Regulation of Leukocyte Function-Associated Antigen 1-Mediated Adhesion by Somatostatin and Substance P in Mouse Spleen Cells

Bit Na Kang, Ho Jun Kim, Kyu Shik Jeong, Sang Joon Park, Sung Ho Kim, Se Ra Kim, Tae Hwan Kim, Si Yun Ryu

Research output: Contribution to journalArticlepeer-review

14 Scopus citations

Abstract

Background: Interaction of the integrin leukocyte function-associated antigen (LFA)-1 (CD11a/CD18) with its ligands, the intercellular adhesion molecules (ICAM)-1, -2, and -3 (CD54, CD102, and CD50), is pivotal to many leukocyte adhesion events. Method: To define the mechanism of the movement of leukocytes to the inflammatory site by somatostatin (SOM) and substance P (SP), we examined the expression of the adhesion molecule LFA-1 and inside-out signals for integrins, protein kinase C (PKC), Ras, Rap1, and phosphoinositide (PI) 3-kinase, in anti-CD3-, anti-CD3+SOM-, anti-CD3+SP-stimulated or unstimulated spleen cells. Results: SOM caused downregulation of LFA-1 mRNA translation as well as of adhesion-stimulating molecules such as Rap1, Ras, and PI 3-kinase. On the other hand, SP slightly induced LFA-1 mRNA translation and activation signals for integrins. The early-phase alteration of LFA-1 mRNA translation after 3 h of culture may be due to the changes of CD8+ T cells rather than changes of CD4+ cells. In adhesion assays, SOM significantly decreased cell adhesion (p < 0.05). Conclusion: These data suggest that SOM treatment of spleen cells, especially in CD8+ T cells, leads to downregulation of LFA-1 mRNA translation, inside-out signaling molecules for integrins (Ras, Rap1 and PI 3-kinase, but not PKC), and consequently to a decrease in the LFA-1-mediated adhesion to ICAM-1.

Original languageEnglish
Pages (from-to)84-92
Number of pages9
JournalNeuroImmunoModulation
Volume11
Issue number2
DOIs
StatePublished - 2004

Keywords

  • CD8+ T cell
  • Cell adhesion
  • Leukocyte function-associated antigen 1
  • Neuropeptide
  • Phosphoinositide 3-kinase
  • Protein kinase C
  • Rap1
  • Ras

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