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

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 (ssR...

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Main Authors: Chalystha Yie Qin Lee, Yee Teng Chan, Yi Ying Cheok, Grace Min Yi Tan, Ting Fang Tang, Heng Choon Cheong, Jamuna Vadivelu, Suhailah Abdullah, Chung Yeng Looi, Won Fen Wong
Format: Article
Language:English
Published: Wiley 2022-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2022/3861518
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author Chalystha Yie Qin Lee
Yee Teng Chan
Yi Ying Cheok
Grace Min Yi Tan
Ting Fang Tang
Heng Choon Cheong
Jamuna Vadivelu
Suhailah Abdullah
Chung Yeng Looi
Won Fen Wong
author_facet Chalystha Yie Qin Lee
Yee Teng Chan
Yi Ying Cheok
Grace Min Yi Tan
Ting Fang Tang
Heng Choon Cheong
Jamuna Vadivelu
Suhailah Abdullah
Chung Yeng Looi
Won Fen Wong
author_sort Chalystha Yie Qin Lee
collection DOAJ
description 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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issn 2314-7156
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publishDate 2022-01-01
publisher Wiley
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series Journal of Immunology Research
spelling doaj-art-c0a628dff8ea4f7fa1d12633525267a22025-02-03T06:12:26ZengWileyJournal of Immunology Research2314-71562022-01-01202210.1155/2022/3861518Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 SignalingChalystha Yie Qin Lee0Yee Teng Chan1Yi Ying Cheok2Grace Min Yi Tan3Ting Fang Tang4Heng Choon Cheong5Jamuna Vadivelu6Suhailah Abdullah7Chung Yeng Looi8Won Fen Wong9Department of Medical MicrobiologyDepartment of Medical MicrobiologyDepartment of Medical MicrobiologyDepartment of Medical MicrobiologyDepartment of Medical MicrobiologyDepartment of Medical MicrobiologyDepartment of Medical MicrobiologyDepartment of MedicineSchool of BioscienceDepartment of Medical MicrobiologyHelicobacter 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.http://dx.doi.org/10.1155/2022/3861518
spellingShingle Chalystha Yie Qin Lee
Yee Teng Chan
Yi Ying Cheok
Grace Min Yi Tan
Ting Fang Tang
Heng Choon Cheong
Jamuna Vadivelu
Suhailah Abdullah
Chung Yeng Looi
Won Fen Wong
Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling
Journal of Immunology Research
title Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling
title_full Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling
title_fullStr Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling
title_full_unstemmed Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling
title_short Helicobacter pylori Infection Elicits Type I Interferon Response in Human Monocytes via Toll-Like Receptor 8 Signaling
title_sort helicobacter pylori infection elicits type i interferon response in human monocytes via toll like receptor 8 signaling
url http://dx.doi.org/10.1155/2022/3861518
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