Introduction
An injury that Carlton received as a result of playing on the beach caused the body’s inflammatory reaction, which is characterized by redness, swelling, and hot and painful sensations in the wounded area. Such a response of an organism ensures that various pathogens that may live on the surface of the shell and sand are effectively neutralized by the body’s immune system. From the physiologic perspective, this process includes several stages.
First of all, after Carlton hurt his leg, the blood vessels in the injured area started growing in size – the process called vasodilation. As a consequence, the wounded area receives more blood (and thus, oxygen) supply (Singh et al., 2017). Moreover, vasodilation leads to increased blood vessel permeability which allows fluid and white blood cells to access the damaged tissue and start fighting against foreign pathogens (Singh et al., 2017). In addition, “cytokines, chemokines, prostaglandins, nitric oxide, proteases,” and other chemical elements are found to mediate the inflammatory response in affected tissue (Mendes et al., 2018, p. 1). Simultaneously, to avoid the extensive loss of blood and prevent pathogens from entering the cardiovascular system, blood clots are formed. Therefore, redness and heat are primarily caused by the increased blood flow in the wounded area, whereas swelling is the result of fluid, leukocytes, and other chemicals entering the damaged tissue.
Once the body successfully addresses the primary impact of the injury, it reaches homeostasis. This, in turn, starts a chain reaction of various processes that lead to healing (Singh et al., 2017). Swelling normally pressures nearby nerve endings and causes the sensation of pain, especially when the injured area is physically affected. This mechanism ensures that Carlton does not touch his foot or otherwise move it, allowing the organism to recover faster.
Inflammatory Response during Internal Organs Damage
Similar to the response that occurs after skin is damaged, there is as well an inflammation that may appear in internal organs. The latter may appear due to physical impacts such as burns, reaction to certain chemicals, cell malfunctioning, and infection as a result of exposure to various bacteria and viruses (Chen et al., 2018). Although both ‘external’ and ‘internal’ body response to damage is associated with redness, swelling, and loss of functioning, there are also some differences. For instance, an individual may not always have a sensation of pain when one of his or her internal organs is inflamed. It happens because not all of the body parts have nerve endings. Additionally, in contrast to external injuries, inflammation in internal organs can cause a change in the temperature of the whole body, fever, and increased blood pressure. However, this process does not occur in all cases and depends on the severity of the damage. For these reasons, the inflammation of the internal organs is generally harder to diagnose. In this regard, when the problem is not treated, it can sometimes lead to organ failure.
Immunologic Response to Injury
Any tissue damage in the non-sterile environment causes both non-specific and specific immunologic responses. As such, the organism starts reacting as soon as the breach in the epidermal barrier is detected. The latter function is realized by keratinocytes – a most widespread cell type that forms an upper skin layer. At approximately the same time, mast cells and dendritic cells become exposed to pathogens and start fighting against intruders. In particular, when the viruses, fungi, or bacteria bind to the former cell’s receptors, it starts releasing histamine, which is toxic to pathogens. Moreover, histamine is a primary mechanism that causes inflammation by signaling blood vessels to expand. Meanwhile, dendritic cells participate in the phagocytosis process of the incoming pathogens and present antigens through major histocompatibility complex class II (MHC II) to T helper cells.
When blood vessels are dilated, various leukocytes can enter the area of damaged tissue. First of all, they include macrophages and neutrophils that eliminate pathogens through phagocytosis (Chen et al., 2018). The major difference between the two is that after ingestion of a foreign body, neutrophils undergo the process of apoptosis, while macrophages can ‘consume’ numerous microorganisms and present parts of antigens through MHC II. Additionally, monocytes which can transform either into macrophages or dendritic cells, and basophils, whose functions are close to those of mast cells, enter the wounded area. All these processes constitute a non-specific immune response to injury and exposure to pathogens.
The immune-specific reaction is achieved by B, T, and Natural Killer (NK) cells. Each group of B cells possesses a unique set of receptors that can only attach to a certain pathogen. When this happens, B cells produce cytokines that attract T helper cells and activate other B cells with similar receptors to search for the intruders. Next, T helper cells that have receptors of a specific shape that matches to pathogen attach to the MHC II of a B cell. It induces the latter to start to differentiate into plasma cells that produce antibodies and memory B cells that will be activated the next time organism is exposed to the same pathogen. Still, foreign organisms can usually infect some of the healthy cells. To address this problem, affected cells present antigen by MHC I, which attracts cytotoxic T cells that destroy the former. In a similar vein, NKs interaction with the infected cell results in its destruction, but in contrast to cytotoxic T cells, they do it by inducing apoptosis.
Wound Healing and Vitamins A and C Deficiency
Shortage of certain important nutrition elements in the body can significantly influence its ability to recover from injuries. In this respect, the two vitamins, namely A and C, are of great importance. As for the former, the previous research identified that individuals who suffer from a shortage of vitamin A are more vulnerable to infectious diseases (Zinder et al., 2019). It happens because this nutrient boosts inflammatory reaction and angiogenesis in response to injury. In particular, vitamin A can suppress the corticosteroid’s anti-inflammatory function and thus, decrease the wound healing time. Moreover, vitamin A plays an important role in epidermal restoration after it is damaged and generally in epidermal turnover (Zinder et al., 2019). For instance, it impacts the production of insulin which is positively associated with faster wound healing. Some studies even suggest that this nutrient promotes the recovery of internal tissues as well, meaning that vitamin A is crucial for both the healing of the skin and internal organs (Zinder et al., 2019). Therefore, vitamin A determines the speed and success of healing during all the periods of wound recovery, including inflammation, proliferation, and remodeling stages.
Similar to vitamin A, vitamin C is related to faster skin recovery. It is found to be a necessary bounding element for collagen, which increases the strength of the tissue (Sarpooshi et al., 2017). Additionally, the shortage of this nutrient can cause vascular fragility, which, in turn, leads to slower wound healing. Likewise, vitamin C deficiency affects the body’s ability to form scar tissues. Last but not least, vitamin C enhances the immune system promoting the organism’s defense against various pathogens. For these reasons, this nutrient plays an important role during inflammation, proliferation, and remodeling periods.
References
Chen, L., Deng, H., Cui, H., Fang, J., Zuo, Z., Deng, J., Li, Y., Wang, X., & Zhao, L. (2018). Inflammatory responses and inflammation-associated diseases in organs.Oncotarget, 9(6), 7204-7218.
Mendes A. F., Cruz M. T., & Gualillo O. (2018). Editorial: The physiology of inflammation – the final common pathway to disease. Frontiers in Physiology, 9, 1-3.
Sarpooshi, H. R., Haddadi, M., Siavoshi, M., & Borghabani, R. (2017). Wound healing with vitamin C.Translational Biomedicine, 8(4), 1-4.
Singh, S., Young, A., & McNaught, C. E. (2017). The physiology of wound healing. Surgery (Oxford), 35(9), 473-477.
Zinder, R., Cooley, R., Vlad, L. G., & Molnar, J. A. (2019). Vitamin A and wound healing.Nutrition in Clinical Practice, 34(6), 839-849.