sCD30, interleukin-1beta-converting enzyme and anti-Annexin V autoantibodies concentrations in heart transplant recipients.
sCD30 and ICE/caspase-1 as apoptosis-regulating factors are suspected to be involved in the survival rate of immunocompetent cells during immunosuppression after allotransplantation. Serum CD30 and ICE/caspase-1 concentrations were estimated and associated with unspecific serum apoptosis marker--anti-Annexin V antibodies and myocardial biopsies results.


METHODS
28 clinically stabile patients--heart transplant recipients at least 3 months after cardiac transplantation performed due to heart failure caused by ischaemic and/or congestive cardiomyopathy or/and primary valvular heart disease (26 men and 2 women, mean age=36.8 years, S.D.=7.6) with normal heart function assessed by use of ultrasound scan--were involved in the trial. The patients were divided and analyzed in two ways: first according to the results of elective endomyocardial biopsies and second to main immunosuppressive agent used. The enzyme immunoassay (CD30, Dako; interleukin-1beta-converting enzyme (ICE)/Caspase-1 ELISA and anti-Annexin V BENDER MedSystem) for soluble CD30, caspase-1 and anti-Annexin V autoantibodies serum levels was used.


RESULTS
sCD30 and caspase-1 concentrations were non-significantly up-regulated in all analysed groups--with or without rejection signs or immunosuppressed with cyclosporine or especially tacrolimus. In contrast anti-Annexin V autoantibodies concentration was non-significantly down-regulated also in all studied groups. Moreover in the group with signs of transplant rejection, strong negative correlation between anti-Annexin antibodies and rejection grade was observed (-0.65, p<0.05). Biopsy results were comparable in groups treated with tacrolimus and cyclosporine A.


CONCLUSIONS
The increasing tendency of sCD30 and caspase-1 as well as the decrease in anti-Annexin V autoantibodies concentrations in heart recipients could be the result of post-transplant apoptosis disturbances. This tendency seems to be inhibited in a greater degree by tacrolimus than by cyclosporine. Anti-Annexin V autoantibodies might be considered as negative rejection markers due to their strong negative correlation with the rejection grade.
Zeglen
Sławomir
S
Chair and Clinical Department of Internal Diseases, Allergology and Clinical Immunology, Medical University of Silesia, 41-800 Zabrze, ul. 3-go Maja 13-15, Poland.
Zakliczyński
Michał
M
Nozyński
Jerzy
J
Rogala
Barbara
B
Zembala
Marian
M
D000328:Adult; D017304:Annexin A5 / Q000276:immunology*; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D001323:Autoantibodies / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D020170:Caspase 1 / Q000097:blood*; D016572:Cyclosporine / Q000627:therapeutic use; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006084:Graft Rejection / Q000097:blood* / Q000276:immunology / Q000517:prevention & control; D016027:Heart Transplantation / Q000276:immunology*; D006801:Humans; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D017730:Ki-1 Antigen / Q000097:blood*; D008297:Male; D008875:Middle Aged; D016559:Tacrolimus / Q000627:therapeutic use
D017304:Annexin A5; D001323:Autoantibodies; D015415:Biomarkers; D007166:Immunosuppressive Agents; D017730:Ki-1 Antigen; D016572:Cyclosporine; D020170:Caspase 1; D016559:Tacrolimus