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The Inflammatory and Immune Response to Helicobacter pylori Infection

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 2534

Special Issue Editors


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Guest Editor
Department of Internal Medicine and Outpatients Therapy, Moscow State University of Medicine and Dentistry, Moscow 127473, Russia
Interests: GI diseases; comorbidity; gastrointestinal microbiota; Helicobacter pylori; microbial metabolism

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Guest Editor
Institute of Experimental Medicine of the North-West Branch of the Russian Academy of Medical Sciences, Saint-Petersburg, Russia
Interests: Lactobacillus helveticus; probiotics; whole genome sequencing; probiotic genes; bacteriocins; gene expression

Special Issue Information

Dear Colleagues,

Helicobacter pylori is generally regarded as a human pathogen and a carcinogen, responsible for about 15% of the total cancer burden globally and up to 90% of all gastric cancer cases. H. pylori is etiologically related to gastric and duodenal ulcers and mucosa-associated lymphoid tissue lymphoma.

Unlike other pathogenic/opportunistic bacteria/pathobionts, H. pylori colonization of infants is facilitated by T helper type 2 immunity and leads to the development of immune tolerance. Most likely, the co-evolution of H. pylori and the human host over millennia has led to the fact that this bacterium is considered a commensal symbiont, not only a pathogen, by the host’s immune system, allowing it to evade the immune response.

The induction of the innate immune response by H. pylori plays a critical role in the outcome of the infection. However, since sequelae of infection occur in only 20% of infected patients, and malignancies occur in <3%, it is clear that other factors and mechanisms regulate the localized non-specific response, including the gastrointestinal microbiota and genetic factors.

Thus, the pathophysiology of H. pylori infection and its clinical outcome should be viewed as a complex interaction between the host, the bacterium, and the gastrointestinal microbiota. This interaction is influenced by the environment and modulated by a variety of largely as yet unidentified factors.

Thus, there is a clear need for studies describing the factors that induce and regulate the immune response during H. pylori infection, as well as for innovative approaches to H. pylori infection management.

This Special Issue will focus on the latest advances in understanding the induction and regulation of the inflammatory and immune response to H. pylori infection, as well as potential tools for its modulation and innovative eradication strategies, including but not limited to novel antibacterials, probiotics, postbiotic metabolites, phytochemicals, and bacteriophages.

Prof. Dr. Leonid B. Lazebnik
Dr. Stanislav Sitkin
Guest Editors

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Keywords

  • adhesion
  • antibiotics resistance
  • bacteriophages
  • chronic inflammation
  • dysbiosis
  • eradication
  • fucosylated glycan
  • gastric cancer
  • gastric microbiota
  • gut microbiota
  • Helicobacter pylori
  • H. pylori-associated gastritis
  • H. pylori differ stamms
  • host immune response
  • inflammasome
  • inflammatory response
  • innate immunity
  • Lewis system antigens
  • matrix metalloproteinases
  • microbial interaction
  • microbial metabolites
  • microRNA
  • molecular mimicry
  • non-coding RNA
  • oxidative stress
  • pathogen-associated molecular patterns
  • pattern recognition receptors
  • phytochemicals
  • postbiotics
  • probiotics
  • synthetic peptides
  • vaccine
  • virulence factors

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Published Papers (1 paper)

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Review

27 pages, 5022 KiB  
Review
Gut Bacteria Provide Genetic and Molecular Reporter Systems to Identify Specific Diseases
by Leon M. T. Dicks
Int. J. Mol. Sci. 2024, 25(8), 4431; https://doi.org/10.3390/ijms25084431 - 17 Apr 2024
Viewed by 2131
Abstract
With genetic information gained from next-generation sequencing (NGS) and genome-wide association studies (GWAS), it is now possible to select for genes that encode reporter molecules that may be used to detect abnormalities such as alcohol-related liver disease (ARLD), cancer, cognitive impairment, multiple sclerosis [...] Read more.
With genetic information gained from next-generation sequencing (NGS) and genome-wide association studies (GWAS), it is now possible to select for genes that encode reporter molecules that may be used to detect abnormalities such as alcohol-related liver disease (ARLD), cancer, cognitive impairment, multiple sclerosis (MS), diabesity, and ischemic stroke (IS). This, however, requires a thorough understanding of the gut–brain axis (GBA), the effect diets have on the selection of gut microbiota, conditions that influence the expression of microbial genes, and human physiology. Bacterial metabolites such as short-chain fatty acids (SCFAs) play a major role in gut homeostasis, maintain intestinal epithelial cells (IECs), and regulate the immune system, neurological, and endocrine functions. Changes in butyrate levels may serve as an early warning of colon cancer. Other cancer-reporting molecules are colibactin, a genotoxin produced by polyketide synthetase-positive Escherichia coli strains, and spermine oxidase (SMO). Increased butyrate levels are also associated with inflammation and impaired cognition. Dysbiosis may lead to increased production of oxidized low-density lipoproteins (OX-LDLs), known to restrict blood vessels and cause hypertension. Sudden changes in SCFA levels may also serve as a warning of IS. Early signs of ARLD may be detected by an increase in regenerating islet-derived 3 gamma (REG3G), which is associated with changes in the secretion of mucin-2 (Muc2). Pro-inflammatory molecules such as cytokines, interferons, and TNF may serve as early reporters of MS. Other examples of microbial enzymes and metabolites that may be used as reporters in the early detection of life-threatening diseases are reviewed. Full article
(This article belongs to the Special Issue The Inflammatory and Immune Response to Helicobacter pylori Infection)
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