Injury responses unite animals from worms to vertebrates
Injury means physiological damage to an organism—humans, other animals, plants, fungi, even choanoflagellates. Causes include mechanical trauma, toxins, other organisms, and harsh abiotic forces. Across many animal phyla, damage sparks inflammation, clotting of blood or body fluid, and wound repair at wildly different speeds.
In animals the narrow meaning is torn or broken anatomy, but the broader sense covers drowning, burns and poisoning too, whether the harm comes from a predator’s attack, a territorial fight, a fall or the weather. Across many phyla the sequence is similar: inflammation, then clotting of blood or body fluid, then repair, which cnidarians manage very fast. Arthropods can partly mend a cracked exoskeleton, and annelids, arthropods, cnidarians, molluscs, nematodes and vertebrates all make antimicrobial peptides after a wound.
Human medicine devotes whole specialties, emergency care and pain management among them, to injury. The World Health Organization sorts human injuries by mechanism, the object or substance involved, location, activity and whether anyone meant it, and it recognises mental aftermaths such as post-traumatic stress and depression.
Plants are damaged by grazing insects and mammals, by bacteria and fungi slipping in through wounds, and by heat, frost, floods, lightning and ozone. Unable to flee, they signal the damage, seal the area, release antimicrobial compounds and, in woody species, grow over the scar. Fungi improvise: partitioned hyphae plug their pores, the largely unpartitioned Mucoromycota turn the cell contents to gel, Trichoderma atroviride regrows broken filaments, and some species respond to damage by producing spores.
The deeper surprise is how much is shared. Plants and animals both flag damage with calcium ions and reactive oxygen species and carry pathogen-sensing receptors; released ATP, detected by P2X receptors found from sponges to chordates and in fungi and green plants, promotes healing. Even choanoflagellates share these pathways. Thibaut Brunet and Detlev Arendt propose that the last common ancestor of all eukaryotes already patched holes in its membrane: incoming calcium made actin-myosin proteins contract, pushing vesicles to fuse with the membrane and close the gap.
Source: Injury
