Role of CD14 in hemorrhagic shock-induced alterations of the monocyte tumor necrosis factor response to endotoxin

Fiemu Nwariaku, Pat Sikes, Ellis Lightfoot, Kendra McIntyre, William Mileski

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Objective: To determine if the shock-induced alterations in whole blood monocyte tumor necrosis factor (TNF) response are mediated by the CD14 receptor. Design: Prospective controlled animal experiments. Materials and Methods: New Zealand White rabbits (n = 15) were subjected to hemorrhage and resuscitation. Blood samples obtained before shock and 24, 72, and 120 hours after shock were stimulated with lipopolysaccharide in the presence or absence of the anti-CD14 monoclonal antibody, 63D3. Tumor necrosis factor was assayed using 1,929 cells. Measurements and Main Results: There was no detectable TNF activity in unstimulated blond. The CD14 inhibition resulted in a 55% reduction in baseline TNF activity. After shock, there was a marked increase in TNF activity with lipopolysaccharide stimulation. Addition of 63D3 resulted in a dose-dependent 95% reduction in TNF activity at 24 and 72 hours after shock, (p < 0.05). Conclusion: The enhanced whole blood monocyte TNF response after hemorrhage is CD14 dependent.

Original languageEnglish (US)
Pages (from-to)564-567
Number of pages4
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume40
Issue number4
DOIs
StatePublished - Apr 1996
Externally publishedYes

Fingerprint

Hemorrhagic Shock
Endotoxins
Monocytes
Tumor Necrosis Factor-alpha
Shock
Lipopolysaccharides
Hemorrhage
Resuscitation
Monoclonal Antibodies
Rabbits

Keywords

  • CD14
  • Cytokine
  • Hypovolemic
  • Inflammation
  • Monocyte
  • Shock

ASJC Scopus subject areas

  • Surgery

Cite this

Role of CD14 in hemorrhagic shock-induced alterations of the monocyte tumor necrosis factor response to endotoxin. / Nwariaku, Fiemu; Sikes, Pat; Lightfoot, Ellis; McIntyre, Kendra; Mileski, William.

In: Journal of Trauma - Injury, Infection and Critical Care, Vol. 40, No. 4, 04.1996, p. 564-567.

Research output: Contribution to journalArticle

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AU - Sikes, Pat

AU - Lightfoot, Ellis

AU - McIntyre, Kendra

AU - Mileski, William

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N2 - Objective: To determine if the shock-induced alterations in whole blood monocyte tumor necrosis factor (TNF) response are mediated by the CD14 receptor. Design: Prospective controlled animal experiments. Materials and Methods: New Zealand White rabbits (n = 15) were subjected to hemorrhage and resuscitation. Blood samples obtained before shock and 24, 72, and 120 hours after shock were stimulated with lipopolysaccharide in the presence or absence of the anti-CD14 monoclonal antibody, 63D3. Tumor necrosis factor was assayed using 1,929 cells. Measurements and Main Results: There was no detectable TNF activity in unstimulated blond. The CD14 inhibition resulted in a 55% reduction in baseline TNF activity. After shock, there was a marked increase in TNF activity with lipopolysaccharide stimulation. Addition of 63D3 resulted in a dose-dependent 95% reduction in TNF activity at 24 and 72 hours after shock, (p < 0.05). Conclusion: The enhanced whole blood monocyte TNF response after hemorrhage is CD14 dependent.

AB - Objective: To determine if the shock-induced alterations in whole blood monocyte tumor necrosis factor (TNF) response are mediated by the CD14 receptor. Design: Prospective controlled animal experiments. Materials and Methods: New Zealand White rabbits (n = 15) were subjected to hemorrhage and resuscitation. Blood samples obtained before shock and 24, 72, and 120 hours after shock were stimulated with lipopolysaccharide in the presence or absence of the anti-CD14 monoclonal antibody, 63D3. Tumor necrosis factor was assayed using 1,929 cells. Measurements and Main Results: There was no detectable TNF activity in unstimulated blond. The CD14 inhibition resulted in a 55% reduction in baseline TNF activity. After shock, there was a marked increase in TNF activity with lipopolysaccharide stimulation. Addition of 63D3 resulted in a dose-dependent 95% reduction in TNF activity at 24 and 72 hours after shock, (p < 0.05). Conclusion: The enhanced whole blood monocyte TNF response after hemorrhage is CD14 dependent.

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