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Host Defense and the Hepatic-Pulmonary Macrophage Axis

Mark P. Callery, MD; Takafumi Kamei, MD; Martin J. Mangino, PhD; M. Wayne Flye, MD, PhD

Arch Surg. 1991;126(1):28-32.

Abstract
• Endotoxin (lipopolysaccharide [LPS]) and tumor necrosis factor (TNF-) have been implicated in the pathogenesis of sepsis-induced adult respiratory distress syndrome. To evaluate the possible interaction of the hepatic-pulmonary macrophage axis in the adult respiratory distress syndrome, we compared the kinetics of immunosuppressive prostaglandin E₂, TNF-, and interleukin 6 production in LPS-stimulated Kupffer cells and alveolar macrophages (AMs). Interleukin 6 production by Kupffer cells was significantly higher than for equal numbers of AMs. Kupffer cell TNF- levels peaked early before decreasing as regulatory prostaglandin E2 levels rose. In contrast, AM TNF- levels rose sharply and remained significantly higher than for Kupffer cells throughout culture coincident with negligible prostaglandin E₂ production. Kupffer cell sequestration of LPS may normally invoke a coordinated cytokine response able to locally induce acute-phase hepatocytes. In hepatic failure, however, LPS spillover to the lung may promote adult respiratory distress syndrome by inducing unregulated AM TNF- production within the pulmonary microenvironment.

(Arch Surg. 1991;126:28-32)

Author Affiliations
From the Department of Surgery, Washington University School of Medicine, St Louis, Mo.

Footnotes
Accepted for publication September 29, 1990.

Read before the Tenth Anniversary Meeting of the Surgical Infection Society, Cincinnati, Ohio, June 14, 1990.

Reprint requests to 1 Barnes Hospital Plaza, Suite 5108, Washington University School of Medicine, St Louis, MO 63110 (Dr Flye).

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