<i>Helicobacter pylori</i> and Antrum Erosion‐Specific Gene Expression Patterns: The Discriminative Role of CXCL13 and VCAM1 Transcripts

Galamb, Orsolya; Győrffy, Balázs; Sípos, Ferenc; Dinya, Elek; Krenács, Tibor; Berczi, Lajos; Szõke, Dominika; Spisák, Sándor; Solymosi, Norbert; Németh, A; Juhász, Márk; Molnár, Béla; Tulassay, Zsolt

doi:10.1111/j.1523-5378.2008.00584.x

Cited by 41 publications

(30 citation statements)

References 39 publications

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“…In H. pylori-associated gastritis, recruitment of T-and B cells, dendritic cells and neutrophil granulocytes is mediated by a variety of chemokines interacting with their cognate receptors such as CCR7, CCR5, CXCR1 and CXCR4 expressed on infiltrating immunological cells. 30,[36][37][38][39][40][41] Consistent with these findings, we also observed upregulated mRNA transcripts of CCR8, CCR9, CXCR3 and CXCR7.…”

Section: Discussionsupporting

confidence: 90%

Chemokine receptors in gastric MALT lymphoma: loss of CXCR4 and upregulation of CXCR7 is associated with progression to diffuse large B-cell lymphoma

et al. 2013

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Chemokine receptors have a crucial role in the development and progression of lymphoid neoplasms. To determine the chemokine receptor expression profile in gastric mucosa-associated lymphoid tissue (MALT) lymphoma, we performed an expression analysis of 19 chemokine receptors at mRNA levels by using real-time RT-PCR, as well as of five chemokine receptors-CCR8, CCR9, CXCR4, CXCR6 and CXCR7-by immunohistochemistry on human tissue samples of Helicobacter pylori-associated gastritis, gastric MALT lymphoma and gastric extranodal diffuse large B-cell lymphoma originating from MALT lymphoma (transformed MALT lymphoma). Following malignant transformation from H. pylori-associated gastritis to MALT lymphoma, an upregulation of CCR7, CXCR3 and CXCR7, and a loss of CXCR4 were detected. The transformation of gastric MALT lymphomas to gastric extranodal diffuse large B-cell lymphoma was accompanied by upregulation of CCR1, CCR5, CCR7, CCR8, CCR9, CXCR3, CXCR6, CXCR7 and XCR1. Remarkably, CXCR4 expression was exclusively found in nodal marginal B-cell lymphomas and nodal diffuse large B-cell lymphomas but not at extranodal manifestation sites, ie, in gastric MALT lymphomas or gastric extranodal diffuse large B-cell lymphomas. Furthermore, the incidence of bone marrow infiltration (16/51 with bone marrow involvement vs 35/51 with bone marrow involvement; Spearman q ¼ 0467 Po0.001) positively correlated with CXCR4 expression. CXCL12, the ligand of CXCR4 and CXCR7, was expressed by epithelial, endothelial and inflammatory cells, MALT lymphoma cells and was most strongly expressed by extranodal diffuse large B-cell lymphoma cells, suggesting at least in part an autocrine signaling pathway. Our data indicate that CXCR4 expression is associated with nodal manifestation and a more advanced stage of lymphomas and hence, might serve as useful clinical prognostic marker.

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Section: Discussionsupporting

confidence: 90%

Chemokine receptors in gastric MALT lymphoma: loss of CXCR4 and upregulation of CXCR7 is associated with progression to diffuse large B-cell lymphoma

et al. 2013

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“…Similar to IL-8, the chemokines CXCL1, CXCL2, and CXCL3 are involved in neutrophil attraction (51), whereas CCL20 attracts immature dendritic cells and memory T cells and plays a role in inflammation on mucosal surfaces (45). In support of previous reports (38,39,(41)(42)(43)(44)(45)(46), we detected increased levels of IL-8, CXCL1, CXCL2, CXCL3, and CCL20 in gastric antrum biopsies from patients infected with H. pylori compared with H. pylori-negative patients. Although ICAM1 expression was detected in all biopsy samples, no statistically significant difference was observed between the two patient groups.…”

Section: Discussionsupporting

confidence: 88%

“…CXCL2 and CXCL3 chemokine secretion was not assayed, because ELISA kits for these proteins were unavailable. Similarly to previous reports (38,39,(41)(42)(43)(44)(45)(46), we detected increased levels of IL-8, CXCL1, CXCL2, CXCL3, and CCL20 in gastric antrum biopsies from H. pylori-positive patients compared with H. pylori-negative patients (Supplemental Fig. 1).…”

Section: H Pylori Lps Induces Il-8 Expression Via Tlr2supporting

confidence: 89%

Tribbles 3: A Novel Regulator of TLR2-Mediated Signaling in Response to Helicobacter pylori Lipopolysaccharide

Smith

Moran

Duggan

et al. 2011

The Journal of Immunology

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Helicobacter pylori causes chronic gastritis, peptic ulcers, and gastric carcinoma. Gastric epithelial cells provide the first point of contact between H. pylori and the host. TLRs present on these cells recognize various microbial products, resulting in the initiation of innate immunity. Although previous reports investigated TLR signaling in response to intact H. pylori, the specific contribution of H. pylori LPS with regard to functional genomics and cell-signaling events has not been defined. This study set out to define downstream signaling components and altered gene expression triggered by H. pylori LPS and to investigate the role of the signaling protein tribbles 3 (TRIB3) during the TLR-mediated response to H. pylori LPS. Cotransfections using small interfering RNA and dominant-negative constructs demonstrated that H. pylori LPS functions as a classic TLR2 ligand by signaling through pathways involving the key TLR signaling components MyD88 adaptor-like, MyD88, IRAK1, IRAK4, TNFR-associated factor 6, IκB kinase β, and IκBα. Microarray analysis, real-time PCR, and ELISA revealed the induction of a discrete pattern of chemokines as a direct effect of LPS:TLR2 signaling. H. pylori infection was associated with decreased expression of TRIB3 in human gastric epithelial cell lines and tissue samples. Additionally, H. pylori decreased expression of C/EBP homologous protein and activating transcription factor 4, the transcription factors involved in the induction of TRIB3 expression. Furthermore, knockdown of TRIB3 and C/EBP homologous protein enhanced TLR2-mediated NF-κB activation and chemokine induction in response to H. pylori LPS. Thus, modulation of TRIB3 by H. pylori and/or its products may be an important mechanism during H. pylori-associated pathogenesis.

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“…These findings suggest that follicular DCs are a specialized form of myofibroblast and, instead, myofibroblasts characterized by a-SMA may produce CXCL13. [26]. On the other hand, the prior [22] and current study showed undetectable immunoreactivity against anti-CXCL13 antibody in the epithelial cells even in the vicinity of colonizing bacteria.…”

Section: Discussioncontrasting

confidence: 43%

Enhanced Expression of CXCL13 in Human Helicobacter pylori-Associated Gastritis

et al. 2011

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Helicobacter pylori and Antrum Erosion‐Specific Gene Expression Patterns: The Discriminative Role of CXCL13 and VCAM1 Transcripts

Abstract: Whole genomic microarray analysis yielded new H. pylori infection and erosion-related gene expression changes. Discriminative genes can be used in mRNA-based diagnostic classification of gastric biopsies.

Cited by 41 publications

References 39 publications

Chemokine receptors in gastric MALT lymphoma: loss of CXCR4 and upregulation of CXCR7 is associated with progression to diffuse large B-cell lymphoma

Chemokine receptors in gastric MALT lymphoma: loss of CXCR4 and upregulation of CXCR7 is associated with progression to diffuse large B-cell lymphoma

Tribbles 3: A Novel Regulator of TLR2-Mediated Signaling in Response to Helicobacter pylori Lipopolysaccharide

Enhanced Expression of CXCL13 in Human Helicobacter pylori-Associated Gastritis

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