Wound Healing & Blood Clotting

Complicated in mammals, but in insects, too

When I was a PhD-student I very much enjoyed recording intracellular responses from visual cells of a variety of insect species. It wasn’t easy, but it was so rewarding when I succeeded in holding a cell for several hours and could determine its sensitivity and visual field. I then had the idea to record from the eyes of an Australian spider, but my supervisor at that time told me that it would not work, because once you’d injure a spider, its blood would coagulate and become jellylike, he said. So, I gave up the idea.

What my supervisor must have been thinking of at that time were observations on the blood of Limulus (the horseshoe crab, which isn’t a crab at all, but related to spiders). It had been studied in 1956 by Fred Bang, who established that its blood can undergo spontaneous gelation. Indeed so famous became Limulus blood that pharmaceutical companies got highly interested in it. So-called gram-negative bacteria that, for example, cause diseases like toxic-shock syndrome, meningitis and typhoid are usually killed by sterilizing medical tools. But the sterilization process does not always remove bacterial compounds from the bacterial cell wall like endotoxins. It is these chemicals that the Limulus blood reacts to. Regarding blood clotting and gelation, they must then be seen as a way to prevent harmful bacteria from entering a wound and spreading. Functionally these roles (and forming a scab over a wound) seem no different in mammals, or are they? I always liked lecturing on the physiology of blood clotting in mammals (rather than the kidney function), because it involves  a fascinating  cascade of events with inputs from vitamin K and calcium ions, but I never discussed the clotting physiology of blood like that of spiders and insects.

In mammals, tissue and blood vessel damage causes the release of thromboplastin from blood platelets and involves calcium ions, factors V and X, to change the inactive prothrombin of the blood plasma into the active thrombin. Thrombin then converts factor I (the molecule fibrinogen) into soluble fibrin strands, while the anti-haemolytic Factor XIII (which depends on fat-soluble vitamin K and is missing in people suffering from haemophilia A, i.e. the bleeder’s disease) together with Factor IX leads to platelet adhesion and in the presence of Factor XIII then stabilizes the fibrin clot, sealing the wound. But white blood cells, especially the granulocytes and eosinophils, also get in on the act, accumulate under the wound and in the case of the granulocytes, aggregate, engulf and ingest bacteria or, in the case of the eosinophils, release a crystalline protein to fight off multicellular parasites: a 2-pronged injury response.

Insects do not possess blood vessels like veins or arteries and the colourless blood in the insect’s body cavity (the haemocoel) does not contain platelets. However, the blood does contain crystal cells and haemocytes, of which granulocytes and plasmatocytes are the most significant ones. The granulocytes are generally amoeboid and one of their roles (like the granulocytes in a mammal) is to encapsulate and digest bacteria. Primarily fighting invading and unwanted micro-organisms, these mobile cells migrate to an injury, coagulate and release a “Factor VIII = vertebrate clotting equivalent”.  Factors promoting the coagulation such as trans-glutaminase are liberated from plasmatocytes (that behave like mammalian macrophages and tackle parasites larger than bacteria) and prophenoloxidase from ruptured crystal cells (a similarity to mammalian eosinophils that also contain crystals, but composed of a protein known as MBP1). A calcium-binding protein known as glutactin, which lines muscles, the central nervous system and basal epithelial cells, is produced by the fat body (= the insect’s liver) and has adhesive properties. It helps building a fibrous or gelatinous clot, sealing the wound.

What all this shows is that there’s also a clotting cascade in insects, but that it is an analogous process: it leads to the same result, but follows a different a pathway. However, that’s not the end of the story, for the clot or the scab will ultimately have to be reabsorbed, right? And that’s different. Vive la différence!

© Dr V.B. Meyer-Rochow and http://www.bioforthebiobuff.wordpress.com, 2022. Unauthorized use and/or duplication of this material without express and written permission from this site’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to V.B Meyer-Rochow and http://www.bioforthebiobuff.wordpress.com with appropriate and specific direction to the original content.