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Exocrine cell-derived microparticles in response to lipopolysaccharide promote endocrine dysfunction in cystic

Andrei Alexandru Constantinescu1, Céline Gleizes2, Mahmoud Alhosin3

  • 1EA7293, Vascular and Tissular Stress in Transplantation, Federation of Translational Medicine of Strasbourg, Faculty of Medicine, University of Strasbourg, 74 route du Rhin, F-67401 Illkirch, Strasbourg, France; Department of Parasitology and Parasitic Diseases and Animal Biology, Faculty of Veterinary Medicine, University of Agronomical Sciences and Veterinary Medicine, 105 spl. Independentei, sector 5, 050097 Bucharest, Romania.

Journal of Cystic Fibrosis : Official Journal of the European Cystic Fibrosis Society
|October 8, 2013
PubMed
Abstract

Insights

Microparticles (MPs) from cystic fibrosis (CF) exocrine cells impair insulin secretion in endocrine cells by activating NF-κB pathways. CFTR dysfunction also reduces insulin secretion and promotes apoptosis.

Area of Science:

  • Pancreatic cell biology
  • Endocrinology
  • Molecular mechanisms of disease

Background:

  • Cystic fibrosis (CF) diabetes involves exocrine pancreas changes and later endocrine dysfunction.
  • Microparticles (MPs) are cell fragments involved in intercellular communication.
  • This study investigates exocrine MPs' role in CF endocrine pancreas dysfunction during infection.

Purpose of the Study:

  • To identify interactions between exocrine and endocrine pancreatic cells mediated by exocrine MPs in CF.
  • To understand the role of microparticles in the context of recurrent infections in CF patients.

Main Methods:

  • Collected MPs from CFTR-mutated (CFPAC-1) and normal (PANC-1) exocrine cells after Pseudomonas aeruginosa LPS treatment.
  • Applied MPs to rat insulin-secreting cells (RIN-m5F) and assessed membrane integration, apoptosis, insulin secretion, and NF-κB activation.
  • Utilized confocal microscopy, flow cytometry, Western blot, and reporter gene assays; inhibited CFTR in normal endocrine cells.

Main Results:

  • Exocrine MPs from CF cells (CFPAC-1) significantly reduced insulin secretion and lysosomal activity in RIN-m5F cells compared to normal MPs.
  • MPs induced NF-κB activation, and inhibiting this pathway restored insulin secretion.
  • CFTR inhibition in normal endocrine cells promoted apoptosis and decreased insulin secretion.

Conclusions:

  • Exocrine MPs contribute to endocrine cell dysfunction via NF-κB pathways during CF-associated recurrent infections.
  • Dysfunctional membrane CFTR is linked to reduced insulin secretion in pancreatic endocrine cells.
Keywords:
Cystic fibrosis-related diabetesInsulin secretionMembrane microparticlesNF-kB

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