wild-type strain induced higher level of Th1 cells than the mutant, and the concentrations of IgG2a and IFN-γ were increased during the early phase of infection. The spontaneous development of Tfh was observed in immunized model, and the serum IL-21 was increased. Conclusion: V. vulnificus VvhA elicited cellular and humoral immune responses by Th1 and Tfh cells to provide protection against VvhA.

Helicobacter pylori (H. pylori) has an essential role in the pathogenesis of gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue lymphoma and gastric cancer. The severity of the host inflammatory responses against the bacteria have been straightly associated with a special bacterial virulence factor, the cag pathogenicity island, which is a type IV secretion system (T4SS) to deliver CagA into the host cells. Besides cag-T4SS, the chromosomes of H. pylori can encode another three T4SSs, including comB, tfs3 and tfs4. In this review, we systematically reviewed the four T4SSs of H. pylori and explored their roles in the pathogenesis of gastroduodenal diseases. The information summarized in this review might provide valuable insights into the pathogenic mechanism for H. pylori.

Helicobacter pylori plays a vital role in the pathogenesis of gastric carcinoma. However, only a relatively small proportion of individuals infected with H. pylori develop gastric carcinoma. Differences in the incidence of gastric carcinoma among infected individuals can be explained, at least partly, by the different genotypes of H. pylori virulence factors. Thus far, many virulence factors of H. pylori, such as Cag PAI, VacA, OMPs and DupA, have been reported to be involved in the development of gastric cancer. The risk of developing gastric cancer during H. pylori infection is affected by specific host–microbe interactions that are independent of H. pylori virulence factors. In this review, we discuss virulence factors of H. pylori and their role in the development of gastric carcinoma that will provide further understanding of the biological interactions of H. pylori with the host.