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Related Experiment Video

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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis

Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis

Published on: March 11, 2017

Complement alternative pathway activation in human nonalcoholic steatohepatitis.

Filip M Segers¹, Froukje J Verdam¹, Charlotte de Jonge²

¹Department of General Surgery, Maastricht University Medical Centre+, Maastricht, the Netherlands.

|October 10, 2014

Summary

The alternative pathway of complement is activated in nonalcoholic steatohepatitis (NASH), contributing to liver inflammation. Targeting this pathway offers a potential therapeutic strategy for NASH.

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Area of Science:

Immunology
Hepatology
Complement System

Background:

Nonalcoholic steatohepatitis (NASH) pathogenesis involves the innate immune system.
Complement activation has been reported in human NASH.
The role of the alternative complement pathway in NASH was previously unclear.

Purpose of the Study:

To investigate the involvement of alternative complement pathway components in NASH.
To assess the correlation between alternative pathway activation and liver inflammation severity in NASH.

Main Methods:

Analysis of liver biopsies from obese subjects with and without NASH.
Quantitative PCR, Western blotting, and immunofluorescence staining were employed.
Assessment of complement components like properdin, C3, factor B, factor D, factor H, and Decay Accelerating Factor.

Main Results:

Properdin accumulated in NASH livers, co-localizing with C3 activation products.
C3 activation status was significantly higher in NASH patients.
Properdin levels correlated positively with C3 activation and lobular inflammation scores.
Factor H expression was downregulated in NASH, while Decay Accelerating Factor showed a trend towards increase.

Conclusions:

Alternative complement pathway activation plays a role in driving hepatic inflammation in NASH.
Alternative pathway factors represent potential therapeutic targets for NASH treatment by inhibiting complement activation.