Background: Helicobacter pylori, gastric cancer‐causing bacteria, survive in their gastric environment of more than 50% of the world population. The presence of H. pylori in the gastric vicinity promotes the development of various diseases including peptic ulcer and gastric carcinoma. H. pylori produce and secret Vacuolating cytotoxin A (VacA), a major toxin facilitating the bacteria against the host defense system. The toxin causes multiple effects in epithelial cells and immune cells, especially T cells, B cells, and Macrophages.Methods: This review describes the diverse functionalities of protein toxin VacA. The specific objective of this review is to address the overall structure, mechanism, and functions of VacA in various cell types. The recent advancements are summarized and discussed and thus conclusion is drawn based on the overall reported evidences.Results: The searched articles on H. pylori VacA were evaluated and limited up to 66 articles for this review. The articles were divided into four major categories including articles on vacA gene, VacA toxin, distinct effects of VacA toxin, and their effects on various cells. Based on these studies, the review article was prepared.Conclusions: This review describes an overview of how VacA is secreted by H. pylori and contributes to colonization and virulence in multiple ways by affecting epithelial cells, T cells, Dendritic cells, B cells, and Macrophages. The reported evidence suggests that the comprehensive outlook need to be developed for understanding distinctive functionalities of VacA.

Helicobacter pylori infection causes chronic active gastritis that after many years of infection can develop into peptic ulceration or gastric adenocarcinoma. The bacterium is highly adapted to surviving in the gastric environment and a key adaptation is the virulence factor urease. Although widely postulated, the requirement of urease expression for persistent infection has not been elucidated experimentally as conventional urease knockout mutants are incapable of colonization. To overcome this constraint, conditional H. pylori urease mutants were constructed by adapting the tetracycline inducible expression system that enabled changing the urease phenotype of the bacteria during established infection. Through tight regulation we demonstrate that urease expression is not only required for establishing initial colonization but also for maintaining chronic infection. Furthermore, successful isolation of tet-escape mutants from a late infection time point revealed the strong selective pressure on this gastric pathogen to continuously express urease in order to maintain chronic infection. In addition to mutations in the conditional gene expression system, escape mutants were found to harbor changes in other genes including the alternative RNA polymerase sigma factor, fliA, highlighting the genetic plasticity of H. pylori to adapt to a changing niche. The tet-system described here opens up opportunities to studying genes involved in the chronic stage of H. pylori infection to gain insight into bacterial mechanisms promoting immune escape and life-long infection. Furthermore, this genetic tool also allows for a new avenue of inquiry into understanding the importance of various virulence determinants in a changing biological environment when the bacterium is put under duress. Helicobacter pylori is a bacterial pathogen that chronically infects half the global population and is a major contributor to the development of peptic ulcers and stomach cancer. H. pylori has evolved to survive in the stomach and one important adaptation is the enzyme urease. The bacteria cannot establish an infection in the host without this enzyme, and although widely postulated, the requirement of urease for chronic infection of the host has not been tested experimentally as conventional urease mutants are incapable of colonization. To overcome this constraint, a genetic system was introduced that allowed for the making of H. pylori strains in which urease expression could be turned off after the bacteria have colonised the stomach. We show for the first time that this enzyme is not only important for initial colonization but that it is also very important for maintaining chronic infection. We also show that if urease is turned off, the bacterium can mutate several different genes in order to restore urease expression. The genetic approach described here opens up opportunities to studying genes involved in the chronic stage of H. pylori infection to gain insight into how the bacterium is able to avoid clearance by the immune system and how it is able to adapt to changing biological environments.

The present study aimed to evaluate the dietary supplementary effects of black soldier fly (Hermetia illucens) (BSF) meal on the bacterial communities in the distal gut, immune response and growth of freshwater crayfish, marron (Cherax cainii) fed poultry-by-product meal (PBM) as an alternative protein source to fish meal (FM). A total of 64 marron were randomly distributed into 16 different tanks with a density of four marron per tank. After acclimation, a 60-days feeding trial was conducted on marron fed isonitrogenouts and isocalorific diets containing protein source from FM, PBM, and a combination of FM + BSF and PBM + BSF. At the end of the trial, weight gain and growth of marron were found independent of any dietary treatment, however, the two diets supplemented with BSF significantly (P< 0.05) enhanced haemolymph osmolality, lysozyme activity, total haemocyte counts, and protein and energy contents in the tail muscle. In addition, the analysis of microbiota and its predicted metabolic pathways via 16s rRNA revealed a significantly (P< 0.05) higher bacterial activity and gene function correlated to biosynthesis of protein, energy and secondary metabolites in PBM + BSF than other dietary groups. Diets FM + BSF and PBM + BSF were seen to be associated with an up-regulation of cytokine genes in the intestinal tissue of marron. Overall, PBM + BSF diet proved to be a superior diet in terms of improved health status, gut microbiota and up-regulated expression of cytokine genes for marron culture.

Infectious diseases caused by microbial pathogens remain a primary contributor to global health burdens. Prompt control and effective prevention of these pathogens are critical for public health and medical diagnostics. Conventional microbial detection methods suffer from high complexity, low sensitivity, and poor selectivity. Therefore, developing rapid and reliable methods for microbial pathogen detection has become imperative. Surface‐enhanced Raman Spectroscopy (SERS), as an innovative non‐invasive diagnostic technique, holds significant promise in pathogenic microorganism detection due to its rapid, reliable, and cost‐effective advantages. This review comprehensively outlines the fundamental theories of Raman Spectroscopy (RS) with a focus on label‐free SERS strategy, reporting on the latest advancements of SERS technique in detecting bacteria, viruses, and fungi in clinical settings. Furthermore, we emphasize the application of machine learning algorithms in SERS spectral analysis. Finally, challenges faced by SERS application are probed, and the prospective development is discussed.