PubMed1995
Bacterial endotoxins (BE) that are lipopolysaccharide complexes (LPS) are a structural component of the external membrane of gram-negative bacteria. In normalcy, BE interact with many types of cells in the mammals. In terms of the concentration, BE may cause cell damage or stimulate the production of many biological mediators, such as interleukins, prostaglandinds, alpha-TNF. Many gastrointestinal bacteria in humans are gram-negative and BE constantly enter the blood. In health, the absence of a toxic response to BE is explained by the presence of natural humoral and cellular antiendotoxic systems and the hepatic absorption of LPS. In patients with hepatitis A and B, the following indices of the blood antiendotoxic systems were determined: the level of antiendotoxic antibodies to Re-chemotype glycolipids was assessed by the passive hemagglutination reaction in the "Antiendotox-1-test"; the count of polymorphonuclear leukocyte (PMNL) fixating LPS on their own surface and endotoxin binding function of PMNL was in vitro measured by the strain ELISA and sandwich ELISA with Re-glycolipids, respectively (LPS-test); the endotoxin fixation function of serum high density lipoproteins (HDL) was also assessed. The humoral and cellular antiendotoxic systems in patients with mild advanced hepatitis A and B was studied when the disease was most clinically significant, at an early convalescence, and at convalescence itself. Finally, the findings indicate that there is a significant decrease in Re-antibody levels and there is a greater absorption ability of HDL than that in the control. Six different types of an antiendotoxic fixation reaction of PMNL were identified in patients with viral hepatitis in the different periods of the disease. The alterations observed may play an important role in the pathogenesis of toxemia in patients with viral hepatitis.