The world can be a hazardous place, with various dangers lurking around us such as bacteria, viruses, accidents, and injuries. Our skin acts as the ultimate shield, providing a steadfast defense against these threats. It serves as the boundary between the internal and external environment and is the
Still, the skin is not immune to harm. It endures daily assaults and still tries to keep us safe by detecting and responding to these dangers. One method is the detection of pathogens, which activates the immune system. However, recent research conducted by Elaine Fuchs at Rockefeller University and published in the journalhas uncovered a new protection mechanism that responds to injury signals in damaged tissue, such as low oxygen levels caused by blood vessel disruption and scab formation.
“IL24 is predominately made by the wound-edge epidermal stem cells, but many cells of the skin—the epithelial cells, the fibroblasts, and the endothelial cells—express the IL24 receptor and respond to the signal. IL24 becomes an orchestrator that coordinates tissue repair,” says Fuchs, head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development.
In collaboration with Daniel Mucida’s lab at Rockefeller, the researchers worked with mice under germ-free conditions and found that the wound-induced IL24 signaling cascade is independent of germs. When the blood vessels are severed and a scab forms, epidermal stem cells at the edge of the wound are starved of oxygen. This state of hypoxia is an alarm bell for cell health and induced a positive feedback loop involving transcription factors HIF1a and STAT3 to amplify IL24 production at the wound edge.
They speculate that IL24 might be involved in the injury response in other body organs featuring epithelial layers, which act as a protective sheath. In recent studies, elevated IL24 activity has been spotted in epithelial lung tissue of patients with severeand in colonic tissue in patients with ulcerative colitis, a chronic inflammatory bowel disease.Linked by function and evolution
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