Infection is the primary cause of death after liver transplantation.
Mannose binding lectin is a recognition molecule of the lectin pathway of complement and a key component of innate immunity.
Mannose binding lectin variant alleles have been described in the coding region of the mannose binding lectin gene.
These are associated with low mannose binding lectin serum concentration and impaired mannose binding lectin structure and function.
Dr Bouwman and colleagues established the role of the liver in production of serum mannose binding lectin.
The investigative team evaluated the effect of mannose binding lectin variant alleles on the susceptibility to infection after liver transplantation.
| Serum conversion was associated with the disappearance of high molecular weight mannose binding lectin|
The team investigated 49 patients undergoing orthotopic liver transplantation.
Mannose binding lectin exon 1 and promoter polymorphisms were determined in patients and in liver donors.
The team determined mannose binding lectin serum concentration before and during 1 year after transplantation.
The incidence of clinically significant infections during this period was assessed.
Transplantation of mannose binding lectin wildtype recipients with donor livers carrying mannose binding lectin variant alleles resulted in a rapid and pronounced decrease of serum mannose binding lectin levels.
The investigators found that this serum conversion was associated with the disappearance of high molecular weight mannose binding lectin.
The team could not obtain an indication for extrahepatic production of serum mannose binding lectin.
The team found an association between the presence of mannose binding lectin variant alleles in the mannose binding lecitn gene of the donor liver and an increase clinically significant infections after transplantation.
However, mannose binding lectin variant alleles in the mannose binding lectin gene in the recipient was not associated with a strongly increased infections after transplantation.
Dr Bouwman's team concluded, “Serum mannose binding lectin is produced by the liver under strong genetic control.”
“After liver transplantation, the mannose binding lectin genotype of the donor liver is a major risk determinant for life-threatening infections.”