1. Helicobacter pylori HP(2-20) induces eosinophil activation and accumulation in superficial gastric mucosa and stimulates VEGF-alpha and TGF-beta release by interacting with formyl-peptide receptors
- Author
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Gianni Marone, Francesca Wanda Rossi, Vittorio Necchi, Vittorio Ricci, Massimo Mascolo, Roberto Fiocca, Stefania Staibano, D. Lamacchia, Paola Ceppa, A. De Paulis, Enrico Solcia, A. Lobasso, Felice Rivellese, N. Prevete, Maurizio Romano, Giuseppe D'Argenio, C. Pelosi, N., Prevete, F. W., Rossi, F., Rivellese, D., Lamacchia, C., Pelosi, A., Lobasso, V., Necchi, E., Solcia, R., Fiocca, P., Ceppa, S., Staibano, M., Mascolo, G., D’Argenio, Romano, Marco, V., Ricci, G., Marone, A., de Paulis, Prevete, Nella, Rossi, FRANCESCA WANDA, Rivellese, Felice, Lamacchia, Donatella, Pelosi, Chiara, Lobasso, Antonio, Necchi, V, Solcia, E, Fiocca, R, Ceppa, P, Staibano, Stefania, Mascolo, Massimo, D., Argenio G, Romano, M, Ricci, V, Marone, Gianni, DE PAULIS, Amato, Prevete, N., Rossi, F. W., Rivellese, F., Lamacchia, D., Pelosi, C., Lobasso, A., Necchi, V., Solcia, E., Fiocca, R., Ceppa, P., Staibano, S., Mascolo, M., D'Argenio, G., Romano, M., Ricci, V., Marone, G., and De Paulis, A.
- Subjects
Formyl peptide ,Male ,Vascular Endothelial Growth Factor A ,Indomethacin ,FPRs ,Eosinophil ,Hp(2-20) ,Peptide Fragment ,Eosinophils ,Helicobacter pylori ,Transforming Growth Factor beta ,Immunology and Allergy ,Receptors, Lipoxin ,Receptor ,Cells, Cultured ,biology ,Chemistry ,Immunohistochemistry ,Chemotaxis, Leukocyte ,medicine.anatomical_structure ,Gastritis ,FPR ,medicine.symptom ,Case-Control Studie ,Human ,Signal Transduction ,Immunology ,Bacterial Protein ,Helicobacter Infections ,Immune system ,Bacterial Proteins ,Microscopy, Electron, Transmission ,TGF beta signaling pathway ,Eosinophil activation ,Gastric mucosa ,medicine ,Animals ,Humans ,RNA, Messenger ,Stomach Ulcer ,Rats, Wistar ,Pharmacology ,Animal ,Gastriti ,biology.organism_classification ,Molecular biology ,Receptors, Formyl Peptide ,Peptide Fragments ,Rats ,Disease Models, Animal ,Gastric Mucosa ,Case-Control Studies ,Chronic Disease ,Rat ,Helicobacter Infection - Abstract
Eosinophils participate in the immune response against Helicobacter pylori, but little is known about their role in the gastritis associated to the infection. We recently demonstrated that the Hp(2-20) peptide derived from H. pylori accelerates wound healing of gastric mucosa by interacting with N-formyl peptide receptors (FPRs) expressed on gastric epithelial cells. The aim of the present study was to investigate whether eosinophils play a role in the repair of gastric mucosa tissue during H. pylori infection. Immunohistochemistry and transmission electron microscopy were used to detect eosinophils in gastric mucosal biopsies. Eosinophil re-distribution occurred in the gastric mucosa of H. pylori-infected patients: their density did not change in the deep mucosal layer, whereas it increased in the superficial lamina propria just below the foveolar epithelium; eosinophils entered the epithelium itself as well as the lumen of foveolae located close to the area harboring bacteria, which in turn were also engulfed by eosinophils. The H. pylori-derived peptide Hp(2-20) stimulated eosinophil migration through the engagement of FPR2 and FPR3, and also induced production of VEGF-A and TGF-β, two key mediators of tissue remodeling. We also demonstrate that Hp(2-20) in vivo induced eosinophil infiltration in rat gastric mucosa after injury brought about by indomethacin. This study suggests that eosinophil infiltrate could modulate the capacity of gastric mucosa to maintain or recover its integrity thereby shedding light on the role of eosinophils in H. pylori infection. Copyright © by BIOLIFE, s.a.s.
- Published
- 2013