HLA-G expression and regulation during Pseudomonas aeruginosa infection in cystic fibrosis patients

Future Microbiol. 2016;11(3):363-73. doi: 10.2217/fmb.15.143. Epub 2016 Mar 2.

Abstract

Background: Deregulated immune response fails to control biofilm-forming bacteria, as Pseudomonas aeruginosa, in the lungs of cystic fibrosis (CF) patients. HLA-G is an immune-modulatory molecule involved in respiratory diseases and infections.

Materials & methods: HLA-G mRNA and protein were analyzed in plasma and exhaled breath condensate from CF patients undergoing intravenous antibiotic treatment, CF cell line and murine model.

Results: Therapy normalizes HLA-G plasmatic in CF patients suggesting a systemic anti-inflammatory role while in CF airway system, higher expression of HLA-G is associated with P. aeruginosa infection. CF cell line and murine model expressed higher HLA-G molecules in the presence of P. aeruginosa.

Conclusion: Plasmatic and lung HLA-G expression suggest a role in reducing systemic inflammation and supporting P. aeruginosa infection.

Keywords: HLA-G; Pseudomonas aeruginosa; cystic fibrosis.

MeSH terms

  • Administration, Intravenous
  • Animals
  • Anti-Bacterial Agents / administration & dosage
  • Anti-Bacterial Agents / therapeutic use
  • Bronchi / immunology
  • Bronchoalveolar Lavage Fluid / immunology
  • Cell Line
  • Cystic Fibrosis / complications*
  • Cystic Fibrosis / genetics*
  • Cystic Fibrosis / microbiology
  • Disease Models, Animal
  • HLA-G Antigens / analysis
  • HLA-G Antigens / blood
  • HLA-G Antigens / genetics*
  • Histocompatibility Antigens Class I / genetics
  • Host-Pathogen Interactions
  • Humans
  • Inflammation
  • Lung / immunology
  • Mice
  • Prospective Studies
  • Pseudomonas Infections / drug therapy
  • Pseudomonas Infections / genetics*
  • Pseudomonas Infections / immunology*
  • Pseudomonas aeruginosa* / immunology
  • Respiratory Mucosa / immunology

Substances

  • Anti-Bacterial Agents
  • HLA-G Antigens
  • Histocompatibility Antigens Class I
  • Q surface antigens