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Immune mechanisms in the process of hepatopathies chronicization. Contribution and role of lymphokines
M Bordea1, C Teleianu, A Popamare
1D. Danielopolu Institute of Normal and Patho-physiology.
Insights
Interleukin-6 (IL-6) plays a key role in chronic hepatitis pathogenesis. Elevated IL-6 serum levels correlate with liver inflammation and disease activity, making it a valuable monitoring tool for chronic hepatitis patients.
Area of Science:
- Hepatology
- Immunology
Background:
- Chronic hepatitis pathogenesis involves complex immune responses.
- Interleukin-6 (IL-6) is a cytokine implicated in inflammatory processes.
Purpose of the Study:
- To evaluate the role of IL-6 in the pathogenesis of chronic hepatitis.
- To assess the correlation between IL-6 serum levels and disease activity.
Main Methods:
- Enzyme immunoassay (EIA) to determine serum IL-6 concentrations.
- Comparison of IL-6 levels in patients with different types of chronic hepatitis and healthy controls.
- Immunologic tests including T-lymphocyte markers and immunoglobulin levels.
Main Results:
- Serum IL-6 levels were significantly higher in patients with chronic active hepatitis (CAH) compared to controls.
- Elevated IL-6 correlated with higher immunoglobulin concentrations, particularly IgM, which was linked to HBsAg presence.
- Increased IL-6 serum concentrations were observed during periods of severe hepatic inflammation (cytolytic syndrome) and decreased as transaminase levels reduced.
Conclusions:
- IL-6 is produced in the liver by activated T lymphocytes and Kupffer cells.
- Serum IL-6 activity reflects the degree of liver inflammation in chronic hepatitis.
- IL-6 can serve as a parameter for monitoring disease progression and activity in chronic hepatitis.
Abstract:
The study attempts to evaluate the role of interleukin-6 (IL-6) in the pathogenesis of chronic hepatitis. We have used EIA sensitive methods to determine the serum concentration in patients with chronic active hepatitis of HB (+) (CAH-HE Ag+) antigen, with chronic active hepatitis of HB(-) (CAH-HBAg-) antigen and in those with persistent chronic hepatitis of HB(+) (CPH-HBAg+) antigen, compared with a group of controls (blood donors) in whom HBAgs, antiHBs, HBAge, antiHBe and anti HBc were absent. Disease status diagnosis was given in accordance with international conventions, immunologic tests included. The fact that the T lymphocytes with a CD56 are present in the liver and that same marker is also encountered on the Kuppfer cells, but not on the T lymphocytes in circulation, shows that in the liver the interleukin 6 is produced by the activated T lymphocytes and by the Kuppfer cells. Therefore, in such conditions, LB stimulation and growth is performed rather by IL-6 and to a lesser extent by IL-8. This statement is also supported by the finding that in the lymphocyte cultures in the peripheral blood there is no difference in the response to polyclonal mitogens between patients with CAH-HBAg(+) and those with CAH-HBAg(-). Also, there are no significant differences in the total immunoglobulin concentrations, but there are differences in the IgM concentration (greater in CAH-HBAg(+). In our investigations, the serum level of IL-6 (40.1 +/- 6.8 pg/ml) was higher in those with higher immunoglobulin concentrations-both IgG, but more particularly IgM. The IgM increase was correlated with the presence of HBAg. Therefore, the highest IL-6 values were found in CAH with HBAg(+). Increases of serum IL-6 concentrations were found during intervals of severe hepatic aggression manifested in a cytolitic syndrome, with transaminase increase. In the case of determinations in dynamics, the values decreased as the enzyme titre decreased. We can state that the serum activity of IL-6 reflects the degree of liver inflammation and can be used as a parameter for monitoring the disease.