O014 Podoplanin (GP38), a marker of synovial inflammation, is an excellent therapeutic target in mouse collagen-induced arthritis

Desanti, GE; Saghir, AN; Naylor, AJ; Kemble, Samuel; Falconer, Jane; Wehmeyer, Corinna; Marshall, J. T. W.; Nakamura, Keizo; Goodall, Margaret; Navarro-Núñez, Leyre; Watson, SP; Buckley, Christopher D.

doi:10.1136/annrheumdis-2018-ewrr2018.14

Cited by 5 publications

(4 citation statements)

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“…The second cluster contains genes that have been associated with the anti-inflammatory responses (Arg1, Spp1, Nqo1, Met, Il1rn, Slc7a2, Nt5e, Chst11, and Pdpn). [39][40][41][42][43][44][45][46][47] These gene were expressed at low levels on the unmodified PDMS surfaces. The opposite response was observed for the expression of these gene clusters on the Z2-Y12 modified surfaces.…”

Section: Lipids Directly Modulate the Transcriptome Of Macrophages Ex...mentioning

confidence: 99%

Lipid Deposition Profiles Influence Foreign Body Responses

et al. 2023

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Fibrosis remains a significant cause of failure in implanted biomedical devices and early absorption of proteins on implant surfaces has been shown to be a key instigating factor. However, lipids can also regulate immune activity and their presence may also contribute to biomaterial‐induced foreign body responses (FBR) and fibrosis. Here it is demonstrated that the surface presentation of lipids on implant affects FBR by influencing reactions of immune cells to materials as well as their resultant inflammatory/suppressive polarization. Time‐of‐flight secondary ion mass spectroscopy (ToF‐SIMS) is employed to characterize lipid deposition on implants that are surface‐modified chemically with immunomodulatory small molecules. Multiple immunosuppressive phospholipids (phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine, and sphingomyelin) are all found to deposit preferentially on implants with anti‐FBR surface modifications in mice. Significantly, a set of 11 fatty acids is enriched on unmodified implanted devices that failed in both mice and humans, highlighting relevance across species. Phospholipid deposition is also found to upregulate the transcription of anti‐inflammatory genes in murine macrophages, while fatty acid deposition stimulated the expression of pro‐inflammatory genes. These results provide further insights into how to improve the design of biomaterials and medical devices to mitigate biomaterial material‐induced FBR and fibrosis.

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Section: Lipids Directly Modulate the Transcriptome Of Macrophages Ex...mentioning

confidence: 99%

Lipid Deposition Profiles Influence Foreign Body Responses

et al. 2023

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“…PDPN has been studied in cancer as a therapeutic target by using antibodies or antagonistic peptides [ 61 , 62 ]. In RA, Christopher D Buckley et al reported in 2018 that anti-PDPN antibodies efficiently protected mice with CIA from arthritis [ 63 ]. THY-1 (CD90) is a highly N-glycosylated, glycosylphosphatidylinositol (GPI)-anchored cell surface protein, first identified for the recognition of thymoma cells, and was found to be expressed on various types of cells, such as mesenchymal stem cells (MSCs) [ 64 ].…”

Section: Strategies For Targeting Pathogenic Fls Subsets In Ramentioning

confidence: 99%

Targeting pathogenic fibroblast-like synoviocyte subsets in rheumatoid arthritis

Qian,

Deng,

Chen

et al. 2024

Arthritis Res Ther

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Fibroblast-like synoviocytes (FLSs) play a central role in RA pathogenesis and are the main cellular component in the inflamed synovium of patients with rheumatoid arthritis (RA). FLSs are emerging as promising new therapeutic targets in RA. However, fibroblasts perform many essential functions that are required for sustaining tissue homeostasis. Direct targeting of general fibroblast markers on FLSs is challenging because fibroblasts in other tissues might be altered and side effects such as reduced wound healing or fibrosis can occur. To date, no FLS-specific targeted therapies have been applied in the clinical management of RA. With the help of high-throughput technologies such as scRNA-seq in recent years, several specific pathogenic FLS subsets in RA have been identified. Understanding the characteristics of these pathogenic FLS clusters and the mechanisms that drive their differentiation can provide new insights into the development of novel FLS-targeting strategies for RA. Here, we discuss the pathogenic FLS subsets in RA that have been elucidated in recent years and potential strategies for targeting pathogenic FLSs.

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“…It has been identified that H. pylori induces expression of an inflammatory protein, podoplanin, via LPS to induce strong proinflammatory IL-1β secretion from macrophages [88]. Podoplanin has been proposed as a treatment target in chronic inflammatory rheumatoid arthritis [89]. Hence, it is not too far-fetched to explore this possibility in the treatment of H. pylori chronic infection.…”

Section: Targeting H Pylori Virulence and Pathogenesis In Treatment And Vaccine Developmentmentioning

confidence: 99%

An Overview of Helicobacter pylori Survival Tactics in the Hostile Human Stomach Environment

et al. 2021

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Helicobacter pylori is well established as a causative agent for gastritis, peptic ulcer, and gastric cancer. Armed with various inimitable virulence factors, this Gram-negative bacterium is one of few microorganisms that is capable of circumventing the harsh environment of the stomach. The unique spiral structure, flagella, and outer membrane proteins accelerate H. pylori movement within the viscous gastric mucosal layers while facilitating its attachment to the epithelial cells. Furthermore, secretion of urease from H. pylori eases the acidic pH within the stomach, thus creating a niche for bacteria survival and replication. Upon gaining a foothold in the gastric epithelial lining, bacterial protein CagA is injected into host cells through a type IV secretion system (T4SS), which together with VacA, damage the gastric epithelial cells. H. pylori does not only establishes colonization in the stomach, but also manipulates the host immune system to permit long-term persistence. Prolonged H. pylori infection causes chronic inflammation that precedes gastric cancer. The current review provides a brief outlook on H. pylori survival tactics, bacterial-host interaction and their importance in therapeutic intervention as well as vaccine development.

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O014 Podoplanin (GP38), a marker of synovial inflammation, is an excellent therapeutic target in mouse collagen-induced arthritis

Cited by 5 publications

References 3 publications

Lipid Deposition Profiles Influence Foreign Body Responses

Lipid Deposition Profiles Influence Foreign Body Responses

Targeting pathogenic fibroblast-like synoviocyte subsets in rheumatoid arthritis

An Overview of Helicobacter pylori Survival Tactics in the Hostile Human Stomach Environment

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