Inflammatory Chaos in Helicobacter pylori Infection
A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Microbiology in Human Health and Disease".
Deadline for manuscript submissions: closed (31 January 2025) | Viewed by 1970
Special Issue Editor
Interests: gastric cancer; Helicobacter pylori; immunology; innate immunity; cytokine biology; cellular microbiology
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
Helicobacter pylori is one of the most common human pathogens and is closely associated with pathogenesis of gastritis, peptic ulcer, gastric cancer and MALT lymphoma. A total of 4.4 billion individuals are estimated to be colonized with H. pylori, which equals to 60% of the world population in the middle of last decade. The prevalence of H. pylori infection is low in developed countries and high in developing countries, ranging between 19% in Switzerland and 88% in Nigeria. The survival of the H. pylori in its niche, the gastric mucosa, can be attributed to the ability of this microbe to manipulate its host’s immunity. H. pylori has evolved strategies to evade or derange innate and adaptive immune responses. This bacterium is generally detected by pattern recognition receptors (PRRs) to mount the different immune responses, whereas H. pylori has evolved strategies for masking the toll-like receptor (TLR) ligands to modulate the sensing which ultimately affects signaling pathways for the production of chemokines and cytokines. In addition, the inflammasome formation and mature IL-1β secretion are critically blocked in H. pylori-infected human immune cells. The major adaptive immune response against H. pylori is driven through Th1 effector functions. The Th1 immune response is mainly controlled by the cagPAI genetic locus-encoded Type IV secretion system (T4SS). TLR5-mediated sensing of H. pylori T4SS proteins CagL or CagY is sufficient to induce a Th1 response in infection models. H. pylori infection also induces a Th2 response through DC-SIGN-mediated activation of an atypical NF-κB pathway. This chronic infection of the gastric mucosa is further producing Treg cells, which complicates the situation. In addition, both M1 and M2 macrophages are involved in H. pylori pathogenesis. Altogether, H. pylori infection is commonly modulating a network of cellular signaling in the production of cytokines and chemokines, which leads to several stochastic events in the bacterial persistence, which are associated with disease pathogenesis, inflammation and resolution. Therefore, this Special Issue focuses on the ‘inflammatory chaos’ and research efforts to understand such dynamic behavior in H. pylori or related infections.
Dr. Suneesh Kumar Pachathundikandi
Guest Editor
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Keywords
- Helicobacter pylori
- cytokine
- chemokine
- TLRs
- inflammasome
- T4SS
- gastric inflammation
- gastric ulcer
- gastric cancer
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