Acute ethanol exposure combined with burn injury enhances IL-6 levels in the murine ileum

Michael T. Scalfani, David M. Chan, Eva L. Murdoch, Elizabeth J. Kovacs, Fletcher White

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Background: Recent studies suggest that ethanol use imposes a greater risk of trauma-associated intestinal injury than trauma alone. The initiating and regulatory factors for multiple organ dysfunction syndromes are not well defined, yet evidence points to the gut as a possible trigger of the systemic inflammatory cascade as well as a potential source of cytokines. In the current study, we hypothesized that ethanol administration would alter cytokine levels and intestinal infiltration by neutrophils within the ileum of mice exposed to burn injury (15% total body surface of dorsal skin). Methods: Ileal samples were collected for histological assessment, myeloperoxidase quantitation and the protein presence of tumor necrosis factor alpha (TNFα), interleukin (IL-) 6, macrophage inflammatory protein-2 (MIP-2; CXCL2) and the anti-inflammatory cytokine, IL-10. Additional ileal tissue samples were examined for localization of the IL-6 immunoreactivity. Results: We did not detect statistically significant cytokine/chemokine differences (MIP-2 and IL-10) between sham control and treatment conditions at either 2 or 24 hours. However, there was a significant decrease in TNFα at 24 hours in both burn injury alone and in combination with ethanol treatment conditions (p <0.05). In addition, there was an increase in IL-6 levels at 24 hours in intestinal tissue obtained from mice subjected to a combination of acute ethanol and burn injury, compared to the mice receiving burn or sham injury (p <0.001). Ileal homogenate increases in IL-6 at 24 hours were concurrent with decreased villus height in the ileum, but no discernable changes in neutrophil infiltration (myeloperoxidase activity levels) at either 2 or 24 hours. Additional immunocytochemical localization studies of ileal tissue revealed that there was a substantial increase of IL-6 in intestinal enterocytes subjected to both burn injury alone, or in combination with acute ethanol exposure. Conclusions: The present study suggests that acute ethanol exposure combined with burn injury enhances levels of IL-6 protein in the ileum. The enhanced levels of ileal IL-6 are likely due to enterocyte production of the cytokine.

Original languageEnglish (US)
Pages (from-to)1731-1737
Number of pages7
JournalAlcoholism: Clinical and Experimental Research
Volume31
Issue number10
DOIs
StatePublished - Oct 2007
Externally publishedYes

Fingerprint

Ileum
Interleukin-6
Ethanol
Wounds and Injuries
Cytokines
Chemokine CXCL2
Tissue
Infiltration
Interleukin-10
Peroxidase
Neutrophil Infiltration
Enterocytes
Tumor Necrosis Factor-alpha
Multiple Organ Failure
Skin
Proteins
Anti-Inflammatory Agents
Placebos

Keywords

  • Burn
  • Interleukin-6
  • Pro-inflammatory Cytokines
  • Small Intestines

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology

Cite this

Acute ethanol exposure combined with burn injury enhances IL-6 levels in the murine ileum. / Scalfani, Michael T.; Chan, David M.; Murdoch, Eva L.; Kovacs, Elizabeth J.; White, Fletcher.

In: Alcoholism: Clinical and Experimental Research, Vol. 31, No. 10, 10.2007, p. 1731-1737.

Research output: Contribution to journalArticle

Scalfani, Michael T. ; Chan, David M. ; Murdoch, Eva L. ; Kovacs, Elizabeth J. ; White, Fletcher. / Acute ethanol exposure combined with burn injury enhances IL-6 levels in the murine ileum. In: Alcoholism: Clinical and Experimental Research. 2007 ; Vol. 31, No. 10. pp. 1731-1737.
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T1 - Acute ethanol exposure combined with burn injury enhances IL-6 levels in the murine ileum

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AU - Chan, David M.

AU - Murdoch, Eva L.

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AU - White, Fletcher

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N2 - Background: Recent studies suggest that ethanol use imposes a greater risk of trauma-associated intestinal injury than trauma alone. The initiating and regulatory factors for multiple organ dysfunction syndromes are not well defined, yet evidence points to the gut as a possible trigger of the systemic inflammatory cascade as well as a potential source of cytokines. In the current study, we hypothesized that ethanol administration would alter cytokine levels and intestinal infiltration by neutrophils within the ileum of mice exposed to burn injury (15% total body surface of dorsal skin). Methods: Ileal samples were collected for histological assessment, myeloperoxidase quantitation and the protein presence of tumor necrosis factor alpha (TNFα), interleukin (IL-) 6, macrophage inflammatory protein-2 (MIP-2; CXCL2) and the anti-inflammatory cytokine, IL-10. Additional ileal tissue samples were examined for localization of the IL-6 immunoreactivity. Results: We did not detect statistically significant cytokine/chemokine differences (MIP-2 and IL-10) between sham control and treatment conditions at either 2 or 24 hours. However, there was a significant decrease in TNFα at 24 hours in both burn injury alone and in combination with ethanol treatment conditions (p <0.05). In addition, there was an increase in IL-6 levels at 24 hours in intestinal tissue obtained from mice subjected to a combination of acute ethanol and burn injury, compared to the mice receiving burn or sham injury (p <0.001). Ileal homogenate increases in IL-6 at 24 hours were concurrent with decreased villus height in the ileum, but no discernable changes in neutrophil infiltration (myeloperoxidase activity levels) at either 2 or 24 hours. Additional immunocytochemical localization studies of ileal tissue revealed that there was a substantial increase of IL-6 in intestinal enterocytes subjected to both burn injury alone, or in combination with acute ethanol exposure. Conclusions: The present study suggests that acute ethanol exposure combined with burn injury enhances levels of IL-6 protein in the ileum. The enhanced levels of ileal IL-6 are likely due to enterocyte production of the cytokine.

AB - Background: Recent studies suggest that ethanol use imposes a greater risk of trauma-associated intestinal injury than trauma alone. The initiating and regulatory factors for multiple organ dysfunction syndromes are not well defined, yet evidence points to the gut as a possible trigger of the systemic inflammatory cascade as well as a potential source of cytokines. In the current study, we hypothesized that ethanol administration would alter cytokine levels and intestinal infiltration by neutrophils within the ileum of mice exposed to burn injury (15% total body surface of dorsal skin). Methods: Ileal samples were collected for histological assessment, myeloperoxidase quantitation and the protein presence of tumor necrosis factor alpha (TNFα), interleukin (IL-) 6, macrophage inflammatory protein-2 (MIP-2; CXCL2) and the anti-inflammatory cytokine, IL-10. Additional ileal tissue samples were examined for localization of the IL-6 immunoreactivity. Results: We did not detect statistically significant cytokine/chemokine differences (MIP-2 and IL-10) between sham control and treatment conditions at either 2 or 24 hours. However, there was a significant decrease in TNFα at 24 hours in both burn injury alone and in combination with ethanol treatment conditions (p <0.05). In addition, there was an increase in IL-6 levels at 24 hours in intestinal tissue obtained from mice subjected to a combination of acute ethanol and burn injury, compared to the mice receiving burn or sham injury (p <0.001). Ileal homogenate increases in IL-6 at 24 hours were concurrent with decreased villus height in the ileum, but no discernable changes in neutrophil infiltration (myeloperoxidase activity levels) at either 2 or 24 hours. Additional immunocytochemical localization studies of ileal tissue revealed that there was a substantial increase of IL-6 in intestinal enterocytes subjected to both burn injury alone, or in combination with acute ethanol exposure. Conclusions: The present study suggests that acute ethanol exposure combined with burn injury enhances levels of IL-6 protein in the ileum. The enhanced levels of ileal IL-6 are likely due to enterocyte production of the cytokine.

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