Inflammation and its role in the aetiopathogenesis of malignant brain tumours

Abstract

The role of inflammation in the aetiopathogenesis of malignant brain tumours is increasingly recognised. Chronic inflammation, characterised by a sustained immune response and tissue remodelling, contributes to the development and progression of tumours. Activated microglia and infiltrating immune cells in the brain release proinflammatory cytokines and reactive oxygen species, creating a neuroinflammatory environment that promotes tumour growth. This persistent inflammation leads to DNA damage, mutations and epigenetic changes, thus favouring malignancy. Epidemiological studies have linked chronic inflammatory diseases and infections to an increased risk of brain tumours. Underlying mechanisms include activating signalling pathways such as nuclear factor kappa B (NF-κB) and signal transducer and activator of transcription 3 (STAT3), which promote cell proliferation and survival. In contrast, inflammatory mediators promote angiogenesis and evasion of the immune system. This text discusses the role of inflammatory markers and chronic bacterial and viral infections in developing brain tumours.