Role of cytosolic and calcium independent phospholipases A(2) in insulin secretion impairment of INS-1E cells infected by S. aureus

• Published in: FEBS letters 2015-12, Vol.589 (24 Pt B), p.3969-3976
• Main Authors: Caporarello, N, Salmeri, M, Scalia, M, Motta, C, Parrino, C, Frittitta, L, Olivieri, M, Toscano, M A, Anfuso, C D, Lupo, G
• Format: Article
• Language: English
• Subjects: Animals; Cell Line, Tumor; Cyclooxygenase 2 - chemistry; Cyclooxygenase 2 - metabolism; Cyclooxygenase 2 Inhibitors - pharmacology; Diabetes Mellitus, Type 1 - etiology; Group IV Phospholipases A2 - metabolism; Group VI Phospholipases A2 - antagonists & inhibitors; Group VI Phospholipases A2 - genetics; Group VI Phospholipases A2 - metabolism; Host-Pathogen Interactions - drug effects; Insulin - metabolism; Insulin Secretion; Insulin-Secreting Cells - drug effects; Insulin-Secreting Cells - enzymology; Insulin-Secreting Cells - metabolism; Insulin-Secreting Cells - microbiology; Kinetics; MAP Kinase Signaling System - drug effects; Methicillin-Resistant Staphylococcus aureus - physiology; Pancreatitis - microbiology; Pancreatitis - physiopathology; Phosphorylation - drug effects; Protein Kinase C-alpha - metabolism; Protein Processing, Post-Translational - drug effects; Rats; RNA Interference; Staphylococcal Infections - microbiology; Staphylococcal Infections - physiopathology
• ISSN: 1873-3468
• DOI: 10.1016/j.febslet.2015.11.035

Cytosolic PLA2 (cPLA2) and Ca(2+)-independent PLA2 (iPLA2) play a significant role in insulin β-cells secretion. Bacterial infections may be responsible of the onset of diabetes. The mechanism by which Staphylococcus aureus infection of INS-1 cells alters glucose-induced insulin secretion has been examined. After acute infection, insulin secretion and PLA2 activities significantly increased. Moreover, increased expressions of phospho-cPLA2, phospho-PKCα and phospho-ERK 1/2 were observed. Chronic infection causes a decrease in insulin release and a significant increase of iPLA2 and COX-2 protein expression. Moreover, insulin secretion in infected cells could be restored using specific siRNAs against iPLA2 isoform and specific COX-2 inhibitor.