Literature DB >> 8614067

Immunosuppression after endotoxin shock: the result of multiple anti-inflammatory factors.

W G Junger1, D B Hoyt, F C Liu, W H Loomis, R Coimbra.   

Abstract

OBJECTIVES: Endotoxin induced suppression of cellular immune function is thought to contribute to septic complications in trauma patients. A rabbit model of endotoxemia was used to determine the relative roles of the anti-inflammatory factors interleukin-4 (IL-4), interleukin-10 (IL-10), transforming growth factor beta1 (TGFbeta1), and prostaglandin E2 (PGE2) in addition to other factors, in inducing immunosuppression.
DESIGN: T-cell suppressive factors (TSF) in serum ultrafiltrates were separated and tested for the presence of the known suppressive factors PGE2, IL-4, IL-10, and TGFbeta1.
MATERIAL AND METHODS: New Zealand rabbits were injected with 50 microg/kg of purified Escherichia coli lipopolysaccharide. Animals were exsanguinated after 48 hours and serum was separated by ultrafiltration (cutoff 50 kd), TSK HW-40 size exclusion chromatography, and Q-Sepharose anion exchange chromatography. TSF activities of chromatographic fractions and serum samples were measured with a mitogen induced in vitro T-cell proliferation assay. Levels of PGE2, IL-4, IL-10, and TGFbeta1 were measured with enzyme immunoassays.
MEASUREMENTS AND MAIN RESULTS: Serum TSF activity, and levels of PGE2, IL-4, IL-10, and TGFbeta1 were increased after endotoxemia. Size exclusion chromatography revealed three major fractions (TSF1-3) with up to 600 times more TSF activity compared with controls. IL-4 and IL-10 were found in TSF1 and TSF3. Further separation of TSF1 by anion exchange chromatography revealed a total of eight different T-cell suppressive factors. TGFbeta1 probably remained in the retentate after ultrafiltration, while PGE2 eluted at a higher retention time. The known anti-inflammatory factors TGFbeta1, IL-10, IL-4, and PGE2 only accounted for 13% of the total serum TSF activity of 614 U/mL.
CONCLUSIONS: Lipopolysaccharide shock results in the release of multiple T-cell suppressive factors in addition to known immunosuppressive factors, all of which contribute to the anti-inflammatory response.

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Year:  1996        PMID: 8614067     DOI: 10.1097/00005373-199605000-00004

Source DB:  PubMed          Journal:  J Trauma        ISSN: 0022-5282


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