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Current research on the interaction between Helicobacter pylori and macrophages

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Abstract

Helicobacter pylori (H. pylori) is a gram-negative bacteria with a worldwide infection rate of 50%, known to induce gastritis, ulcers and gastric cancer. The interplay between H. pylori and immune cells within the gastric mucosa is pivotal in the pathogenesis of H. pylori-related disease. Following H. pylori infection, there is an observed increase in gastric mucosal macrophages, which are associated with the progression of gastritis. H. pylori elicits macrophage polarization, releases cytokines, reactive oxygen species (ROS) and nitric oxide (NO) to promote inflammatory response and eliminate H. pylori. Meanwhile, H. pylori has developed mechanisms to evade the host immune response in order to maintain the persistent infection, including interference with macrophage phagocytosis and antigen presentation, as well as induction of macrophage apoptosis. Consequently, the interaction between H. pylori and macrophages can significantly impact the progression, pathogenesis, and resolution of H. pylori infection. Moreover, macrophages are emerging as potential therapeutic targets for H. pylori-associated gastritis. Therefore, elucidating the involvement of macrophages in H. pylori infection may provide novel insights into the pathogenesis, progression, and management of H. pylori-related disease.

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Data availability

No datasets were generated or analysed during the current study.

Abbreviations

H. pylori :

Helicobacter pylori

ROS:

Reactive oxygen species

NO:

Nitric oxide

CAG:

Chronic atrophic gastritis

IM:

Intestinal metaplasia

CG:

Gastric adenocarcinoma

IL:

Interleukin

IFN-γ:

Interferon gamma

TNF-α:

Tumor necrosis factor alpha

COX-2:

Cyclooxygenase-2

PRRs:

Pattern recognition receptor proteins

TLRs:

Toll-like receptors

NODs:

Nucleotide-binding oligomeric domains

NLRs:

NOD-like receptors

PAMPs:

Pathogen-associated molecular patterns

MyD88:

Bone marrow differentiation primary response 88

PG:

Peptidoglycan

TRIF:

TIR domain-containing adaptor-induced interferon-β

IRFs:

Interferon regulators

TRAF:

Tumor necrosis factor receptor-associated factor

iNOS:

Inducible nitric oxide synthase

TGF-β:

Transforming growth factor-β

Arg-1:

Arginase-1

TRPM2:

Transient receptor potential melastatin 2

cagPAI:

Cytotoxin-associated gene pathogenicity island

T4SS:

Type 4 secretion system

BRD4:

Bromopolyamine protein 4

HO-1:

Heme oxygenase-1

SP1:

Specificity protein 1

LCN2:

Lipocalin 2

miRNAs:

MicroRNAs

LECT2:

Leukocyte cell-derived chemotaxin 2

SMO:

Spermine oxidase

CTH:

Cystathionine γ-lyase

VacA:

Vacuolating cytotoxin A

CGT:

Cholesterol-α-glucosyltransferase

CG:

Cholesterol-α-glucoside

APCs:

Antigen-presenting cells

HLA II:

Human leukocyte antigen class II

Th:

T helper

MHC:

Major histocompatibility complex

CIITA:

Class II transactivator

PA:

Patchouli alcohol

PAO1:

Polyamine oxidase 1

ODC:

Ornithine decarboxylase

BMDMs:

Bone marrow-derived macrophages

HMDMs:

Human monocyte-derived macrophages

Hoph:

H.pylori outer membrane protein H

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Acknowledgements

The work was financially supported by grants from National Natural Science Foundation of China (Grant No. 81970496). The figures are edited on the Figdraw website (https://www.figdraw.com/).

Funding

The work was financially supported by grants from National Natural Science Foundation of China (Grant No. 81970496).

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Yan-Fei Wei conceived and designed this study. Shu-Tian Zhang and Si-An **e edited and revised the manuscript. All authors have contributed to the manuscript and approved the final version.

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Wei, YF., **e, SA. & Zhang, ST. Current research on the interaction between Helicobacter pylori and macrophages. Mol Biol Rep 51, 497 (2024). https://doi.org/10.1007/s11033-024-09395-8

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