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 1797

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Guest Editor
Department of Environmental Microbiology, Babasaheb Bhimrao Ambedkar University, Vidya Vihar, Raebareli Road, Lucknow 226025, Uttar Pradesh, India
Interests: gastric cancer; Helicobacter pylori; immunology; innate immunity; cytokine biology; cellular microbiology
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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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Published Papers (1 paper)

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Review

20 pages, 9893 KiB  
Review
The Influence of Gastric Microbiota and Probiotics in Helicobacter pylori Infection and Associated Diseases
by Jagriti Verma, Md Tanveer Anwar, Bodo Linz, Steffen Backert and Suneesh Kumar Pachathundikandi
Biomedicines 2025, 13(1), 61; https://doi.org/10.3390/biomedicines13010061 - 30 Dec 2024
Viewed by 1392
Abstract
The role of microbiota in human health and disease is becoming increasingly clear as a result of modern microbiome studies in recent decades. The gastrointestinal tract is the major habitat for microbiota in the human body. This microbiota comprises several trillion microorganisms, which [...] Read more.
The role of microbiota in human health and disease is becoming increasingly clear as a result of modern microbiome studies in recent decades. The gastrointestinal tract is the major habitat for microbiota in the human body. This microbiota comprises several trillion microorganisms, which is equivalent to almost ten times the total number of cells of the human host. Helicobacter pylori is a known pathogen that colonizes the gastric mucosa of almost half of the world population. H. pylori is associated with several gastric diseases, including gastric cancer (GC) development. However, the impact of the gastric microbiota in the colonization, chronic infection, and pathogenesis is still not fully understood. Several studies have documented qualitative and quantitative changes in the microbiota’s composition in the presence or absence of this pathogen. Among the diverse microflora in the stomach, the Firmicutes represent the most notable. Bacteria such as Prevotella sp., Clostridium sp., Lactobacillus sp., and Veillonella sp. were frequently found in the healthy human stomach. In contrast, H.pylori is very dominant during chronic gastritis, increasing the proportion of Proteobacteria in the total microbiota to almost 80%, with decreasing relative proportions of Firmicutes. Likewise, H. pylori and Streptococcus are the most abundant bacteria during peptic ulcer disease. While the development of H. pylori-associated intestinal metaplasia is accompanied by an increase in Bacteroides, the stomachs of GC patients are dominated by Firmicutes such as Lactobacillus and Veillonella, constituting up to 40% of the total microbiota, and by Bacteroidetes such as Prevotella, whereas the numbers of H. pylori are decreasing. This review focuses on some of the consequences of changes in the gastric microbiota and the function of probiotics to modulate H. pylori infection and dysbiosis in general. Full article
(This article belongs to the Special Issue Inflammatory Chaos in Helicobacter pylori Infection)
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