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Mark L. Jordan, MD; Ann Carlson; Rosemary A. Hoffman; Richard L. Simmons, MD

Arch Surg. 1988;123(2):182-187.

Abstract
• Alterations in macrophage function may render the immunocompromised host more susceptible to infectious complications. Although allograft recipients are at increased risk of infection primarily because of pharmacologic immunosuppression, whether the process of allosensitization per se alters this risk is unknown. We therefore studied the effects of cloned allosensitized murine helper or cytotoxic T cells on both interleukin 1 (IL-1) and prostaglandin E₂ (PGE₂) production by syngeneic resident murine peritoneal macrophages. Endotoxin (lipopolysaccharide [LPS]) stimulated both IL-1 and PGE₂ production in macrophages. Cloned T cells alone, with or without LPS pretreatment, produced neither IL-1 nor PGE₂. After 48 hours of coculture with LPS-treated macrophages, cloned helper cells augmented IL-1 release by macrophages but inhibited PGE₂ production. In contrast, cytotoxic T cells not only reduced IL-1 production by macrophages but also potentiated PGE₂ release. These effects were not observed when macrophages were not first exposed to LPS. Thus, endotoxin renders macrophages more susceptible to allosensitized "help" ( IL-1, PGE₂) or "suppression" ( IL-1, PGE₂) by cytotoxic T cells. We hypothesize that, even in the absence of immunosuppression, the process of allosensitization itself may modulate the response to sepsis by altering host macrophage function.

(Arch Surg 1988;123:182-187)

Author Affiliations
From the Division of Urology, Toronto Western Hospital, University of Toronto (Dr Jordan), and the Department of Surgery, Veterans of Foreign Wars Cancer Research Center, University of Minnesota, Minneapolis (Mss Carlson and Hoffman and Dr Simmons).

Footnotes
Accepted for publication Aug 3, 1987.

Read before the Seventh Annual Meeting of the Surgical Infection Society, Philadelphia, May 11, 1987.

Reprint requests to Suite 8-304, 399 Bathurst St, Toronto, Ontario, Canada M5T 2S8 (Dr Jordan).

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