Children's Health Queensland Clinical Unit, School of Clinical Medicine, Faculty of Medicine, Mater Research, University of Queensland, St Lucia, Brisbane, Queensland 4078, Australia; School of Biomedical Sciences, Faculty of Medicine, University of Queensland, St Lucia, Brisbane, Queensland 4078, Australia. Electronic address: [Email]
Inflammation occurs as a result of acute trauma, invasion of the host by different pathogens, pathogen-associated molecular patterns (PAMPs) or chronic cellular stress generating damage-associated molecular patterns (DAMPs). Thus inflammation may occur under both sterile inflammatory conditions including certain cancers, autoimmune or autoinflammatory diseases (Rheumatic arthritis (RA)) and infectious diseases including sepsis, pneumonia-associated acute lung inflammation (ALI) or acute respiratory distress syndrome (ARDS). The pathogenesis of inflammation involves dysregulation of an otherwise protective immune response comprising of various innate and adaptive immune cells and humoral (cytokines and chemokines) mediators secreted by these immune cells upon the activation of signaling mechanisms regulated by the activation of different pattern recognition receptors (PRRs). However, the pro-inflammatory and anti-inflammatory action of these immune cells is determined by the metabolic stage of the immune cells. The metabolic process of immune cells is called immunometabolism and its shift determined by inflammatory stimuli is called immunometabolic reprogramming. The article focuses on the involvement of various immune cells generating the inflammation, their interaction, immunometabolic reprogramming, and the therapeutic targeting of the immunometabolism to manage inflammation.
