Suppression of atopic dermatitis in mice model by reducing inflammation utilizing phosphatidylserine-coated biodegradable microparticles

J Biomater Sci Polym Ed. 2015;26(18):1465-74. doi: 10.1080/09205063.2015.1100844. Epub 2015 Oct 22.

Abstract

Controlling inflammatory response is important to avoid chronic inflammation in many diseases including atopic dermatitis (AD). In this research, we tried using a phosphatidylserine (PS)-coated microparticles in the AD mouse model for achieving the modulation of the macrophage phenotype to an anti-inflammatory state. Here, we prepared poly (D,L-lactic acid) microparticle coated with PS on the outside shell. We confirmed the cellular uptake of the PS-coated microparticle, which leads to the significant downregulation of the inflammatory cytokine production. In the mouse model of AD, the PS-coated microparticle was injected subcutaneously for a period of 12 days. The mice showed significant reduction in the development of AD symptoms comparing with the mice treated with the PC-coated microparticle.

Keywords: atopic dermatitis; microparticle; phosphatidylserine; subcutaneous injection.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / administration & dosage*
  • Cattle
  • Cells, Cultured
  • Dermatitis, Atopic / drug therapy*
  • Dermatitis, Atopic / immunology*
  • Dermatitis, Atopic / pathology
  • Dermatologic Agents / administration & dosage*
  • Disease Models, Animal
  • Down-Regulation / drug effects
  • Drug Delivery Systems / methods*
  • Egg Proteins / chemistry
  • Female
  • Injections, Subcutaneous
  • Macrophages / drug effects
  • Macrophages / immunology
  • Macrophages / pathology
  • Mice, Inbred C57BL
  • Phosphatidylserines / administration & dosage*
  • Skin / drug effects
  • Skin / immunology
  • Skin / pathology
  • Treatment Outcome
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Dermatologic Agents
  • Egg Proteins
  • Phosphatidylserines
  • Tumor Necrosis Factor-alpha