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,
Departments of
*
Urology and
Immunology, Cleveland Clinic Foundation, Cleveland, OH 44195;
Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109; and
Department of Pathology, Case Western Reserve University School of Medicine, Cleveland, OH 44106
The identification of early inflammatory events after transplant in
solid tissue organ grafts that may direct T cell recruitment and
promote acute allograft rejection remain largely unknown. To better
understand temporal aspects of early inflammatory events in
vascularized organ grafts, we tested the intragraft expression of four
different chemokines in heterotopically transplanted A/J
(H-2a) and syngeneic heart grafts in C57BL/6
(H-2b) recipient mice from 1.5 to 48 h after
transplant. Similar temporal expression patterns and equivalent levels
of chemokine expression were observed in both syngeneic and allogeneic
cardiac allografts during this time period. Expression of the
neutrophil chemoattractant growth-related oncogene 
(KC) was
observed first and reached peak levels by 6 h after transplant and
was followed by the monocyte/macrophage chemoattractant protein-1 (JE)
and then macrophage inflammatory proteins 1
and 1. Administration
of rabbit KC antiserum to allograft recipients within 30 min of cardiac
transplantation attenuated downstream events including intra-allograft
expression of the T cell chemoattractants IFN-
-inducible protein-10
and monokine induced by IFN-, cellular infiltration into the
allograft, and graft rejection. Similarly, depletion of recipient
neutrophils at the time of transplantation significantly extended
allograft survival from day 8 to 10 in control-treated recipients up to
day 21 after transplant. These results indicate the induction of highly
organized cascades of neutrophil and macrophage chemoattractants in
cardiac grafts and support the proposal that early inflammatory events
are required for optimal recruitment of T cells into allografts during
the progression of acute rejection of cardiac
allografts.
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