Transforming growth factor-β: an important mediator in Helicobacter pylori-associated pathogenesis

Li, Nianshuang; Xie, Chuan; Lü, Nonghua

doi:10.3389/fcimb.2015.00077

Cited by 29 publications

(22 citation statements)

References 95 publications

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“…TGF-ß has an important role in mediating inflammation in gastric cancer. Helicobacter pylori-associated inflammation is mainly induced by TGF-ß [ 55 ]. In addition, TGF-ß plays an important role in epithelial-mesenchymal transition of gastric cancer cells [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

Inflammatory cytokines are associated with response and prognosis in patients with esophageal cancer

et al. 2017

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BackgroundEsophageal cancer is often marked by aggressive tumor growth and poor prognosis. Patient groups who benefit from perioperative therapy are not yet defined. The tumor microenvironment and circulating factors as possible predictors of response and prognosis gain interest. This study aimed to investigate cytokines in patients’ serum and tumor tissue with regard to response and prognosis.ResultsMedian survival between SCC and AC was not different (published previously). Lower levels of CCL11 (Eotaxin-1) and CXCL10 (IP-10) in the tumor tissue were associated with a better prognosis (p = 0.022; p = 0.002). In the AC subgroup higher concentrations of TGF-β3 in serum and corresponding tumor tissue were associated with adverse prognosis (p = 0.035; p = 0.006). An association with histopathological response was found for IL-12(p70) and CXCL10 in patients’ sera (p = 0.041; p = 0.032). The tissue levels of TGF-β1 and TGF-β2 were significantly lower in histopathological responders than in nonresponders (p = 0.033; p = 0.007). A similar trend was seen for TGF-β3, without statistical significance (p = 0.097).Materials and MethodsPreoperative serum samples and corresponding tumor tissue (n = 54), only serum (n = 20) or only tissue (n = 4) were collected from patients undergoing surgery for cT3/4 esophageal squamous cell cancer (SCC) (n = 34) and adenocarcinoma (AC) (n = 44). All samples were taken after neoadjuvant treatment. All patients received perioperative chemo(radio)therapy. Cytokine levels of 17 different cytokines were measured by multiplex immunoassay and correlated with clinicopathological factors.ConclusionsTwo chemokines (CCL11 and CXCL10) in posttherapeutic tumor tissue were associated with prognosis in patients with esophageal cancer, lower levels indicating a better prognosis. Lower levels of TGF-β were associated with better response and prognosis in patients with AC.

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Section: Discussionmentioning

confidence: 99%

Inflammatory cytokines are associated with response and prognosis in patients with esophageal cancer

et al. 2017

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“…The TGF-β/TGF-β-RII signalling pathway has been show to comprise a tumour suppressor pathway (Hahm et al, 2002;Takeno et al, 2002) deregulated in gastric cancer (Li et al, 2015). Dominant negative mutant TGF-β-RII mice infected by H. pylori has been shown to present greater cell proliferation, and to develop gastric adenocarcinoma in the same time frame that wild type mice develop chronic gastritis only.…”

Section: Discussionmentioning

confidence: 99%

Interaction between inflammatory mediators and miRNAs in Helicobacter pylori infection

Rossi

Cadamuro

Biselli

et al. 2016

Cellular Microbiology

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Summary Helicobacter pylori cause chronic inflammation favouring gastric carcinogenesis, and its eradication may prevent malignant transformation. We evaluated whether H. pylori infection and its eradication modify the expression of inflammatory mediators in patients with chronic gastritis. Furthermore, we assessed whether microRNAs modulate inflammatory pathways induced by H. pylori and identified miRNA–gene interaction networks. mRNA and protein expression of TNFA, IL6, IL1B, IL12A, IL2 and TGFBRII and miRNAs miR‐103a‐3p, miR‐181c‐5p, miR‐370‐3p, miR‐375 and miR‐223‐3p were evaluated in tissue samples from 20 patients with chronic gastritis H. pylori negative (Hp−) and 31 H. pylori positive (Hp+), before and three months after bacterium eradication therapy, in comparison with a pool of Hp− normal gastric mucosa. Our results showed that H. pylori infection leads to up‐regulation of TNFA, IL6, IL12A and IL2 and down‐regulation of miRNAs. Bacterium eradication reduces the expression of TNFA and IL6 and up‐regulates TGFBRII and all investigated miRNAs, except miR‐223‐3p. Moreover, transcriptional profiles of inflammatory mediators and miRNAs after eradication are different from the non‐infected group. Deregulated miRNA–mRNA interaction networks were observed in the Hp+ group before and after eradication. Therefore, miRNAs modulated cytokine expression in the presence of H. pylori and after its eradication, suggesting that miRNAs participate in the pathological process triggered by H. pylori in the gastric mucosa.

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“…56 In the canonical signaling pathway, binding of mature TGF-β1 to either TGF-βRIII or the heterodimeric receptor consisting of the TGF-βRI and TGF-βRII subunits results in the dimerization of SMAD2 and SMAD3, which subsequently form a complex with SMAD4 that can translocate to the nucleus and induce gene transcription. 57 Non-canonical signaling is mediated by various kinase pathways, including the Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and extracellular signal-regulated kinase (ERK) pathways. 57 TGF-β1 signaling is critical for Treg cell differentiation due to its ability to induce Foxp3 gene expression.…”

Section: Immunomodulatory Pathwaysmentioning

confidence: 99%

Immunomodulatory Bonds of the Partnership between Dendritic Cells and T Cells

Bourque

Hawiger

2018

Crit Rev Immunol

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By acquiring, processing, and presenting both foreign and self-antigens, dendritic cells (DCs) initiate T cell activation that is shaped through the immunomodulatory functions of a variety of cell-membrane-bound molecules including BTLA-HVEM, CD40-CD40L, CTLA-4-CD80/CD86, CD70-CD27, ICOS-ICOS-L, OX40-OX40L, and PD-L1-PD-1, as well as several key cytokines and enzymes such as interleukin-6 (IL-6), IL-12, IL-23, IL-27, transforming growth factor-beta 1 (TGF-β1), retinaldehyde dehydrogenase (Raldh), and indoleamine 2,3-dioxygenase (IDO). Some of these distinct immunomodulatory signals are mediated by specific subsets of DCs, therefore contributing to the functional specialization of DCs in the priming and regulation of immune responses. In addition to responding to the DC-mediated signals, T cells can reciprocally modulate the immunomodulatory capacities of DCs, further refining immune responses. Here, we review recent studies, particularly in experimental mouse systems, that have delineated the integrated mechanisms of crucial immunomodulatory pathways that enable specific populations of DCs and T cells to work intimately together as single functional units that are indispensable for the maintenance of immune homeostasis.

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Transforming growth factor-β: an important mediator in Helicobacter pylori-associated pathogenesis

Cited by 29 publications

References 95 publications

Inflammatory cytokines are associated with response and prognosis in patients with esophageal cancer

Inflammatory cytokines are associated with response and prognosis in patients with esophageal cancer

Interaction between inflammatory mediators and miRNAs in Helicobacter pylori infection

Immunomodulatory Bonds of the Partnership between Dendritic Cells and T Cells

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