Active cell migration in retransplanted rat cardiac allografts during the course of chronic rejection

Citation
S. Kitagawa-sakakida et al., Active cell migration in retransplanted rat cardiac allografts during the course of chronic rejection, J HEART LUN, 19(6), 2000, pp. 584-590
Citations number
25
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF HEART AND LUNG TRANSPLANTATION
ISSN journal
1053-2498 → ACNP
Volume
19
Issue
6
Year of publication
2000
Pages
584 - 590
Database
ISI
SICI code
1053-2498(200006)19:6<584:ACMIRR>2.0.ZU;2-0
Abstract
Background: Chronic allograft vasculopathy (CAV) is caused by the infiltrat ion of host immune cells to a graft, but it has been technically difficult to monitor the movements of the cells in graft rejection. Methods: We used a male-specific gene, SRY, as a marker to investigate the dynamics of host cells in a model of CAV in which immunosuppression was unn ecessary and anti-male responses were practically negligible. Fluorescent-b ased real-time quantitative polymerase chain reaction (PCR) was adapted to estimate the fraction of host cells in a graft by the ratio of SRY to IL-2 gene. Using this technique, we studied the turnover and migration of host c ells during the course of CAV progression by retransplanting female allogra fts from male to female or from female to male rats. Results: We detected histologic CAV 60 days after retransplantation in allo grafts retransplanted to the F-1 progeny of donor x recipient on the 5th da y, but not in those retransplanted on the 3rd day, regardless of the mismat ches in the genders. Most: of the initial infiltrating cells disappeared ra pidly in both cases. The fraction of migrating cells from the second recipi ent, however, continuously increased in allografts developing CAV, and 60 d ays after retransplantation exceeded 50%, whereas it stayed at 5% to 15% in those not developing CAV. ED-1-positive macrophages/monocytes were likely candidates for the migrated cells. Conclusions: We have developed a simple method to measure the migration of host cells into a graft. This technique was useful, at least in certain rat strains, to investigate the cellular mechanisms of chronic cardiac allogra ft rejection.