Date of Award

7-2009

Degree Type

Thesis

Degree Name

MS Biology

Department

Biology

Advisor

Heping Zhou

Committee Member

Allan Blake

Committee Member

Jane Ko

Keywords

Lipopolysaccharide, LPS-induced activation of hepatic map kinases

Abstract

Lipopolysaccharide (LPS) is a potent inflammagen that has been found to be primarily responsible for many symptoms caused by gram-negative bacterial infections. The LPS-initiated signal transduction pathways involve several terminal kinases, mainly p42/44 mitogen-activated protein kinase (MAPK), p38 MAPK and c-Jun N-terminal kinase (JNK), ultimately leading to increased expression of genes encoding such inflammatory cytokines as interleukin (IL )-1 �. IL-6 and tumor necrosis factors (TNF)-u. In this study, the effects of age on LPS-induced activation of MAPKs in the liver of rats were examined. Results show that the basal level of phosphorylated p42/44 MAPK was increased in postnatal day (P) 21 and P70 compared to P 1 animals treated with saline, and that LPS significantly increased the phosphorylation of p42/44 MAPK at P21 and P70. On the other hand, both basal and phosphorylated p38 MAPK did not show significant changes in P21 and P70 liver compared to PI. The effects of maternal exposure to LPS on the activation of MAPKs in P21 offspring liver were also examined. Results show that p42/44 MAPK activation was significantly decreased in the liver of pups born to LPS-treated dams as compared to those born to saline-treated dams following LPS stimulation. However, p38 MAPK and JNK activation was not affected by maternal exposure to LPS. These results indicate that MAPKs are differentially modulated by age and maternal exposure to LPS.

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