scholarly journals Helicobacter pyloriHp(2–20) Promotes Migration and Proliferation of Gastric Epithelial Cells by Interacting with Formyl Peptide Receptors In Vitro and Accelerates Gastric Mucosal Healing In Vivo

2009 ◽  
Vol 183 (6) ◽  
pp. 3761-3769 ◽  
Author(s):  
Amato de Paulis ◽  
Nella Prevete ◽  
Francesca W. Rossi ◽  
Felice Rivellese ◽  
Fiamma Salerno ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mucosal Healing ◽  
Gastric Epithelial Cells ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide

scholarly journals Interleukin-10 Expands Transit-Amplifying Cells While Depleting Lgr5+ Stem Cells via Inhibition of Wnt and Notch Signaling

2020 ◽  
Author(s):  
Fan Deng ◽  
Jingjuan Hu ◽  
Xiao Yang ◽  
Yifan Wang ◽  
Kexuan Liu
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Interleukin 10 ◽  
Mucosal Healing ◽  
Mucosal Barrier ◽  
Inflammatory Factor ◽  
Epithelial Regeneration ◽  
Immune Mediated

Abstract Background & Aims: Epithelial regeneration is essential for homeostasis and mucosal barrier repair. In infectious and immune-mediated intestinal diseases, interleukin (IL)-10 is thought to enhance these processes. We aimed to define the mechanism by which IL-10 played in mucosal healing or injury.Methods: Intestinal stem cells (ISCs) cultures and mice were treated with recombinant mice IL-10 (rmIL-10). The level of cell proliferation, differentiation, death and related signaling pathways for self-renewal of ISCs were measured in vitro and in vivo.Results: It was uncovered that rmIL-10 increased the size and death, but reduced the total number of organoids. In addition, rmIL-10 depleted Lgr5+ ISCs and reduced epithelial proliferation, but enhanced the differentiation of epithelial cells and expanded numbers of transit-amplifying (TA) cells. These changes are related to the decrease of Wnt and Notch signals in vivo and in vitro. Meanwhile, increased expression of Paneth cells and decreased expression of enteroendocrine cells and goblet cells were induced by rmIL-10.Conclusions: IL-10 reduces the survival of Lgr5+ ISCs and proliferation of epithelial cells by inhibiting Notch and Wnt signaling, but promotes enhanced the differentiation of epithelial cells and expanded numbers of TA cells. Therefore, IL-10 acts as an anti-inflammatory factor, but may damage intestinal mucosa repair and maybe a potential target for the treatment of intestinal injury.

scholarly journals Mesoglycan connects Syndecan‐4 and VEGFR2 through Annexin A1 and formyl peptide receptors to promote angiogenesis in vitro

FEBS Journal ◽  
2021 ◽  
Author(s):  
Emanuela Pessolano ◽  
Raffaella Belvedere ◽  
Nunzia Novizio ◽  
Amelia Filippelli ◽  
Mauro Perretti ◽  
...  
Keyword(s):  
Annexin A1 ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide

scholarly journals Formyl peptide receptors in the mucosal immune system

2020 ◽  
Vol 52 (10) ◽  
pp. 1694-1704
Author(s):  
Yu Sun Jeong ◽  
Yoe-Sik Bae
Keyword(s):  
Epithelial Cells ◽  
Reproductive Tract ◽  
Host Cells ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Mucosal Surfaces ◽  
Wide Range ◽  
Formyl Peptide ◽  
Monocytes And Macrophages ◽  
Mucosal Homeostasis

Abstract Formyl peptide receptors (FPRs) belong to the G protein-coupled receptor (GPCR) family and are well known as chemotactic receptors and pattern recognition receptors (PRRs) that recognize bacterial and mitochondria-derived formylated peptides. FPRs are also known to detect a wide range of ligands, including host-derived peptides and lipids. FPRs are highly expressed not only in phagocytes such as neutrophils, monocytes, and macrophages but also in nonhematopoietic cells such as epithelial cells and endothelial cells. Mucosal surfaces, including the gastrointestinal tract, the respiratory tract, the oral cavity, the eye, and the reproductive tract, separate the external environment from the host system. In mucosal surfaces, the interaction between the microbiota and host cells needs to be strictly regulated to maintain homeostasis. By sharing the same FPRs, immune cells and epithelial cells may coordinate pathophysiological responses to various stimuli, including microbial molecules derived from the normal flora. Accumulating evidence shows that FPRs play important roles in maintaining mucosal homeostasis. In this review, we summarize the roles of FPRs at mucosal surfaces.

scholarly journals Regulation of Human β-Defensins by Gastric Epithelial Cells in Response to Infection with Helicobacter pylori or Stimulation with Interleukin-1

2000 ◽  
Vol 68 (9) ◽  
pp. 5412-5415 ◽  
Author(s):  
Deborah A. O'Neil ◽  
Sheri P. Cole ◽  
Edith Martin-Porter ◽  
Michael P. Housley ◽  
Lide Liu ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Interleukin 1 ◽  
Peptide Antibiotic ◽  
Gastric Epithelial Cells ◽  
Proinflammatory Mediators ◽  
H Pylori

ABSTRACT Gastric epithelial cells in vitro and in vivo are shown to constitutively express the peptide antibiotic human β-defensin type 1 (hBD-1). In contrast, hBD-2 expression is regulated in gastric epithelial cells and increases in response to infection withHelicobacter pylori or stimulation with the proinflammatory cytokine interleukin-1. These data suggest that hBD-2 is a component of the regulated host gastric epithelial cell response to H. pylori infection and proinflammatory mediators.

scholarly journals N-Acetylcysteine Reduces ROS-Mediated Oxidative DNA Damage and PI3K/Akt Pathway Activation Induced by Helicobacter pylori Infection

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Chuan Xie ◽  
Jian Yi ◽  
Jing Lu ◽  
Muwen Nie ◽  
Meifang Huang ◽  
...  
Keyword(s):  
Dna Damage ◽  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Oxidative Dna Damage ◽  
Akt Pathway ◽  
Gastric Epithelial Cells ◽  
H Pylori

Background. H. pylori infection induces reactive oxygen species- (ROS-) related DNA damage and activates the PI3K/Akt pathway in gastric epithelial cells. N-Acetylcysteine (NAC) is known as an inhibitor of ROS; the role of NAC in H. pylori-related diseases is unclear. Aim. The aim of this study was to evaluate the role of ROS and the protective role of NAC in the pathogenesis of H. pylori-related diseases. Method. An in vitro coculture system and an in vivo Balb/c mouse model of H. pylori-infected gastric epithelial cells were established. The effects of H. pylori infection on DNA damage and ROS were assessed by the comet assay and fluorescent dichlorofluorescein assay. The level of PI3K/Akt pathway-related proteins was evaluated by Western blotting. The protective role of N-acetylcysteine (NAC) was also evaluated with in vitro and in vivo H. pylori infection models. Results. The results revealed that, in vitro and in vivo, H. pylori infection increased the ROS level and induced DNA damage in gastric epithelial cells. NAC treatment effectively reduced the ROS level and inhibited DNA damage in GES-1 cells and the gastric mucosa of Balb/c mice. H. pylori infection induced ROS-mediated PI3K/Akt pathway activation, and NAC treatment inhibited this effect. However, the gastric mucosa pathological score of the NAC-treated group was not significantly different from that of the untreated group. Furthermore, chronic H. pylori infection decreased APE-1 expression in the gastric mucosa of Balb/c mice. Conclusions. An increased ROS level is a critical mechanism in H. pylori pathogenesis, and NAC may be beneficial for the treatment of H. pylori-related gastric diseases linked to oxidative DNA damage.

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