Age-dependent differences of interleukin-6 activity in cardiac function after burn complicated by sepsis

Lin Wang, Jiexia Quan, William E. Johnston, David L. Maass, Jureta W. Horton, James A. Thomas, Weike Tao

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Interleukin (IL)-6 is a pleiotropic cytokine that is activated after acute injuries, and plays an important role during aging. We aim to define the role of IL-6 on myocardial dysfunction following a 40% total body surface area burn followed by late (7 days) Streptococcus pneumoniae sepsis (burn plus sepsis) in 2- and 14-month-old wild type and IL-6-/- mice. We measured global hemodynamic and cardiac contractile function with left ventricular pressure-volume analysis 24 h after sepsis induction, and measured phosphorylated signal transducer and activator of transcription 3 (p-STAT-3), tumor necrosis factor (TNF)-α, and IL-1β in the heart with Western blot analysis. We also measured mRNA expression of IL-6, TNF-α, and IL-1β. Sham injured mice did not manifest any appreciable level of p-STAT-3 or functional deficiencies regardless of age or presence of the IL-6 gene. Burn plus sepsis injury was associated with a significant deterioration of global hemodynamic and cardiac contractile function in WT mice in both age groups. This dysfunction was attenuated by IL-6 deficiency at age 2 months, but accentuated at age 14 months. Aging was associated with an increase in mRNA expression of IL-6 (WT mice), TNF-α, and IL-1β (all mice). At age 14 months, IL-6 deficient mice exhibited a greater TNF-α mRNA expression than the wild type mice. We conclude aging is associated with changed cytokine gene transcription, and burn plus sepsis injury further intensifies such gene responses. IL-6 deficiency does not abrogate STAT-3 phosphorylation and it may enhance expression of other inflammatory cytokines. The differential effects of IL-6 deficiency on the cardiac function in young and aging mice cannot be explained by cytokine gene expression alone, and require further studies.

Original languageEnglish (US)
Pages (from-to)232-238
Number of pages7
JournalBurns
Volume36
Issue number2
DOIs
StatePublished - Mar 2010

Fingerprint

Interleukin-6
Sepsis
Tumor Necrosis Factor-alpha
Interleukin-1
Cytokines
STAT3 Transcription Factor
Messenger RNA
Wounds and Injuries
Hemodynamics
Genes
Body Surface Area
Ventricular Pressure
Streptococcus pneumoniae
Age Groups
Western Blotting
Phosphorylation
Gene Expression
mouse interleukin-6

Keywords

  • Aging
  • Burn
  • Cytokines
  • Heart
  • Interleukin-6
  • Sepsis

ASJC Scopus subject areas

  • Emergency Medicine
  • Critical Care and Intensive Care Medicine
  • Surgery

Cite this

Age-dependent differences of interleukin-6 activity in cardiac function after burn complicated by sepsis. / Wang, Lin; Quan, Jiexia; Johnston, William E.; Maass, David L.; Horton, Jureta W.; Thomas, James A.; Tao, Weike.

In: Burns, Vol. 36, No. 2, 03.2010, p. 232-238.

Research output: Contribution to journalArticle

Wang, Lin ; Quan, Jiexia ; Johnston, William E. ; Maass, David L. ; Horton, Jureta W. ; Thomas, James A. ; Tao, Weike. / Age-dependent differences of interleukin-6 activity in cardiac function after burn complicated by sepsis. In: Burns. 2010 ; Vol. 36, No. 2. pp. 232-238.
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abstract = "Interleukin (IL)-6 is a pleiotropic cytokine that is activated after acute injuries, and plays an important role during aging. We aim to define the role of IL-6 on myocardial dysfunction following a 40{\%} total body surface area burn followed by late (7 days) Streptococcus pneumoniae sepsis (burn plus sepsis) in 2- and 14-month-old wild type and IL-6-/- mice. We measured global hemodynamic and cardiac contractile function with left ventricular pressure-volume analysis 24 h after sepsis induction, and measured phosphorylated signal transducer and activator of transcription 3 (p-STAT-3), tumor necrosis factor (TNF)-α, and IL-1β in the heart with Western blot analysis. We also measured mRNA expression of IL-6, TNF-α, and IL-1β. Sham injured mice did not manifest any appreciable level of p-STAT-3 or functional deficiencies regardless of age or presence of the IL-6 gene. Burn plus sepsis injury was associated with a significant deterioration of global hemodynamic and cardiac contractile function in WT mice in both age groups. This dysfunction was attenuated by IL-6 deficiency at age 2 months, but accentuated at age 14 months. Aging was associated with an increase in mRNA expression of IL-6 (WT mice), TNF-α, and IL-1β (all mice). At age 14 months, IL-6 deficient mice exhibited a greater TNF-α mRNA expression than the wild type mice. We conclude aging is associated with changed cytokine gene transcription, and burn plus sepsis injury further intensifies such gene responses. IL-6 deficiency does not abrogate STAT-3 phosphorylation and it may enhance expression of other inflammatory cytokines. The differential effects of IL-6 deficiency on the cardiac function in young and aging mice cannot be explained by cytokine gene expression alone, and require further studies.",
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