High plasma sST2 levels in gastric cancer and their association with metastatic disease

Bergis, Dominik; Kassis, Valentin; Radeke, Heinfried H.

doi:10.3233/cbm-150547

Cited by 23 publications

(26 citation statements)

References 29 publications

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“…In line with previous findings in other cancers, like myeloproliferative disorders, hepatic cancer, and breast cancer, we found increased serum concentrations of ST2 in MF. Moreover, ST2 concentrations were significantly higher in more advanced stages of MF.…”

Section: Discussionsupporting

confidence: 92%

Interleukin‐33 polymorphisms and serum concentrations in mycosis fungoides

et al. 2019

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Background Mycosis fungoides (MF) skin lesions are characterized by low-grade inflammation, which may be sustained by proinflammatory cytokines as probably interleukin-33 (IL-33). We compared serum concentrations of IL-33 and its receptor ST2 and the frequency of selected IL-33 single nucleotide polymorphisms (SNPs) between patients with MF and healthy controls.Methods In 88 patients with MF and 66 healthy controls, we analyzed SNPs in the 9894 and 11877 loci of the IL-33 gene. Moreover, we measured serum concentrations of IL-33 and its receptor ST2.Results There were no statistically significant differences in the frequencies of both IL-33 SNPs between patients and controls. Compared with controls, patients with MF had similar IL-33 serum concentrations (P = 0.71) but significantly increased ST2 concentrations (P < 0.001). Patients in MF-IA stage had significantly lower ST2 serum concentrations than those with the remaining MF stages (P = 0.002). The studied variables were not related to pruritus severity. Patients with the C(+) IL-33 11877 SNP had lower ST2 serum concentrations than patients with the C(À) 11877 SNP (P = 0.043).Conclusions It was published before that the knockout of the ST2 gene after injection of IL-33 is associated with a reduced inflammatory reaction in the skin, as well as that IL-33 plays a role in allergic and neoplastic disorders. Concerning the difference in ST2 concentration between control and MF group, and C IL-33 11877 SNP possibly influencing the ST2 concentration, the role of IL-33/ST2 signaling, needs further studies.

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Section: Discussionsupporting

confidence: 92%

Interleukin‐33 polymorphisms and serum concentrations in mycosis fungoides

et al. 2019

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“…This suggests a link between sST2 levels and immune response involving CD8 + T-cell expansion during EHI. In addition, we investigated whether using IL-33/sST2 ratio may represent a better marker of disease progression [ 27 ]; and this ratio did not improve the link with disease progression (data not shown).…”

Section: Resultsmentioning

confidence: 99%

The plasma levels of soluble ST2 as a marker of gut mucosal damage in early HIV infection

Mehraj

Jenabian

Ponte

et al. 2016

Aids

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Objective:Following tissue barrier breaches, interleukin-33 (IL-33) is released as an ‘alarmin’ to induce inflammation. Soluble suppression of tumorigenicity 2 (sST2), as an IL-33 decoy receptor, contributes to limit inflammation. We assessed the relationship between the IL-33/ST2 axis and markers of gut mucosal damage in patients with early (EHI) and chronic HIV infection (CHI) and elite controllers.Design:Analyses on patients with EHI and CHI were conducted to determine IL-33/sST2 changes over time.Methods:IL-33 and sST2 levels were measured in plasma. Correlations between sST2 levels and plasma viral load, CD4+ and CD8+ T-cell counts, expression of T-cell activation/exhaustion markers, gut mucosal damage, microbial translocation and inflammation markers, as well as kynurenine/tryptophan ratio were assessed.Results:Plasma sST2 levels were elevated in EHI compared with untreated CHI and uninfected controls, whereas IL-33 levels were comparable in all groups. In EHI, sST2 levels were positively correlated with the CD8+ T-cell count and the percentage of T cells expressing activation and exhaustion markers, but not with viral load or CD4+ T-cell count. Plasma sST2 levels also correlated with plasma levels of gut mucosal damage, microbial translocation and kynurenine/tryptophan ratio and for some markers of inflammation. Prospective analyses showed that early antiretroviral therapy had no impact on sST2 levels, whereas longer treatment duration initiated during CHI normalized sST2.Conclusion:As sST2 levels were elevated in EHI and were correlated with CD8+ T-cell count, immune activation, and microbial translocation, sST2 may serve as a marker of disease progression, gut damage and may directly contribute to HIV pathogenesis.

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“…Lysophosphatidic acid has also been shown to increase sST2 production by human bronchial epithelial cells in an NF-κB- or JNK-dependent manner (66). Enhanced sST2 plasma circulation has been correlated with pulmonary fibrosis (67), acute myocardial infarction (39), subclinical brain injury and stroke (68), celiac disease (69), gastric cancer (70), HBV-related acute-on-chronic liver failure (71), HIV progression (72), and GVHD (17–24). …”

Section: St2/il-33 Signalingmentioning

confidence: 99%

The ST2/IL-33 Axis in Immune Cells during Inflammatory Diseases

2017

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Il1rl1 (also known as ST2) is a member of the IL-1 superfamily, and its only known ligand is IL-33. ST2 exists in two forms as splice variants: a soluble form (sST2), which acts as a decoy receptor, sequesters free IL-33, and does not signal, and a membrane-bound form (ST2), which activates the MyD88/NF-κB signaling pathway to enhance mast cell, Th2, regulatory T cell (Treg), and innate lymphoid cell type 2 functions. sST2 levels are increased in patients with active inflammatory bowel disease, acute cardiac and small bowel transplant allograft rejection, colon and gastric cancers, gut mucosal damage during viral infection, pulmonary disease, heart disease, and graft-versus-host disease. Recently, sST2 has been shown to be secreted by intestinal pro-inflammatory T cells during gut inflammation; on the contrary, protective ST2-expressing Tregs are decreased, implicating that ST2/IL-33 signaling may play an important role in intestinal disease. This review will focus on what is known on its signaling during various inflammatory disease states and highlight potential avenues to intervene in ST2/IL-33 signaling as treatment options.

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High plasma sST2 levels in gastric cancer and their association with metastatic disease

Abstract: Soluble ST2 is associated with advanced and metastatic disease in GC patients and significantly correlates with the duration of the disease. The IL-33/sST2 ratio may offer a new, interesting approach in identifying GC patients.

Cited by 23 publications

References 29 publications

Interleukin‐33 polymorphisms and serum concentrations in mycosis fungoides

Interleukin‐33 polymorphisms and serum concentrations in mycosis fungoides

The plasma levels of soluble ST2 as a marker of gut mucosal damage in early HIV infection

The ST2/IL-33 Axis in Immune Cells during Inflammatory Diseases

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