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: UNIPROT:P17174 (
aspartate aminotransferase
)
14,872
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
