Innate Immunity Crosstalk with Helicobacter pylori: Pattern Recognition Receptors and Cellular Responses

Cheok, Yi Ying; Tan, Guan Huat; Lee, Chalystha Yie Qin; Abdullah, Suhailah; Looi, Chung Yeng; Wong, Won Fen

doi:10.3390/ijms23147561

Cited by 16 publications

(13 citation statements)

References 83 publications

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“…H. pylori infection triggers activation of the innate immune system in the host through recognition by multiple PRRs including TLRs [ 36 ]. Although both TLR7 and TLR8 are well established as viral RNA sensors, the role of TLR8 in bacterial RNA recognition has only begun to be uncovered in the past decade [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling

Lee

Chan

Cheok

et al. 2022

Journal of Immunology Research

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Helicobacter pylori colonization and persistence could precede gastric adenocarcinoma. Elucidating immune recognition strategies of H. pylori is therefore imperative to curb chronic persistence in the human host. Toll-like receptor 7 (TLR7) and TLR8 are widely known as viral single-stranded RNA (ssRNA) sensors yet less studied in the bacteria context. Here, we investigated the involvement of these receptors in the immunity to H. pylori. Human THP-1 monocytic cells were infected with H. pylori, and the expression levels of human Toll-like receptors (TLRs) were examined. The roles of TLR7 and TLR8 in response to H. pylori infection were further investigated using receptor antagonists. Among all TLR transcripts examined, TLR8 exhibited the most prominent upregulation, followed by TLR7 in the THP-1 cells infected with H. pylori J99 or SS1 strains. H. pylori infection-mediated IFN-α and IFN-β transactivation was significantly abrogated by the TLR7/8 (but not TLR7) antagonist. Additionally, TLR7/8 antagonist treatment reduced H. pylori infection-mediated phosphorylation of interferon regulatory factor 7 (IRF7). Our study suggests a novel role of TLR8 signaling in host immunity against H. pylori through sensing live bacteria to elicit the production of type I interferon.

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Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling

Lee

Chan

Cheok

et al. 2022

Journal of Immunology Research

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“…Besides, H. pylori promotes mitochondrial membrane depolarisation and hydrogen peroxide secretion which induce apoptotic program in macrophages (267, 268). Persisting a life-long H. pylori infection in the host depends on the inhibition of macrophage-mediated functions including phagocytosis, human leukocyte antigen-II (HLA-II) expression and IFN-γ production which results in T-cell suppression (269). Via the glucosylation of cholesterol, H. pylori escapes from macrophage phagocytosis and could survive (270).…”

Section: Interaction Between H Pylori and The Human Host Immune Syste...mentioning

confidence: 99%

Helicobacter pylorivirulence factors: subversion of host immune system and development of various clinical outcomes

Mohammadzadeh,

Menbari,

Pishdadian

et al. 2023

Expert Rev. Mol. Med.

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Helicobacter pylori (H. pylori) is a worldwide spread bacterium, co-evolving with humans for at least 100 000 years. Despite the uncertainty about the mode of H. pylori transmission, the development of intra-gastric and extra-gastric diseases is attributed to this bacterium. The morphological transformation and production of heterogenic virulence factors enable H. pylori to overcome the harsh stomach environment. Using numerous potent disease-associated virulence factors makes H. pylori a prominent pathogenic bacterium. These bacterial determinants are adhesins (e.g., blood group antigen-binding adhesin (BabA)/sialic acid-binding adhesin (SabA)), enzymes (e.g., urease), toxins (e.g., vacuolating cytotoxin A (VacA)), and effector proteins (e.g., cytotoxin-associated gene A (CagA)) involved in colonisation, immune evasion, and disease induction. H. pylori not only cleverly evades the immune system but also robustly induces immune responses. This insidious bacterium employs various strategies to evade human innate and adaptive immune responses, leading to a life-long infection. Owing to the alteration of surface molecules, innate immune receptors couldn't recognise this bacterium; moreover, modulation of effector T cells subverts adaptive immune response. Most of the infected humans are asymptomatic and only a few of them present severe clinical outcomes. Therefore, the identification of virulence factors will pave the way for the prediction of infection severity and the development of an effective vaccine. H. pylori virulence factors are hereby comprehensively reviewed and the bacterium evasion from the immune response is properly discussed.

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“…Innate immune cells, such as neutrophils, macrophages, and dendritic cells (DCs) are activated through direct interaction with H. pylori components or through activated GECs, resulting in the secretion of proinflammatory cytokines, such as Interleukin (IL‐8) and IL‐1β. Tregs are activated to increase IL‐10 secretion, leading to bacterial persistence 27 . Helicobacter pylori can alter several proinflammatory signaling pathways to sustain stomach inflammation 25 .…”

Section: B7 Family During Helicobacter Pylori Infectionmentioning

confidence: 99%

“…26 Helicobacter pylori components and virulence factors are recognized by human pattern recognition receptors (PRRs) expressed on innate immune cells or GECs, the first step in immune activation elicited by H. pylori. 27 For GECs, recognition initiates downstream signaling pathways, promoting apoptosis and proliferation TA B L E 1 B7 family member function and expression upon Helicobacter pylori infection. and inhibiting the regeneration thereof.…”

Section: B7 Family During H Elicobac Ter Pylori Infec Ti Onmentioning

confidence: 99%

The expression and function of the B7 family in Helicobacter pylori infection and gastric carcinogenesis process

Zhang

Zhao

et al. 2023

Helicobacter

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Gastric cancer (GC) was the fifth most common cancer and the fourth leading cause of cancer-related deaths worldwide in 2020. 1 In 2010-2014, the 5-year-survival was very high in Korea (69%) and Japan (60%), but in China, it was only 35.9%, 2 where initial asymptomatic development and subsequent nonspecific symptoms result in a diagnosis at advanced stages with a poor prognosis. Assuming that the current incidence rates remain the same, the annual number of new GC cases are predicted to increase from 1.09 million cases to 1.77 million cases by 2040. 3 Helicobacter pylori is an important GC risk factor. 4 The Correa model 5 demonstrates the progression of human gastric carcinogenesis from the normal gastric mucosa to cancer. Persistent H. pylori

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Innate Immunity Crosstalk with Helicobacter pylori: Pattern Recognition Receptors and Cellular Responses

Cited by 16 publications

References 83 publications

Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling

Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling

Helicobacter pylorivirulence factors: subversion of host immune system and development of various clinical outcomes

The expression and function of the B7 family in Helicobacter pylori infection and gastric carcinogenesis process

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