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Type I Hypersensitivity as Self-Defense Mechanism
The case presented with a 24-year-old man, RT, who got a bee sting and had adverse consequences, has several essential points to discuss. When an individual interacts with an allergen, it can immediately respond to the immune system. It is defined as an allergy and is most likely associated with a type I hypersensitivity. RT had a health record previously with an allergy to bee stings; thus, it can be stated that allergy is dangerous for RT, and insect venom can be considered as hazardous because his body is sensitized to bee stings.
A primary IgE antibody response appears when the first interaction with the allergen occurs that sensitizes RT to type I hypersensitivity reaction before a subsequent response ( Hypersensitivities, n.d.). Increased itching throat and tightness with breathing are indicators of the systemic reaction to bee allergen, and anaphylaxis appears due to the significant emission of anaphylactic and inflammatory mediators ( Hypersensitivities, n.d.). It is clear that the bee sting provokes a multiple-organ system reaction; thus, the treatment should be provided carefully and promptly. The dosing of epinephrine can vary but should be evaluated before administering any intramuscular manipulations.
The cellular pathophysiology has resulted in the local inflammation that can be explained. The insect venom causes sensitization of breathing organs and skin that experience allergic reactions. In the venom-allergic individuals, specific IgE to the venom is raised and triggers an immediate hypersensitivity reaction (atopic allergy). In the case of RT, he has an immediate- and delayed-type hypersensitivity because it appears after several hours. The latter reaction is triggered by T cell responses and results in dermatitis that RT has with a hand with inflammation (Kany et al., 2019). T cells and their derived cytokines aim to control the immune reactions against venom substances (Kany et al., 2019).
Specific IgE antibodies that combat toxin components launch the work of mast cells and basophilic granulocytes, triggering the development of mediators that result in acute manifestations of that allergic sensitivity (Galli & Tsai, 2012). Pathogenic factors impact inflammation by causing tissue damage and cellular changes (Chen et al., 2017). Vasculature around the sting site reacts by increasing blood flow and enhancing vascular permeability, which is reflected in tenderness and redness of the skin. In response to tissue inflammation, cells can launch a signaling phase of cells that aim to develop a healing effect for tissues (Chen et al., 2017). Activated from the signaling stage, leukocytes produce cytokines that induce an inflammatory reaction.
The kinin system would have a substantial effect on the course of inflammation and the level of pain. Wasp and bee kinins are stored in venom but can act locally in humans. Wasp kinins are of interest because they occur in humans, produced by plasma kallikreins and tissue kallikreins (Gowder, 2014). Kinins are crucial mediators of inflammatory reactions that can potentially produce pain and increase vascular permeability and vasodilation (Abdulkhaleq et al., 2018). A great taxonomic diversity peptides of bee kinins in the venom have a potential to initialize long-lasting pharmacological effects in humans because they can act internally transferring from the bees venom.
Kinins are autacoid peptides and main neuromediators engaged in cardiovascular flows, inflammation, and pain (Golias et al., 2007, para. 8). The kinin system has the potential to initiate reflexes by triggering sensory nerve endings, which leads to inflammatory pain. Kinins evoke histamine production from mast cells, prostaglandin synthesis in different cells; therefore, the main effects would include vasodilation, smooth muscle contraction, pain that are related to other mediators, such as prostaglandins.
References
Abdulkhaleq, L. A., Assi, M. A., Abdullah, R., Zamri-Saad, M., Taufiq-Yap, Y. H., & Hezmee, M. (2018). The crucial roles of inflammatory mediators in inflammation: A review. Veterinary world, 11(5), 627635.
Chen, L., Deng, H., Cui, H., Fang, J., Zuo, Z., Deng, J., Li, Y., Wang, X., & Zhao, L. (2017). Inflammatory responses and inflammation-associated diseases in organs. Oncotarget, 9(6), 72047218.
Galli, S. J., & Tsai, M. (2012). IgE and mast cells in allergic disease. Nature medicine, 18(5), 693704.
Golias, C., Charalabopoulos, A., Stagikas, D., & Charalabopoulos, K.A. & Batistatou, A. (2007). The kinin systemBradykinin: Biological effects and clinical implications. Multiple role of the kinin systemBradykinin. Hippokratia, 11, 124-128.
Gowder, S. (2014). Pharmacology and Therapeutics. BoD Books on Demand.
Hypersensitivities. (n.d.). Lumen Learning.
Kany, S., Vollrath, J. T., & Relja, B. (2019). Cytokines in Inflammatory Disease. International journal of molecular sciences, 20(23), 6008.
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