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Tumor Necrosis Factor α Gene Expression in Human Peritoneal Macrophages Is Suppressed by Extra-abdominal Trauma

Carl J. Hauser, MD; Sandhya Lagoo, MD, PhD; Anand Lagoo, MD, PhD; Enatra Hale; Kenneth J. Hardy, MD, PhD; W. Henry Barber, MD, DPhil; J. David Bass, PhD; Galen V. Poole, MD
Arch Surg. 1995;130(11):1186-1192. doi:10.1001/archsurg.1995.01430110044008.
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Background:  Trauma is believed to activate immunocytes but paradoxically also increases the risk of intraperitoneal infection.

Objective:  To investigate these events by evaluating changes in the cytokine control networks of human peritoneal macrophages (PMø) early after trauma.

Design:  Case-control study comparing cytokine messenger RNA (mRNA) expression by PMø from patients with extra-abdominal trauma with that of both peripheral blood mononuclear cells (PBM) and PMø obtained from healthy individuals.

Setting:  Level I trauma center and basic science laboratory in a university hospital center.

Patients:  Six patients with polytrauma (Injury Severity Score, ≥15) with clinically negative diagnostic peritoneal lavages performed on routine indications at admission to the emergency department and six healthy age- and sex-matched individuals undergoing inguinal herniorrhaphy under local anesthesia.

Interventions:  Peritoneal macrophages were isolated from diagnostic peritoneal lavages in trauma patients. Identical lavages were performed through the hernia sac in the control group.

Measurements:  Cellular RNA was assayed for tumor necrosis factor α (TNF-α), interleukin-1β, IL-6, and IL-10 message by semiquantitative reverse-transcription polymerase chain reaction.

Results:  Normal PMø expressed high levels of TNF-α mRNA relative to PBM, but expression of the other proinflammatory cytokines was equivalent to that of PBM. Peritoneal macrophage expression of TNF-α mRNA was markedly (64-fold) decreased after trauma (P<.001), when PBM expression of IL-10 mRNA was increased (P=.03).

Conclusions:  Human PMø constitutively show high levels of TNF-α message expression, and this is down-regulated by polytrauma. This might constitute a functionally "primed" state. If so, TNF-α down-regulation might contribute to functional PMø suppression after systemic injury.(Arch Surg. 1995;130:1186-1192)


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