Effect of chronic ethanol consumption on the expression of complement components and acute-phase proteins in liver.

• The complement system can provoke but also participate in the repair of liver injury. Here we investigated by microarray analysis the effect of chronic ethanol consumption on hepatic mRNA expression of complement components and acute-phase proteins in complement C3-deficient (C3(-/-)) and wild-type (C3(+/+)) mice. Up-regulation by ethanol of factor B, C1qA-chain and clusterin but down-regulation of factor H, Masp-2, factor D and the terminal components C6, C8alpha and C9 was seen in both strains. Ethanol up-regulated C2 and down-regulated C4bp only in C3(+/+) mice, while in C3(-/-) mice up-regulation of C1qB-chain and vitronectin was observed. The expression of factor B, C6, C1qB and factor I was lower but that of factor D higher in C3(-/-) than in C3(+/+) mice. Ethanol induced mRNA synthesis of many acute-phase proteins including SPARC and lipocalin-2, but reduced the expression of SAP. The induction of early classical and alternative pathway components and suppression of terminal pathway components and soluble regulators may thus contribute to alcohol-induced liver injury. Lipocalin-2 and SPARC emerge as new candidate markers for early detection of liver damage.

Nyckelord

Acute-Phase Proteins

biosynthesis

genetics

immunology

Alcohol Drinking

genetics

immunology

metabolism

Animals

Complement System Proteins

biosynthesis

genetics

immunology

Ethanol

administration & dosage

toxicity

Gene Expression

Liver

immunology

Liver Diseases

Alcoholic

genetics

immunology

Male

Mice

Mice

Inbred C57BL

Oligonucleotide Array Sequence Analysis

methods

Oncogene Proteins

biosynthesis

immunology

Osteonectin

biosynthesis

immunology

RNA

Messenger

biosynthesis

genetics

Reverse Transcriptase Polymerase Chain Reaction

methods

Publikations- och innehållstyp

ref (ämneskategori)

art (ämneskategori)