The genes downregulated in biofilm were involved in metabolism and translation, whereas the biofilm upregulated genes encoded the envelope proteins involved in stress response and construction of flagella. In a comparative transcriptomic analysis performed by Hathroubi et al, 8% of the genes studied were found to be differentially expressed between H pylori biofilm and planktonic cells. 2 Helicobacter pylori downregulates the expression of two transporters of cellular bicarbonate in the duodenal epithelium: (a) the cystic fibrosis transmembrane conductance regulator (CFTR) and (b) the solute linked carrier 26 gene family A6 (ALC26A6), through the transforming growth factor beta (TGFβ)-mediated p38 mitogen-activated protein kinase (MAPK) signaling pathway. Helicobacter pylori-induced reduction of mucosal bicarbonate secretion, which protects the gastric barrier against acid-induced mucosal injury, was suggested to play a role in duodenal ulcer development.
1 These data allow to link acid adaptation of H pylori and nickel homeostasis. Jones and Zamble showed the effects of a drop in cytosolic pH on H pylori, exposed to external pH 2.0 mimicking the conditions in human stomach it resulted in a nickel-responsive transcription factor (HpNikR)-dependent activation of ureA gene transcription illustrating the mechanism of adaptation of these bacteria to the harsh acidic environment. All these new data illustrate further progress in understanding H pylori pathogenicity and facilitate the search for new therapeutic targets as well as development of immunoprophylaxis methods based on new chimeric UreB and HpA proteins.ġ GASTRIC TISSUE COLONIZATION AND CHRONIC INFECTION 1.1 Response to the harsh environment in the stomach The role of molecular mimicry between a common sequence (ATVLA) of H pylori heat shock protein (Hsp) B and human Hsp60 in the induction of potentially autoreactive antibodies is discussed. Furthermore, we shall describe molecular and functional studies on new aspects of VacA and CagA virulence, including the role of urease in the upregulation of VacA toxicity, an epithelial-mesenchymal transition mediated by CagA, and the role of interaction of HopQ adhesin with carcinoembryonic antigen-related cell adhesion molecules (CEACAMs) in CagA translocation into the host cells by the type IV secretion system (T4SS). The role of the membrane vesicles of these bacteria has been emphasized as an important source of virulence factors. In this review, we shall focus on the last year progression understanding the pathogenesis of Helicobacter pylori infection in the light of recent data related to adaptation of H pylori to the harsh acidic environment in the stomach, colonization of gastric mucosa via interaction with mucin 5 (MUC5AC) and other host cell receptors, the ability to form biofilm, interference with the host metabolic pathways, and induction of neuroimmune cross-talk as well as downregulation of gastric barrier homeostasis and its consequences for the disease development.