Extracellular Signal-Regulated Protein Kinase Mediates Interleukin 17 (IL-17)-Induced IL-8 Secretion in Helicobacter pylori-Infected Human Gastric Epithelial Cells

Sebkova, Ladislava; Pellicanò, A.; Monteleone, Giovanni; Grazioli, Barbara; Guarnieri, Giovanni; Imeneo, Maria; Pallone, Francesco; Luzza, Francesco

doi:10.1128/iai.00071-14

Cited by 6 publications

(8 citation statements)

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“…Firstly, Luzza et al reported that increased production of active IL-17A during H. pylori infection may play an important role in the inflammatory response to H. pylori colonization [16]. Thereafter, several studies revealed that IL-17, a key regulator of neutrophil chemotaxis, is produced in excess in H pylori-infected stomachs [17,23]. These results suggest that IL-17A may contribute to H. pylori-induced gastric inflammation.…”

Section: Discussionmentioning

confidence: 91%

Genetic polymorphisms of IL17A and pri-microRNA-938, targeting IL17A 3′-UTR, influence susceptibility to gastric cancer

et al. 2012

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Section: Discussionmentioning

confidence: 91%

Genetic polymorphisms of IL17A and pri-microRNA-938, targeting IL17A 3′-UTR, influence susceptibility to gastric cancer

et al. 2012

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“…Pathway analysis demonstrates that CCL8 and IL‐8 are both involved in the ERK 1/2 signaling pathway. ERK 1/2 are protein kinases, ERK1 and ERK2 belonging to one of the three major mitogen‐activated protein kinase (MAPK) families (Sebkova et al ., ). IL‐8 induction is transcriptionally controlled through multiple promoter elements, and MAPK signaling pathways are associated with inflammatory stimuli that regulate IL‐8 production (Dong et al ., ; Hoffmann et al ., ).…”

Section: Discussionmentioning

confidence: 97%

Loperamide‐induced expression of immune and inflammatory genes in Collies associated with ivermectin sensitivity

Zhu

Yancy

Deaver

et al. 2015

Vet Pharm & Therapeutics

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This study evaluated the impact of the ABCB1-1Δ mutation in Collies which exhibited toxicity toward ivermectin, on changes in gene expression when given the unrelated ABCB1 substrate loperamide, to identify potential biomarkers predictive of drug safety. Thirty-two healthy intact Collies consisting of dogs with either a wild-type, heterozygous mutant, or homozygous mutant genotype were used. Whole blood samples were collected from Collies at 0 or 5 h following administration of loperamide at a dose of 0.10 mg/kg. Whole-genome gene expression microarray was conducted to examine for changes in gene expression. Microarray analysis identified loperamide-induced changes in gene expression which were specifically associated with ivermectin-sensitive phenotypes in Collies possessing the ABCB1-1Δ mutation. Gene pathway analysis further demonstrated that the altered genes are involved in immunological disease, cell death and survival, and cellular development. Thirteen genes, including CCL8 and IL-8, were identified. Collie dogs harboring ABCB1-1Δ mutation which also exhibited toxicity toward ivermectin demonstrated systematic responses following loperamide treatment exhibited by altered expression of genes involved in immune and inflammatory signaling pathways. Genes such as CCL8 and IL-8 are potential biomarkers in whole blood that may predict the safety of loperamide in dogs with ABCB1-1∆ mutation associated with ivermectin sensitivity.

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“…IL‐17 family cytokines per se do not possess chemotactic activity (Zou and Restifo, ) but instead trigger cell‐mediated immune responses by inducing secretion of unrelated cytokines and chemokines. Following H. pylori infection IL‐17A induces secretion of IL‐8, by activation of the ERK 1/2 MAP kinase cascade (Sebkova et al ., ; Kabir, ). IL‐17 may therefore indirectly promote cell‐mediated immunity, in part, by triggering release of IL‐8, a potent chemoattractant for neutrophils.…”

Section: H Pylori Stat3 and Il‐17mentioning

confidence: 99%

STAT3: a critical component in the response toHelicobacter pyloriinfection

2015

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Summary STAT3 imparts a profound influence on both the epithelial and immune components of the gastric mucosa, and through regulation of key intracellular signal transduction events, is well placed to control inflammatory and oncogenic outcomes in the context of Helicobacter (H.) pylori infection. Here we review the roles of STAT3 in the host immune response to H. pylori infection, from both gastric mucosal and systemic perspectives, as well as alluding more specifically to STAT3‐dependent mechanisms that might be exploited as drug targets.

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Extracellular Signal-Regulated Protein Kinase Mediates Interleukin 17 (IL-17)-Induced IL-8 Secretion in Helicobacter pylori-Infected Human Gastric Epithelial Cells

Abstract: During preparation of figures showing the results of Western blots, the following bands from control samples were inadvertently duplicated:

Cited by 6 publications

References 0 publications

Genetic polymorphisms of IL17A and pri-microRNA-938, targeting IL17A 3′-UTR, influence susceptibility to gastric cancer

Genetic polymorphisms of IL17A and pri-microRNA-938, targeting IL17A 3′-UTR, influence susceptibility to gastric cancer

Loperamide‐induced expression of immune and inflammatory genes in Collies associated with ivermectin sensitivity

STAT3: a critical component in the response toHelicobacter pyloriinfection

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