Background: Surgical stress has been reported to induce immunosuppression.
The mechanisms giving rise to T-cell dysfunction following surgery are stil
l unclear. The cellular mechanisms behind T-cell dysfunction following surg
ery were investigated, based on the induction of T-cell apoptosis and downr
egulation of T-cell signalling molecules.
Methods: Peripheral blood T cells were collected and separated before and a
fter surgery in patients who had oesophagectomy, gastrectomy or cholecystec
tomy, and studied for their ability to produce cytokines, the induction of
T-cell apoptosis with terminal deoxynucleotidyl transferase-mediated dUPT-b
iotin nick end labelling methods, and the expression of T-cell signalling z
eta (TCR zeta) molecules with intracellular staining.
Results: The increased degree of T-cell apoptosis, downregulation of TCR ze
ta molecules and impaired cytokine production of T cells were significant o
n days 1 and 3 after operation in patients who had oesophagectomy, but not
after gastrectomy or cholecystectomy. A higher level of T-cell apoptosis wa
s observed in the co-culture with postoperative monocytes than with preoper
ative monocytes.
Conclusion: Peripheral blood T cells obtained after oesophagectomy underwen
t apoptosis that correlated with the downregulation of TCR zeta molecules.
Postoperative monocytes induced by surgical stress were able to mediate the
T-cell apoptosis.