Obese Patients With Nonalcoholic Fatty Liver Disease Have an Increase in Soluble Plasma CD163 and a Concurrent...

Area of Science:

• Hepatology
• Immunology
• Metabolic Diseases

Background:

• Macrophages are key players in nonalcoholic fatty liver disease (NAFLD) pathogenesis and progression to nonalcoholic steatohepatitis (NASH).
• The macrophage scavenger receptor CD163 and its soluble form (sCD163) are implicated in liver inflammation and fibrosis.
• Obesity is a major risk factor for NAFLD and NASH, highlighting the need to understand immune cell roles in this population.

Purpose of the Study:

• To investigate the association between hepatic CD163 expression and plasma sCD163 levels with NAFLD severity in obese patients.
• To evaluate sCD163 as a potential non-invasive biomarker for NASH diagnosis.
• To explore the relationship between macrophage markers and liver disease progression.

Main Methods:

• Analysis of paired liver biopsies and plasma samples from 61 obese patients (BMI ≥35) with varying degrees of NAFLD.
• Quantification of hepatic CD163 expression using immunohistochemistry and mass spectrometry.
• Measurement of plasma sCD163 levels via ELISA and mass spectrometry.
• Assessment of NAFLD stage and activity using established scoring systems (Kleiner fibrosis and NASH-CRN).

Main Results:

• Plasma sCD163 levels were significantly elevated in patients with NASH and correlated positively with NAFLD severity.
• sCD163 demonstrated good predictive value for NASH (AUC = 0.78).
• Hepatic CD163 expression was negatively associated with NAFLD severity and fibrosis stage, and inversely correlated with plasma sCD163 levels.

Conclusions:

• Increased plasma sCD163 is a promising biomarker for predicting NASH in obese individuals.
• Decreased hepatic CD163 expression, alongside elevated sCD163, is strongly linked to the presence and severity of NAFLD in obese patients.
• These findings underscore the complex role of macrophage CD163 in NAFLD pathogenesis and suggest sCD163 as a potential diagnostic tool.