The role of keratinocyte-derived chemokine in hemorrhage-induced acute lung injury in mice

J Korean Med Sci. 2009 Oct;24(5):775-81. doi: 10.3346/jkms.2009.24.5.775. Epub 2009 Sep 23.

Abstract

Dominant inflammatory cytokines might be different depending on the underlying causes of acute lung injury (ALI). The role of kertinocyte-derived chemokine (KC), a potent chemoattractant for neutrophils, has not been clearly established in hemorrhage-induced ALI. In this study, lung injury and cytokine expression were evaluated in LPS- or hemorrhage-induced ALI models of BALB/c mice. The myeloperoxidase activities at 4 hr after hemorrhage and LPS-injection were 47.4+/-13.0 and 56.5+/-16.4 U/g, respectively. NF-kappaB activity peaked at 4 hr after hemorrhage, which was suppressed to the control level by anti-high mobility group B1 (HMGB1) antibody. Lung expressions of TNF-alpha, MIP-2, and IL-1beta were increased by LPS injection. However, there was only a minimal increase in IL-1beta and no expressions of TNF-alpha or MIP-2 in hemorrhage-induced ALI. In contrast, lung KC increased significantly at 4 hr after hemorrhage compared to control levels (83.1+/-12.3 vs. 14.2+/-1.6 pg/mL/mg by ELISA) (P<0.05). By immunohistochemical staining, lung neutrophils stained positive for KC. Increased KC was also observed in bronchoalveolar lavage fluid and plasma. KC plays an important role in hemorrhage-induced ALI.

Keywords: Acute Lung Injury; Hemorrhage; Keratinocyte-derived Chemokines; LPS.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / etiology
  • Acute Lung Injury / metabolism*
  • Animals
  • Antibodies / immunology
  • Antibodies / metabolism
  • Chemokine CXCL2 / analysis
  • Chemokines / analysis
  • Chemokines / blood
  • Chemokines / physiology*
  • Chickens
  • HMGB1 Protein / metabolism
  • Humans
  • Interleukin-1beta / analysis
  • Lipopolysaccharides / toxicity
  • Mice
  • Mice, Inbred BALB C
  • NF-kappa B / metabolism
  • Neutrophils / immunology
  • Neutrophils / metabolism
  • Peroxidase / analysis
  • Shock, Hemorrhagic / complications*
  • Time Factors
  • Tumor Necrosis Factor-alpha / analysis

Substances

  • Antibodies
  • Chemokine CXCL2
  • Chemokines
  • HMGB1 Protein
  • Interleukin-1beta
  • Lipopolysaccharides
  • NF-kappa B
  • Tumor Necrosis Factor-alpha
  • keratinocyte-derived chemokines
  • Peroxidase