Modulation of PMN-endothelial cells interactions by cyclic nucleotides

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Yukio Sato1

  • 1Division of Thoracic Surgery, Department of Surgery, Jichi Medical School, Japan. tcvysato@jichi.ac.jp

Current Pharmaceutical Design
|February 5, 2004
PubMed

Insights

Cyclic nucleotides like cGMP and cAMP inhibit polymorphonuclear leukocyte (PMN) interactions with endothelial cells (EC). Modulating these cyclic nucleotides may treat inflammatory diseases like asthma and acute respiratory distress syndrome.

Area of Science:

  • Cellular Biology
  • Immunology
  • Physiology

Background:

  • Polymorphonuclear leukocytes (PMN) interact with endothelial cells (EC) in systemic and pulmonary circulations.
  • Adhesion molecules are key regulators, but pulmonary circulation has unique conditions affecting PMN deformability.
  • Dysregulated PMN-EC interactions can cause tissue injury in conditions like acute respiratory distress syndrome.

Purpose of the Study:

  • To review the modulation of PMN-EC interactions by cyclic nucleotides (cGMP and cAMP).
  • To explore the role of these interactions in inflammatory diseases and tissue injury.

Main Methods:

  • Literature review focusing on studies investigating cGMP, cAMP, and PMN-EC interactions.
  • Analysis of the effects of cyclic nucleotides on PMN functions like rolling, adhesion, migration, and deformability.

Main Results:

  • Both cGMP and cAMP demonstrate inhibitory effects on critical PMN-EC interaction events.
  • These cyclic nucleotides influence PMN rolling, adhesion, migration, and changes in deformability.

Conclusions:

  • Modulation of cGMP and cAMP levels offers potential therapeutic strategies for inflammatory conditions.
  • Targeting cyclic nucleotides could be beneficial for treating local diseases (e.g., asthma) and systemic injuries (e.g., ARDS).

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