TY - JOUR
T1 - Regulation of Leukocyte Function-Associated Antigen 1-Mediated Adhesion by Somatostatin and Substance P in Mouse Spleen Cells
AU - Kang, Bit Na
AU - Kim, Ho Jun
AU - Jeong, Kyu Shik
AU - Park, Sang Joon
AU - Kim, Sung Ho
AU - Kim, Se Ra
AU - Kim, Tae Hwan
AU - Ryu, Si Yun
PY - 2004
Y1 - 2004
N2 - 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.
AB - 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.
KW - CD8+ T cell
KW - Cell adhesion
KW - Leukocyte function-associated antigen 1
KW - Neuropeptide
KW - Phosphoinositide 3-kinase
KW - Protein kinase C
KW - Rap1
KW - Ras
UR - http://www.scopus.com/inward/record.url?scp=0842299502&partnerID=8YFLogxK
U2 - 10.1159/000075317
DO - 10.1159/000075317
M3 - Article
C2 - 14758054
AN - SCOPUS:0842299502
SN - 1021-7401
VL - 11
SP - 84
EP - 92
JO - NeuroImmunoModulation
JF - NeuroImmunoModulation
IS - 2
ER -