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Contribution of tumor necrosis factor alpha to endotoxin-induced mucosal dysfunction in the feline jejunum

Departments of Large Animal Medicine and Physiology and Pharmacology, University of Georgia, Athens, Georgia, USA

Susan C. Eades

Departments of Large Animal Medicine and Physiology and Pharmacology, University of Georgia, Athens, Georgia, USA

James N. Moore

Departments of Large Animal Medicine and Physiology and Pharmacology, University of Georgia, Athens, Georgia, USA

Michelle H. Barton

Departments of Large Animal Medicine and Physiology and Pharmacology, University of Georgia, Athens, Georgia, USA

Tumor necrosis factor (TNF) occupies a pivotal role in the development of shock and tissue injury during endotoxemia and septicemia, and may be an important trigger in the pathogenesis of endotoxin-induced intestinal mucosal dysfunction. This study investigated the contribution of TNF to endotoxin-induced mucosal dysfunction and the efficacy of polyclonal anti-TNF antibody in preventing endotoxin-induced mucosal dysfunction.

To evaluate mucosal dysfunction, jejunal blood-to-lumen clearances of chromium 51-labeled ethylenediaminetetraacetate ([⁵¹Cr]-EDTA) were measured in cats administered fetal calf serum (controls), endotoxin, TNF, or polyclonal anti-TNF antibody and endotoxin. Serum TNF activity was determined using a modified in vitro cytotoxicity bioassay using the murine fibrosarcoma cell line, WEHI-164 clone 13.

Endotoxin and TNF induced jejunal mucosal dysfunction as indicated by increases in [⁵¹ Cr]-EDTA clearance. Mucosal dysfunction was accompanied by marked increases in serum TNF activity. Furthermore, pretreatment with polyclonal anti-TNF antibody prevented endotoxin-induced mucosal dysfunction and markedly reduced the associated increase in serum TNF activity. The findings of this study suggest that TNF is an important mediator of endotoxin-induced mucosal epithelial barrier dysfunction.

Innate Immunity, Vol. 3, No. 4, 323-332 (1996)
DOI: 10.1177/096805199600300406


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