Chapters authored
Vascular Endothelial Growth Factor (VEGF) in Liver Disease
Vascular endothelial growth factor (VEGF) is the most potent stimulating factor for angiogenesis. Its expression is related to inflammation and hypoxia. In normal conditions, VEGF is important in the wound healing process. The binding of VEGF with its receptors triggers angiogenesis and lymphangiogenesis and increases vascular permeability. Liver diseases comprise acute and chronic ones. Liver diseases cause inflammation and hypoxia, which increase VEGF level. If they occur chronically, persistent high VEGF levels will promote the risk of chronic liver diseases, including hepatic viral infections, alcoholic and nonalcoholic fatty liver diseases, liver cirrhosis, and finally hepatocellular carcinoma (HCC). High VEGF level is also associated with progressive disease course and poorer outcomes. Tissue remodeling by replacement of normal liver tissue with fibrous tissue occurs. Due to the importance of VEGF in angiogenesis and liver diseases, therapeutic agents targeting VEGF have been developed. Drugs that neutralize VEGF and modulate VEGF receptors have been approved for treating various disorders, including liver disease. Additionally, VEGF is a promising modality for diagnosing liver cirrhosis and HCC. VEGF may also be utilized to predict the outcome of the liver and to monitor the therapeutic response of patients.
Part of the book: Tumor Angiogenesis and Modulators
Immunology of Helicobacter pylori Infection
Helicobacter pylori (H. pylori) is the most common infecting microorganism in humans. H. pylori had coexisted with humans for 30,000 years ago and developed extensive survival adaptations. The infection is both active and chronic and leads to several disorders from chronic gastritis to gastric adenocarcinoma. The prevalence of H. pylori infection is still high in developing countries. The burden of disease due to infection is also heavy. The persistence of infection is the basis of diseases. H. infection activates innate and adaptive immune responses but the immune response fails to eradicate the infection. H. pylori is able to evade both innate and adaptive immune responses. It can neutralize gastric acid, elicit autoimmunity toward parietal cells, prevent phagocytosis, induce apoptosis of immune cells, inhibit lymphocyte proliferation, disrupt imbalance between humoral and cellular adaptive immune responses, promote regulatory T cell activity, and trigger genetic rearrangement. Host factor is involved in the incidence of H. pylori infection and its complications. Reinfection after eradication is common. Multiple drug resistance has also emerged. Vaccination is a promising management approach to eradicate H. pylori and prevent diseases it caused. The development of the vaccine itself needs to consider the immune escape mechanism of H. pylori.
Part of the book: Immunology of the GI Tract