NOD1 is required for<i>Helicobacter pylori</i>induction of IL-33 responses in gastric epithelial cells

Tran, Le Son; Tran, Darren; Paoli, Amanda De; D’Costa, Kimberley; Creed, Sarah J.; Ng, Garrett Z.; Le, Lena; Sutton, Philip; Nachbur, Ueli; Ferrero, Richard L.

doi:10.1111/cmi.12826

Cited by 30 publications

(47 citation statements)

References 45 publications

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“…26 Consistent with this finding, chronic H pylori infection in Nod1 +/+ mice was associated with enhanced Th2 responses, as characterized by increased levels of gastric IL-33 and splenic interleukin-13 (IL-13) production, but decreased IFN-γ production, when compared with Nod1 −/− animals. 1,2 Specifically, H pylori activation of NOD1 signaling, via its adaptor protein receptor-interacting serine-threonine kinase 2 (RIPK2), was found to promote epithelial cell production of processed interleukin-33 (IL-33), which is associated with a Th2 signature.…”

Section: Downregulation Of Host Immune Responses and Induction Of Tsupporting

confidence: 61%

“…1,2 Specifically, H pylori activation of NOD1 signaling, via its adaptor protein receptor-interacting serine-threonine kinase 2 (RIPK2), was found to promote epithelial cell production of processed interleukin-33 (IL-33), which is associated with a Th2 signature. 26 Consistent with this finding, chronic H pylori infection in Nod1 +/+ mice was associated with enhanced Th2 responses, as characterized by increased levels of gastric IL-33 and splenic interleukin-13 (IL-13) production, but decreased IFN-γ production, when compared with Nod1 −/− animals. 26 Thus, NOD1-driven IL-33 production during chronic H pylori infection may protect against excessive inflammatory responses and favor bacterial persistence.…”

Section: Downregulation Of Host Immune Responses and Induction Of Tsupporting

confidence: 61%

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Review: Helicobacter: Inflammation, immunology, and vaccines

Lehours

Ferrero

2019

Helicobacter

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Chronic inflammation induced by Helicobacter pylori infection is a critical factor in the development of peptic ulcer disease and gastric cancer. Central to this inflammation is the initiation of pro‐inflammatory signaling cascades within epithelial cells, in particular those mediated by two sensors of bacterial cell wall components, nucleotide‐binding oligomerization domain‐containing protein 1 (NOD1) and alpha‐protein kinase 1 (ALPK1). H pylori is, however, also highly adept at mitigating inflammation in the host, thereby restricting tissue damage and favoring bacterial persistence. H pylori modulates host immune responses by altering cytokine signaling in epithelial and myeloid cells, which results in increased proliferation of regulatory T cells and downregulation of effector T‐cell responses. H pylori vacuolating cytotoxin A (VacA) has been shown to play an important role in the dampening of immune responses and induction of immune tolerance capable of protecting against asthma. It is also possible to generate protective immune responses by immunization with various H pylori antigens or their epitopes, in combination with an adjuvant, though this for now has only been shown in mouse models. Novel non‐toxic adjuvants, consisting of modified bacterial enterotoxins or nanoparticles, have recently been developed that may not only enhance vaccine efficacy, but also help translate candidate vaccines to the clinic. This review will summarize the main discoveries in the past year regarding host immune responses to H pylori infection, as well as the design of new vaccine approaches against this infection.

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Section: Downregulation Of Host Immune Responses and Induction Of Tsupporting

confidence: 61%

Section: Downregulation Of Host Immune Responses and Induction Of Tsupporting

confidence: 61%

Review: Helicobacter: Inflammation, immunology, and vaccines

Lehours

Ferrero

2019

Helicobacter

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“…Indeed, the mouse GEC line GSM06 infected with H. pylori releases the anti‐inflammatory cytokine IL‐33 by a NOD1‐dependent pathway; this was confirmed in primary GECs from wild type (WT) and Nod1 ‐deficient mice . Similar to that, the human AGS cells transfected with shRNA specific for NOD1 or with a NOD1 knockout using CRISPR/Cas9 technology failed to produce IL‐33 in response to H. pylori . As expected, the NOD1‐dependent production of IL‐33 was orchestrated by a functional T4SS .…”

Section: Inflammationsupporting

confidence: 66%

“…Nod1-deficient mice. 15 Similar to that, the human AGS cells transfected with shRNA specific for NOD1 or with a NOD1 knockout using CRISPR/Cas9 technology failed to produce IL-33 in response to H. pylori. 15 As expected, the NOD1-dependent production of IL-33 was orchestrated by a functional T4SS.…”

Section: Regulation Of Inflammation By Cellular Receptorsmentioning

confidence: 55%

“…Tran et al investigated whether NOD1 can also dampen the inflammatory response by inducing the cytokine IL‐33. Indeed, the mouse GEC line GSM06 infected with H. pylori releases the anti‐inflammatory cytokine IL‐33 by a NOD1‐dependent pathway; this was confirmed in primary GECs from wild type (WT) and Nod1 ‐deficient mice . Similar to that, the human AGS cells transfected with shRNA specific for NOD1 or with a NOD1 knockout using CRISPR/Cas9 technology failed to produce IL‐33 in response to H. pylori .…”

Section: Inflammationmentioning

confidence: 63%

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Helicobacter: Inflammation, immunology, and vaccines

et al. 2018

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Helicobacter pylori infection induces a chronic gastric inflammation which can lead to gastric ulcers and cancer. The mucosal immune response to H. pylori is first initiated by the activation of gastric epithelial cells that respond to numerous bacterial factors, such as the cytotoxin-associated gene A or the lipopolysaccharide intermediate heptose-1,7-bisphosphate. The response of these cells is orchestrated by different receptors including the intracellular nucleotide-binding oligomerization domain-containing protein 1 or the extracellular epidermal growth factor receptor. This nonspecific response leads to recruitment and activation of various myeloid (macrophages and dendritic cells) and T cells (T helper-17 and mucosal-associated invariant T cells), which magnify and maintain inflammation. In this review, we summarize the major advances made in the past year regarding the induction, the regulation, and the role of the innate and adaptive immune responses to H. pylori infection. We also recapitulate efforts that have been made to develop efficient vaccine strategies.

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A new isolation method for bacterial extracellular vesicles providing greater purity and improved proteomic detection of vesicle proteins

Steele

Ying

et al. 2023

J of Extracellular Bio

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Contaminants within cell culture media often co-isolate with eukaryotic extracellular vesicles (EVs) thus affecting their biological properties. It has yet to be investigated if this is also true for bacterial EVs (BEVs), especially for organisms grown in complex culture media containing animal-derived products. To address this question, we isolated BEVs from the fastidious bacterium Helicobacter pylori grown in either standard Brain Heart Infusion (BHI) medium or BHI depleted of animal-derived products (D-BHI). We show that BEVs prepared from bacteria grown in D-BHI medium have similar morphologies, size ranges and yields to those prepared from standard medium. Similarly, no differences were found in the ability of H. pylori BEVs to induce IL-8 responses in epithelial cells. However, H. pylori BEVs prepared from D-BHI medium were of higher purity than those prepared from standard medium. Importantly, proteomic analyses detected 3.4-fold more H. pylori proteins and 10-fold fewer bovine-derived proteins in BEV samples prepared from D-BHI rather than the standard method. Fifty-seven H. pylori proteins were uniquely detected in BEV samples prepared from D-BHI. In conclusion, we have described an improved method for BEV isolation. Furthermore, we demonstrate how animal-derived products in bacteriological culture media may adversely affect proteomic analyses of BEVs. K E Y WO R D S bacterial extracellular vesicles, Helicobacter pylori, outer membrane vesicles, proteomics  INTRODUCTIONCells belonging to all three domains of life release spherical membrane-bound nanostructures, known as extracellular vesicles (EVs) (Gill et al., 2019). The EVs produced by bacteria (BEVs) are 20-400 nm in size and contain a range of products, such as proteins, nucleic acids, lipopolysaccharide and peptidoglycan, which may contribute to infection and to horizontal gene transfer (Gao & van der Veen, 2020;Kaparakis-Liaskos & Ferrero, 2015) BEVs are generally isolated by either ultracentrifugation or ultrafiltration, though both techniques result in relatively crude preparations (Klimentová & Stulík, 2015). Ultracentrifugation has been reported to promote vesicle and extra-vesicle proteinThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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NOD1 is required forHelicobacter pyloriinduction of IL-33 responses in gastric epithelial cells

Cited by 30 publications

References 45 publications

Review: Helicobacter: Inflammation, immunology, and vaccines

Review: Helicobacter: Inflammation, immunology, and vaccines

Helicobacter: Inflammation, immunology, and vaccines

A new isolation method for bacterial extracellular vesicles providing greater purity and improved proteomic detection of vesicle proteins

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