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The alkaline phosphatase activity in DBA/2 and A/JAX mouse strains injected with mouse hepatitis virus 3: a
Abstract:
ALP activity has been studied during hepatitis (infection) in two genetically controlled mouse strains having different degrees of susceptibility ot MHV3 virus: A/JAX (resistant) and DBA/2 (susceptible). During the 8 days following viral infection we have compared ALP activity in serum and liver homogenates with ALP cytological localization in liver tissue (light and electron microscopy). Firstly, liver ALP activity has been demonstrated in the Disse's spaces, on the membrane of the hepatocytes microvilli whilst serum ALP was still very low. The serum ALP activity begins to increase markedly since the third day in sensitive mice (DBA/2), i.e., when the electron microscopy hepatocytes look very damaged; hepatocytes have lost most of their microvilli; necrotic vesicles, degenerative cytoplasmic organelles, lipid vesicles occurred in numerous hepatocytes. ALP activity has disappeared at the biliary pole of the cells whilst it increased at the vascular pole. Moreover, electron microscopic studies demonstrated that ALP positive cells are exclusively of lymphoid type whereas Kupffer cells remain ALP negative.
Insights
This study investigated alkaline phosphatase (ALP) activity during viral hepatitis in mice. In susceptible mice, liver damage correlated with changes in ALP localization and increased serum ALP levels, primarily in lymphoid cells.
Area of Science:
- Hepatology
- Immunology
- Biochemistry
Background:
- Viral hepatitis can cause significant liver damage.
- Alkaline phosphatase (ALP) is an enzyme found in liver cells and other tissues.
- Understanding ALP's role during infection can provide insights into disease progression.
Purpose of the Study:
- To investigate changes in alkaline phosphatase (ALP) activity and localization in the liver during viral hepatitis.
- To compare ALP activity in susceptible and resistant mouse strains following MHV3 virus infection.
- To correlate ALP changes with liver damage and cellular changes observed via microscopy.
Main Methods:
- Studied ALP activity in serum and liver homogenates of A/JAX (resistant) and DBA/2 (susceptible) mice post-MHV3 infection.
- Utilized light and electron microscopy to examine ALP cytological localization in liver tissue.
- Monitored changes over an 8-day period following viral infection.
Main Results:
- Initially, liver ALP was localized in Disse's spaces and on hepatocyte microvilli before serum ALP increased.
- In susceptible DBA/2 mice, serum ALP markedly increased by day 3, coinciding with severe hepatocyte damage.
- Electron microscopy revealed ALP activity primarily in lymphoid cells, not Kupffer cells, and a shift in localization from the biliary to the vascular pole of hepatocytes.
Conclusions:
- Hepatocyte damage during viral hepatitis is associated with altered ALP localization and increased serum levels.
- Lymphoid cells appear to be a significant source of ALP during the inflammatory response to viral hepatitis.
- Mouse models provide valuable insights into the biochemical and cellular changes during liver disease.