Evidence for Kupffer cell activation by burn injury and pseudomonas exotoxin A

Y. L. Dong, F. Ko, T. Yan, H. Q. Huang, David Herndon, J. P. Waymack

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Postburn metabolic and immunological alterations may in part be due to translocation of gut exotoxin and endotoxin, which can result in tumour necrosis factor (TNF) and prostaglandin E (PGE) production by macrophages. We evaluated the effect of burn injury, plus exotoxin and endotoxin on TNF-α and PGE production by Kupffer cells, and peritoneal macrophages. Adult Wistar rats underwent 30 per cent TBSA burn or sham burn. Kupffer cells were harvested from rat livers and peritoneal macrophages from the abdominal cavity 24 h postburn. They were cultured overnight at 1 × 106 cells/ml and stimulated with saline, 5 μg/ml of Pseud. aeruginosa Exotoxin A (Exo-A), 5 μg/ml of Pseud. aeruginosa Endotoxin (Endo), Exo-A + Endo, or Exo-A + Endo + the PGE derivative 16,16 dimethyl-PGE (dPGE) (10μg/ml). The supernatants were harvested after 4, 24 and 48 h of culture and assayed for TNF-α and PGE. Results showed that burn injury induced an increase in TNF-α and PGE production by Kupffer cells stimulated with Exo-A, Endo, and both Exo-A + Endo (P < 0.05). The release of TNF-α by Kupffer cells was downregulated by exogenous PGE (P < 0.05). The increased TNF-α production was inversely related to PGE levels. In conclusion, both burn injury and Exo-A potentiate the responsiveness of Kupffer cells and peritoneal macrophages to endotoxin as measured by the rate of production of TNF-α and PGE. PGE may locally downregulate the immune response by limiting Kupffer cells' and peritoneal macrophages' TNF-α production.

Original languageEnglish (US)
Pages (from-to)12-16
Number of pages5
JournalBurns
Volume19
Issue number1
DOIs
StatePublished - 1993

Fingerprint

Kupffer Cells
Exotoxins
Prostaglandins E
Endotoxins
Tumor Necrosis Factor-alpha
Wounds and Injuries
Peritoneal Macrophages
Down-Regulation
Pseudomonas aeruginosa toxA protein
Abdominal Cavity
Wistar Rats
Macrophages

ASJC Scopus subject areas

  • Emergency Medicine
  • Surgery

Cite this

Dong, Y. L., Ko, F., Yan, T., Huang, H. Q., Herndon, D., & Waymack, J. P. (1993). Evidence for Kupffer cell activation by burn injury and pseudomonas exotoxin A. Burns, 19(1), 12-16. https://doi.org/10.1016/0305-4179(93)90094-O

Evidence for Kupffer cell activation by burn injury and pseudomonas exotoxin A. / Dong, Y. L.; Ko, F.; Yan, T.; Huang, H. Q.; Herndon, David; Waymack, J. P.

In: Burns, Vol. 19, No. 1, 1993, p. 12-16.

Research output: Contribution to journalArticle

Dong, YL, Ko, F, Yan, T, Huang, HQ, Herndon, D & Waymack, JP 1993, 'Evidence for Kupffer cell activation by burn injury and pseudomonas exotoxin A', Burns, vol. 19, no. 1, pp. 12-16. https://doi.org/10.1016/0305-4179(93)90094-O
Dong, Y. L. ; Ko, F. ; Yan, T. ; Huang, H. Q. ; Herndon, David ; Waymack, J. P. / Evidence for Kupffer cell activation by burn injury and pseudomonas exotoxin A. In: Burns. 1993 ; Vol. 19, No. 1. pp. 12-16.
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AB - Postburn metabolic and immunological alterations may in part be due to translocation of gut exotoxin and endotoxin, which can result in tumour necrosis factor (TNF) and prostaglandin E (PGE) production by macrophages. We evaluated the effect of burn injury, plus exotoxin and endotoxin on TNF-α and PGE production by Kupffer cells, and peritoneal macrophages. Adult Wistar rats underwent 30 per cent TBSA burn or sham burn. Kupffer cells were harvested from rat livers and peritoneal macrophages from the abdominal cavity 24 h postburn. They were cultured overnight at 1 × 106 cells/ml and stimulated with saline, 5 μg/ml of Pseud. aeruginosa Exotoxin A (Exo-A), 5 μg/ml of Pseud. aeruginosa Endotoxin (Endo), Exo-A + Endo, or Exo-A + Endo + the PGE derivative 16,16 dimethyl-PGE (dPGE) (10μg/ml). The supernatants were harvested after 4, 24 and 48 h of culture and assayed for TNF-α and PGE. Results showed that burn injury induced an increase in TNF-α and PGE production by Kupffer cells stimulated with Exo-A, Endo, and both Exo-A + Endo (P < 0.05). The release of TNF-α by Kupffer cells was downregulated by exogenous PGE (P < 0.05). The increased TNF-α production was inversely related to PGE levels. In conclusion, both burn injury and Exo-A potentiate the responsiveness of Kupffer cells and peritoneal macrophages to endotoxin as measured by the rate of production of TNF-α and PGE. PGE may locally downregulate the immune response by limiting Kupffer cells' and peritoneal macrophages' TNF-α production.

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