Effect of indomethacin and impact liquid diet administration on inflammatory mediator production by murine splenocytes after burn injury

Ramon Zapata Sirvent, John F. Hansbrough

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Production of prostlaglandin E2 (PGE2) and tumor necrosis factor-α (TNF-α) by various cells is increased after injury, and these mediators are implicated in the downregulation of immune responses. We attempted to modulate the production of immune suppressive mediators by inhibiting prostaglandin production in a murine model that had a burn covering 25% of the total body surface area. Two treatments were performed. One was the intraperitoneal administration of indomethacin after burn injury at 2 mg/kg day for 10 days. The control group received saline solution injections. The other treatment was the ad libitum administration of a commercial diet after burn injury for 10 days. This diet contained mixed fats, including omega-3 and omega-6 fatty acids. The control group received standard mouse food. On days 1, 5, and 10 after burn injury, spleens were removed aseptically, and splenocyte cultures were established and stimulated with phytohemagglutinin. TNF-α and PGE2 concentrations were determined in culture supernatants at 48 hours with the use of commencai enzyme-linked immunosorbent assay kits. Splenocytes from burned animals produced elevated levels of both mediators in culture supernatants, reaching significant levels of TNF-α on day 10 after burn injury and of PGE2 on days 5 and 10 after burn injury. Neither the administration of indomethacin for 10 days nor the administration of the commercial diet for 10 days decreased production of these mediators in culture. However, cells in culture may escape the in vivo regulating effects of biologic modifying agents.

Original languageEnglish (US)
Pages (from-to)538-545
Number of pages8
JournalJournal of Burn Care and Rehabilitation
Volume13
Issue number5
DOIs
StatePublished - Jan 1 1992
Externally publishedYes

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Indomethacin
Diet
Wounds and Injuries
Tumor Necrosis Factor-alpha
Omega-6 Fatty Acids
Control Groups
Body Surface Area
Biological Factors
Phytohemagglutinins
Sodium Chloride
Prostaglandins
Down-Regulation
Spleen
Cell Culture Techniques
Enzyme-Linked Immunosorbent Assay
Fats
Food
Injections
Therapeutics

ASJC Scopus subject areas

  • Surgery
  • Nursing(all)
  • Emergency Medicine
  • Rehabilitation
  • Health Professions(all)

Cite this

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abstract = "Production of prostlaglandin E2 (PGE2) and tumor necrosis factor-α (TNF-α) by various cells is increased after injury, and these mediators are implicated in the downregulation of immune responses. We attempted to modulate the production of immune suppressive mediators by inhibiting prostaglandin production in a murine model that had a burn covering 25{\%} of the total body surface area. Two treatments were performed. One was the intraperitoneal administration of indomethacin after burn injury at 2 mg/kg day for 10 days. The control group received saline solution injections. The other treatment was the ad libitum administration of a commercial diet after burn injury for 10 days. This diet contained mixed fats, including omega-3 and omega-6 fatty acids. The control group received standard mouse food. On days 1, 5, and 10 after burn injury, spleens were removed aseptically, and splenocyte cultures were established and stimulated with phytohemagglutinin. TNF-α and PGE2 concentrations were determined in culture supernatants at 48 hours with the use of commencai enzyme-linked immunosorbent assay kits. Splenocytes from burned animals produced elevated levels of both mediators in culture supernatants, reaching significant levels of TNF-α on day 10 after burn injury and of PGE2 on days 5 and 10 after burn injury. Neither the administration of indomethacin for 10 days nor the administration of the commercial diet for 10 days decreased production of these mediators in culture. However, cells in culture may escape the in vivo regulating effects of biologic modifying agents.",
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N2 - Production of prostlaglandin E2 (PGE2) and tumor necrosis factor-α (TNF-α) by various cells is increased after injury, and these mediators are implicated in the downregulation of immune responses. We attempted to modulate the production of immune suppressive mediators by inhibiting prostaglandin production in a murine model that had a burn covering 25% of the total body surface area. Two treatments were performed. One was the intraperitoneal administration of indomethacin after burn injury at 2 mg/kg day for 10 days. The control group received saline solution injections. The other treatment was the ad libitum administration of a commercial diet after burn injury for 10 days. This diet contained mixed fats, including omega-3 and omega-6 fatty acids. The control group received standard mouse food. On days 1, 5, and 10 after burn injury, spleens were removed aseptically, and splenocyte cultures were established and stimulated with phytohemagglutinin. TNF-α and PGE2 concentrations were determined in culture supernatants at 48 hours with the use of commencai enzyme-linked immunosorbent assay kits. Splenocytes from burned animals produced elevated levels of both mediators in culture supernatants, reaching significant levels of TNF-α on day 10 after burn injury and of PGE2 on days 5 and 10 after burn injury. Neither the administration of indomethacin for 10 days nor the administration of the commercial diet for 10 days decreased production of these mediators in culture. However, cells in culture may escape the in vivo regulating effects of biologic modifying agents.

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