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Injury

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(Redirected from Injuries)
This article is about damage to organisms. For other uses, see Injury (disambiguation).

BERJAYA
A crabeater seal injured by a predator

Injury is physiological damage to an organism. The response to injury, whether in humans, in other animals, in plants, in fungi, or in single-celled eukaryotes such as choanoflagellates, is substantially shared, implying that the mechanisms are ancient.

Injuries can be caused in many ways, including mechanical trauma, toxins, interactions with other organisms, or abiotic factors in the environment. In many animal taxa, injury prompts an inflammatory response that initiates wound healing. In both plants and animals, substances are released to help to occlude the wound, limiting loss of fluids and the entry of pathogens. Many organisms secrete antimicrobial chemicals which limit wound infection; animals have immune responses for the same purpose. Both plants and animals have regrowth mechanisms that may result in complete or partial healing over the injury.

Taxonomic range

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Animals

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Main article: Injury in animals
BERJAYA
A female sand lizard that has shed its tail when attacked by a predator, and has started to regrow a tail from the site of the injury

Injury in animals is sometimes defined as mechanical damage to an anatomical structure,[1] but it has a wider connotation of physical damage with any cause, including drowning, burns, and poisoning.[2] Such damage may result from attempted predation, territorial fights, falls, and abiotic factors.[2]

Injury triggers an inflammatory response in animals of many different phyla.[3] This prompts coagulation of the blood or body fluid,[4] followed by wound healing, which may be rapid, as in cnidarians.[3] Arthropods are able to repair injuries to the cuticle that forms their exoskeleton to some extent.[5]

Animals in several phyla, including annelids, arthropods, cnidarians, molluscs, nematodes, and vertebrates, are able to produce antimicrobial peptides to fight off infection following an injury.[1]

Humans

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Main article: Injury in humans
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Injuries to humans elicit an elaborate response including emergency medicine, trauma surgery (illustrated), and pain management.

Injury in humans has been studied extensively for its importance in medicine. Much of medical practice, including emergency medicine and pain management, is dedicated to the treatment of injuries.[6][7] The World Health Organization has developed a classification of injuries in humans by categories, including mechanism, objects/substances producing injury, place of occurrence, activity when injured, and the role of human intent.[8] In addition to physical harm, injuries can cause psychological harm, including post-traumatic stress disorder.[9][10]

Plants

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Main article: Injury in plants
BERJAYA
Oak tree split by lightning, an abiotic cause of injury.

In plants, injuries result from the eating of plant parts by herbivorous animals including insects and mammals,[11] from damage to tissues by plant pathogens such as bacteria and fungi, which may gain entry after herbivore damage or in other ways,[12] and from abiotic factors such as heat,[13] freezing,[14] flooding,[15] lightning,[16] and pollutants[17] such as ozone.[18] Plants respond to injury by signalling that damage has occurred,[19] secreting materials that seal off the damaged area,[20] producing antimicrobial chemicals,[21][22] and, in woody plants, regrowing over wounds.[23][24][25]

Fungi

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Fungi with septate hyphae, or filaments with partitions, are able to block septal pores if a hypha is injured.[26] In the Mucoromycota, which mostly lack septa, wounding a hypha produces a rapid response in which the protoplasm inside the hypha forms a gel.[26] Some fungi, such as the ascomycete Trichoderma atroviride, respond to mechanical damage by regenerating damaged hyphae, effectively healing the injury. In the basidiomycetes Schizophyllum commune and Sclerotium rolfsii, damage to the mycelium (the mat of hyphae) triggers the production of reproductive conidia. Several species of Trichoderma also produce conidia in response to injury.[27]

Ancient eukaryote mechanism

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Plants cannot move away from a source of injury as animals do, nor are their immune reactions as elaborate as those in animals. However, there are multiple parallels between plant and animal responses to injury. Both signal damage with calcium ions, which activate receptors to launch a response.[28] Both also signal damage with reactive oxygen species, which drive changes in metabolism, such as enabling cells to multiply to repair damaged tissues.[28][29] Both have pattern recognition receptors on the surfaces of their cells, triggered by invading pathogens. Both have a "primitive" inflammation response that causes the release of antimicrobial peptides; additionally, animals have mobile immune cells capable of more complex responses. Both have mechanisms for sealing up the site of a wound. Finally, plants, and many animals, have the ability to regenerate some damaged parts.[28]

Several of these mechanisms, including receptors, calcium signalling, reactive oxygen species, adenosine triphosphate release, kinase cascades, and oxylipin signalling, are also found in fungi such as Trichoderma.[27] Single-celled eukaryotes, such as choanoflagellates, substantially share the pathways found in plants and animals for detecting damage and pathogens.[1] Extracellular adenosine triphosphate is a signal that promotes healing of wounds to the epithelium in both bilateria (such as vertebrates) and in non-bilaterians such as cnidaria. The signal is detected by a P2X receptor; these receptors occur across the animal kingdom in phyla including sponges, cnidaria, placozoa, mollusca, arthropoda, and chordata, and in both fungi and green plants.[30] Such sharing between eukaryote groups implies that these damage response mechanisms are ancient and have been conserved in evolution.[27][30]

Thibaut Brunet and Detlev Arendt propose that the last eukaryotic common ancestor (LECA) possessed a calcium-based wound healing response. They argue that the mechanism's purpose was to detect and heal a potentially fatal opening in the cell membrane. They propose that it worked by detecting an inflow of calcium ions, which provoked a contraction in muscle-like actomyosin proteins. This in turn caused vesicles to fuse with the cell membrane (exocytosis), healing the opening and preventing the cell from splitting open.[31]

References

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  1. ^ a b c Rennolds, Corey W.; Bely, Alexandra E. (29 September 2022). "Integrative biology of injury in animals". Biological Reviews. 98 (1): 34–62. doi:10.1111/brv.12894. PMC 10087827. PMID 36176189.
  2. ^ a b de Ramirez, Sarah Stewart; Hyder, Adnan A.; Herbert, Hadley K.; Stevens, Kent (2012). "Unintentional injuries: magnitude, prevention, and control". Annual Review of Public Health. 33: 175–191. doi:10.1146/annurev-publhealth-031811-124558. PMID 22224893.
  3. ^ a b Sparks, Albert (1972). Invertebrate Pathology Noncommunicable Diseases. Academic Press. pp. 20, 133. ISBN 978-0-323-15196-2.
  4. ^ Cerenius, Lage; Söderhäll, Kenneth (6 November 2010). "Coagulation in Invertebrates". Journal of Innate Immunity. 3 (1): 3–8. doi:10.1159/000322066. PMID 21051883. S2CID 20798250.
  5. ^ Parle, Eoin; Dirks, Jan-Henning; Taylor, David (2016). "Bridging the gap: wound healing in insects restores mechanical strength by targeted cuticle deposition". Journal of the Royal Society Interface. 13 (117) 20150984. doi:10.1098/rsif.2015.0984. PMC 4874426. PMID 27053653.
  6. ^ Maerz, Linda L.; Davis, Kimberly A.; Rosenbaum, Stanley H. (2009). "Trauma". International Anesthesiology Clinics. 47 (1): 25–36. doi:10.1097/AIA.0b013e3181950030. PMID 19131750. S2CID 220567282.
  7. ^ Ahmadi, Alireza; Bazargan-Hejazi, Shahrzad; Heidari Zadie, Zahra; et al. (2016). "Pain management in trauma: A review study". Journal of Injury and Violence Research. 8 (2): 89–98. doi:10.5249/jivr.v8i2.707. PMC 4967367. PMID 27414816.
  8. ^ "International Classification of External Causes of Injury (ICECI)". World Health Organization. Archived from the original on 17 October 2004. Retrieved 22 September 2023.
  9. ^ Agarwal, Tulika Mehta; Muneer, Mohammed; Asim, Mohammad; et al. (2020). "Psychological trauma in different mechanisms of traumatic injury: A hospital-based cross-sectional study". PLOS ONE. 15 (11) e0242849. Bibcode:2020PLoSO..1542849A. doi:10.1371/journal.pone.0242849. PMC 7703890. PMID 33253298.
  10. ^ Jones, Kristen; Boschen, Mark; Devilly, Grant; Vogler, Jessica; Flowers, Harley; Winkleman, Charlotte; Wullschleger, Martin (2024). "Risk and protective factors that predict posttraumatic stress disorder after traumatic injury: A systematic review". Health Sciences Review. 10 100147. doi:10.1016/j.hsr.2023.100147.
  11. ^ Tarr, S. A. J. (1972). "Plant injury due to insects, mites, nematodes and other pests". Principles of Plant Pathology. London: Macmillan. pp. 126–137. doi:10.1007/978-1-349-00355-6_9. ISBN 978-1-349-00357-0.
  12. ^ Cappelli, Seraina Lisa; Koricheva, Julia (2 July 2021). "Interactions between mammalian grazers and plant pathogens: an elephant in the room?". New Phytologist. 232 (1): 8–10. Bibcode:2021NewPh.232....8C. doi:10.1111/nph.17533. PMID 34213785. S2CID 235708670.
  13. ^ Smillie, R.M.; Nott, R. (1979). "Heat Injury in Leaves of Alpine, Temperate and Tropical Plants". Functional Plant Biology. 6 (1). CSIRO Publishing: 135. doi:10.1071/pp9790135.
  14. ^ Burke, M. J.; Gusta, L. V.; Quamme, H. A.; Weiser, C. J.; Li, P. H. (1976). "Freezing and Injury in Plants". Annual Review of Plant Physiology. 27 (1): 507–528. doi:10.1146/annurev.pp.27.060176.002451.
  15. ^ Kramer, Paul J. (1 October 1951). "Causes of Injury to Plants Resulting from Flooding of the Soil". Plant Physiology. 26 (4): 722–736. doi:10.1104/pp.26.4.722. PMC 437542. PMID 16654407.
  16. ^ Nelson, Scot C. (July 2008). "Lightning Injury to Plants" (PDF). Plant Disease. College of Tropical Agriculture and Human Resources, University of Hawaiʻi at Mānoa. PD-40. Archived (PDF) from the original on 11 March 2026. Retrieved 21 September 2023.
  17. ^ Heath, R. L. (1980). "Initial Events in Injury to Plants by Air Pollutants". Annual Review of Plant Physiology. 31 (1): 395–431. doi:10.1146/annurev.pp.31.060180.002143.
  18. ^ Hill, A. C.; Pack, M. R.; Treshow, M. (1961). "Plant injury induced by ozone". Phytopathology. 51. OSTI 5518148. Archived from the original on 12 August 2025. Retrieved 21 September 2023.
  19. ^ Turlings, Ted C.; Tumlinson, James H. (1992). "Systemic release of chemical signals by herbivore-injured corn". Proceedings of the National Academy of Sciences. 89 (17): 8399–8402. Bibcode:1992PNAS...89.8399T. doi:10.1073/pnas.89.17.8399. PMC 49926. PMID 11607325.
  20. ^ Sun, Qiang; Rost, Thomas L.; Matthews, Mark A. (2008). "Wound-induced vascular occlusions in Vitis vinifera (Vitaceae): Tyloses in summer and gels in winter". American Journal of Botany. 95 (12). Wiley: 1498–1505. doi:10.3732/ajb.0800061. PMID 21628157.
  21. ^ Shigo, Alex L. (1985). "Compartmentalization of Decay in Trees". Scientific American. 252 (4): 96–103. Bibcode:1985SciAm.252d..96S. doi:10.1038/scientificamerican0485-96. hdl:2027/uva.x002416568. Archived from the original on 15 January 2025. Retrieved 21 September 2023.
  22. ^ González-Lamothe, Rocío; Mitchell, Gabriel; Gattuso, Mariza; Diarra, Moussa; Malouin, François; Bouarab, Kamal (31 July 2009). "Plant Antimicrobial Agents and Their Effects on Plant and Human Pathogens". International Journal of Molecular Sciences. 10 (8): 3400–3419. doi:10.3390/ijms10083400. PMC 2812829. PMID 20111686.
  23. ^ Shigo, Alex L. (1985). "How tree branches are attached to trunks". Canadian Journal of Botany. 63 (8): 1391–1401. Bibcode:1985CaJB...63.1391S. doi:10.1139/b85-193.
  24. ^ O'Hara, Kevin L. (2007). "Pruning Wounds and Occlusion: A Long-Standing Conundrum in Forestry". Journal of Forestry. 105 (3): 131–138. doi:10.1093/jof/105.3.131. S2CID 10075580. Archived from the original on 7 January 2024. Retrieved 23 June 2026.
  25. ^ "Tree pruning guide". US Forest Service for the US Department of Agriculture. Archived from the original on 26 April 2007.
  26. ^ a b Nguyen, Tu Anh; Le, Shimin; Lee, Michelle; Fan, Jing-Song; Yang, Daiwen; Yan, Jie; Jedd, Gregory (12 November 2020). "Fungal wound healing through instantaneous protoplasmic gelation". Current Biology. 31 (2): 271–282. doi:10.1016/j.cub.2020.10.016. PMID 33186551. Archived from the original on 20 September 2024. Retrieved 24 June 2026.
  27. ^ a b c Hernández-Oñate, M. A.; Herrera-Estrella, A. (2015). "Damage response involves mechanisms conserved across plants, animals and fungi". Current Genetics. 61 (3): 359–372. doi:10.1007/s00294-014-0467-5. PMID 25572693.
  28. ^ a b c Byatt, Timothy C.; Martin, Paul (2023). "Parallel repair mechanisms in plants and animals" (PDF). Disease Models & Mechanisms. 16 (1) dmm049801. doi:10.1242/dmm.049801. PMC 9903144. PMID 36706000. dmm049801.
  29. ^ Suzuki, Nobuhiro; Mittler, Ron (2012). "Reactive oxygen species-dependent wound responses in animals and plants" (PDF). Free Radical Biology and Medicine. 53 (12): 2269–2276. doi:10.1016/j.freeradbiomed.2012.10.538. PMID 23085520.
  30. ^ a b Lee, Elizabeth E. L.; O'Malley-Krohn, Isabel; Edsinger, Eric; Wu, Stephanie; Malamy, Jocelyn (1 November 2023). "Epithelial wound healing in Clytia hemisphaerica provides insights into extracellular ATP signaling mechanisms and P2XR evolution". Scientific Reports. 13 (1) 18819. doi:10.1038/s41598-023-45424-5. PMC 10620158. PMID 37914720. these organisms [cnidarians] can reveal the evolutionary origin of wound healing mechanisms and likely identify mechanisms that are conserved across the tree of life.
  31. ^ Brunet, Thibaut; Arendt, Detlev (5 January 2016). "From damage response to action potentials: early evolution of neural and contractile modules in stem eukaryotes". Philosophical Transactions of the Royal Society B. 371 (371 (1685)) 20150043. doi:10.1098/rstb.2015.0043. PMC 4685582. PMID 26598726. 20150043.
  32. ^ Brunet & Arendt 2016.
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