Selective defects of T lymphocyte function in patients with lethal intraabdominal infection.
BACKGROUND
In recent models, compensatory antiinflammatory immune reactions triggered in response to systemic inflammation were considered important for the outcome of sepsis. The present study investigated T-cell functions in patients with postoperative sepsis due to intra-abdominal infection.


METHODS
Peripheral T cells were purified from 32 sepsis patients and 41 healthy controls. Proliferation and production of interferon (IFN)-gamma, interleukin (IL)-2, IL-4, tumor necrosis factor (TNF), and IL-10 were stimulated by cross-linking of CD3 and CD28.


RESULTS
T-cell proliferation and production of IL-2 and TNF were severely suppressed in patients with lethal intraabdominal infection as compared with survivors and healthy controls. Sepsis survivors showed normal T-cell proliferation and IL-2 release, whereas secretion of TNF was reduced. However, TNF suppression in survivors was less severe than in nonsurviving patients. Defective T-cell functions were observed at the onset of sepsis and persisted throughout the entire observation period. T-cell production of IL-4 and IL-10 was not affected by postoperative intraabdominal infection.


CONCLUSIONS
Defective T-cell proliferation and secretion of IL-2 and TNF correlate with sepsis mortality, thus indicating an important role of T 'cells for the immune defense against postoperative infection. Immune defects were evident at the onset of sepsis, suggesting that immunosuppression may develop as a primary response to sepsis without preceding immune hyperactivity.
Heidecke
C D
CD
Department of Surgery, Klinikum rechts der Isar, Technische Universität, Munich, Germany.
Hensler
T
T
Weighardt
H
H
Zantl
N
N
Wagner
H
H
Siewert
J R
JR
Holzmann
B
B
D000005:Abdomen; D000368:Aged; D002455:Cell Division; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis; D007378:Interleukins / Q000096:biosynthesis; D008297:Male; D008875:Middle Aged; D011183:Postoperative Complications / Q000276:immunology / Q000503:physiopathology*; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology / Q000503:physiopathology*; D013601:T-Lymphocytes / Q000276:immunology / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D007378:Interleukins; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma