Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.6.1.2 (
alanine aminotransferase
)
26,722
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
IL-19
, a proinflammatory cytokine, belongs to the IL-10 family.
IL-19
is induced in systemic inflammatory response syndrome, but its pathophysiological function in sepsis is unclear. Our aim was to determine the roles of
IL-19
in endotoxin-induced tissue damage in vivo and in vitro. We examined serum levels of
IL-19
in sepsis patients and healthy volunteers, determined the in vitro effects of
IL-19
on lung epithelial cells, liver cells, and neutrophils, and analyzed the tissue expression of
IL-19
and its receptors in murine endotoxic shock. Electroporation-mediated gene transfer of mouse
IL-19
-soluble receptor plasmid DNA was used to determine the effects of
IL-19
depletion in preventing endotoxic shock-induced tissue damage in mice. We found that serum levels of
IL-19
were higher in patients than in healthy volunteers (n = 28, P = 0.001).
IL-19
induced apoptosis in lung epithelial cells and reactive oxygen species production in liver cells in vitro.
IL-19
also promoted neutrophil chemotaxis, reduced neutrophil apoptosis, and induced the production of proinflammatory cytokines and chemokines (IL-1[beta], IL-6, IL-8, CCL5, and CXCL9) in lung epithelial cells. In LPS-challenged mice, transcripts of
IL-19
and its receptors were up-regulated in heart, lung, liver, and kidney tissue. Neutrophil infiltration in lung and liver tissue, and serum levels of
alanine transaminase
and aspartate transaminase, were lower in mice electroporated with
IL-19
-soluble receptor plasmid DNA before LPS treatment compared with control mice. These results suggest that up-regulated
IL-19
may be involved in lung and liver tissue injury in murine endotoxic shock.
...
PMID:IL-19 is involved in the pathogenesis of endotoxic shock. 1824 2
Interleukin (IL)-19 is a cytokine clustered in the IL-20 cytokine superfamily with both anti-inflammatory and pro-inflammatory aspects depending on the etiology of inflammatory disease. The function of
IL-19
has been evaluated in cutaneous and inflammatory bowel diseases, but has not been studied in liver diseases. Here, we examined the effect of
IL-19
on acute liver failure (ALF) using two mouse models of ALF: lipopolysaccharide and D-galactosamine (LPS/GalN)-induced model and concanavalin A (ConA)-induced model. In the LPS/GalN-induced ALF model, which is mainly caused by the innate immune response of liver macrophages,
IL-19
knockout (KO) mice showed increased plasma level of liver deviation enzymes, aspartate aminotransferase (AST) and
alanine aminotransferase
(
ALT
) compared with wild-type (WT) mice. In histopathology of liver sections,
IL-19
KO mice exacerbated liver injury with marked hemorrhagic lesions and hepatocellular death in the liver compared with WT mice. In this model, mRNA expressions of pro-inflammatory chemokines, CCL2 and CCL5 were increased in liver tissue from
IL-19
KO mice compared with WT mice. Moreover, the mRNA expressions of
IL-19
and its receptor subunit were induced in liver tissue by LPS/GalN administration. However, there is no difference in liver injury between WT and IL-19KO in the ConA-induced ALF model induced by CD4
+
T cell activation. These data suggest that
IL-19
has a protective effect against inflammation-mediated liver injury, which is dependent on the etiology.
...
PMID:Deficiency of interleukin-19 exacerbates lipopolysaccharide/D-galactosamine-induced acute liver failure. 3277 17
