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*
Department of Surgery, Klinikum rechts der Isar, and
Institute for Medical Microbiology, Immunology, and Hygiene, Technische Universität, Munich, Germany
IL-12 is a potent immunoregulatory cytokine that is essential for
the development of protective immunity, as demonstrated by numerous
animal models of infection. Here, we provide evidence for a critical
role of IL-12 in human sepsis. The results of a prospective study of
184 patients undergoing major elective surgery of the upper and lower
gastrointestinal tract revealed that, in contrast to patients showing
uneventful recovery, monocyte IL-12 production was severely and
selectively impaired in patients developing postoperative sepsis.
Moreover, the extent of monocyte IL-12 suppression correlated with the
severity of postoperative sepsis. Monocyte IL-12 secretion was
suppressed before surgery and remained low until the onset of sepsis.
Therefore, the suppression of IL-12 secretion preceded the onset of
postoperative sepsis but did not occur as a consequence of major
surgery. In contrast, IL-1ß production was only reduced during the
late postoperative course in patients developing postoperative sepsis,
and TNF-
release was even increased at different time intervals
before the onset of sepsis. Thus, reduced IL-12 release does not
reflect a general defect in monocyte cytokine production. Consequently,
these results establish a critical role for IL-12 in early resistance
to postoperative infection and may allow for the development of novel
therapeutic strategies designed to stimulate host defense mechanisms
and to reduce the incidence and severity of septic
complications.
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