Ltb, or leukotriene B4, is a lipid mediator derived from arachidonic acid. It acts as a chemoattractant for inflammatory leukocytes and is a key mediator in a cascade involving complement, lipid, cytokine, and chemokine, which initiates and sustains neutrophilic inflammation in inflammatory arthritis [1,3]. Ltb binds to two receptors, the high-affinity receptor BLT1 and the low-affinity receptor BLT2, and the Ltb/BLT1 axis is involved in leukocyte recruitment to infected sites and pathogen elimination [2].

In Chronic Granulomatous Disease (CGD), a Ltb4/CD11b self-amplifying loop drives pyogranuloma formation. Antagonizing BLT1 blocked neutrophil aggregation in an ex vivo system of pyogranuloma formation using peritoneal cells of zymosan-treated CGD (gp91phox-/-) mice, indicating the importance of Ltb in this hyperinflammatory condition [4]. In Lyme arthritis, macrophages from 5-lipoxygenase (5-LOX)-/-mice, which are defective in Ltb production, showed impaired phagocytosis of Borrelia burgdorferi. Exogenous Ltb addition augmented phagocytic capability, suggesting Ltb's role in macrophage phagocytosis [5].

In conclusion, Ltb is crucial in inflammatory processes, leukocyte recruitment, and phagocytosis. Studies using gene-knockout mouse models, such as in CGD and Lyme arthritis, have revealed its role in specific disease-related biological processes, providing insights into potential therapeutic targets for inflammatory diseases.