Figure 1.

Mediators of neutrophil dysfunction present in T1D and T2D. The microenvironment of T1D and T2D presents a complex interplay of mediators of neutrophil dysfunction. Hyperglycaemia and the formation of advanced glycation end products in the circulation and the bone marrow modify circulating neutrophils and myeloid precursors. Metabolic perturbations in lipid metabolism and increased synthesis of circulating free fatty acids further contribute to aberrant dysfunction. Resulting activated neutrophils produce pro-inflammatory mediators adding to a cycle of inflammation. Increased age further impacts neutrophil function, in addition to co-morbidities and infection, where altered neutrophil functions are previously shown e.g chronic obstructive pulmonary disease (COPD) sepsis and COVID-19. Figure created with BioRender.com.