Inflammation and proliferation – a causal event of host response to Helicobacter pylori infection

The importance of Helicobacter pylori in the development of gastric MALT lymphoma — induction of proliferation and immune suppression

“…Modified protein induces tyrosine phosphatase 2 (SHP-2) and this activates extracellular signal-regulated kinases 1/2 (Erk1/2). The unphosphorylated CagA protein induces Erk1/2 kinase through an alternative Ras-Raf signalling pathway [2,16]. Both processes contribute to activating the NF-kB transcription factor and increased IL-8 expression [17].…”

“…VacA is a highly immunogenic 95 kDa protein causing a number of pathological changes in the targeted host cells. Among these, is its ability to form anion-selective pores in cell membranes, interfere with cytoskeleton-dependent cell function and induce apoptosis via the mitochondrial cytochrome c release [2,4]. In addition, VacA has in vivo antiproliferative activity against lymphocytes and the ability of modulating immune system processes [6].…”

“…The cagPAI pathogenic island is a 40 kb DNA fragment containing 27 to 31 genes; eighteen of which encode information for proteins forming the IV secretory system (T4SS), which facilitates CagA oncoprotein and peptidoglycan fragment translocation [2]. CagA is a 120-145 kDa protein produced by 60-70% of H. pylori strains.…”

“…This process occurs most often during early childhood and lasts throughout life in the absence of any adequate eradication therapy [1]. Not all people colonized with this bacteria exhibit disease symptoms, but importantly this condition predisposes towards their development [2]. It is estimated that over 90% of chronic gastritis is a result of prolonged H. pylori infection.…”

“…Increased production of proinflammatory cytokines involved in gastric tissue degradation, (including IL-1b, IL-6, IL-8, IL-12, TNF-a, CCL2-5, CCL20 and CXCL1-3), is the consequence [4]. Inflammatory mediators cause the following: epithelial lesion formation, changes in proliferation and apoptosis processes along with modulating host gene expression [2]. The acute phase is followed by a decreased antimicrobial response of the host organism and chronic H. pylori infection.…”