Introduction
In many cases, inflammation response includes redness, loss of function, swelling, heat, and pain. Inflammation refers to the immune response of the body resulting from tissue injury, attack by pathogens, and effects from chemicals and radiation (Abdulkhaleq et al., 2018). In the provided case study, the physiological mechanism causing Carlton’s foot to swell, become painful, and red, and produce heat is acute inflammation. Clinically, the cardinal signs of acute inflammation encompass redness, heat, swelling, loss of function, and pain. Acute inflammation is the body’s first response when there is damage to the tissues. Carlton’s foot skin showed an inflammatory reaction that began from the entry of pathogens at the wound, making the damaged site compromise the epithelial tissue of the skin. The cut in the foot permitted the admission of pathogens, subsequently activating the body’s innate immune system, which is regarded as the immediate swift response to support in averting infection. Innate immunity uses chemical, physical, molecular, and cellular defenses of the body.
It involves the mobilization of the immune system and inflammatory mediators, often causing blood vessels to swell. The vascular system within and around the injured location triggers high blood flow and improves vascular permeability due to the tightening of endothelial cells in the nearby capillaries and allowing extracellular spaces. The torrent of protein-concentrated fluid usually accompanies the enhanced vascular penetrability into the extravascular places. The situation activates an enhanced interstitial osmotic compression, making the osmotic pressure of the capillary decrease following the loss of proteins (Hannoodee & Nasuruddin, 2021). The combination of these factors makes the inflamed site turn red and generate heat. Heat in the injured place is also triggered by the increased supply of blood at the body’s main temperature into the usual cooler skin.
Acute inflammation is accompanied by the travel of inflammatory cells from the blood to the site of injury followed by fluid exudation. Carlton’s foot appeared edematous because of the accumulation of fluid in the injured area. Moreover, he is also feeling pain at the site of injury due to the generation of inflammatory mediators coupled with chemical stimulation of the nerve endings that have sensory endothelial tissues. Specifically, the release of histamine and bradykinin hormones during inflammatory response aggravates the nerves, leading sending of pain signals to the brain (Hannoodee & Nasuruddin, 2021). Inflammatory response on internal organs is slightly different from the acute inflammatory reaction Carlton received on his foot. The dissimilarity might arise from the fact that the internal organs can develop complications resulting in chronic inflammation. Moreover, visceral inflammation presents a slight difference from that of local inflammation. For example, there is a reduced occurrence of heat since the core temperature is conserved within the homeostatic range while pain becomes ostensible when stretch receptors present on the viscera surfaces are activated.
Immunological Events
The immunological events that happened to Carlton’s injured foot occurred in the cellular phase of the normal acute inflammatory response that exhibits a concentration of granulocytes. Four steps occur in the cellular stage and encompass margination and grip to the endothelial tissue, migration across the endothelial tissue, chemotaxis, and activation coupled with phagocytosis. Margination and grip by leukocytes to the endothelium leads to a decrease in their number followed by their sticking to the endothelial. Adhesion is facilitated by the production of cytokines by the leukocytes. The process of transmigration then initiates after the occurrence of adhesion. Transmigrations happen with specific leukocytes traveling through the endothelial walls and then moving to the tissue (Hannoodee & Nasuruddin, 2021). Following their migration into the tissue, the process is then followed by chemotaxis to the site of infection, and the whole process is completed through chemoattractant. The arrival of leukocytes at the injured place precedes the process of phagocytosis, which involves neutrophils, tissue macrophages, and monocytes. The steps involved in phagocytosis encompass the recognition of invading pathogens/antigens, ingestion, and intracellular microbial killing. The phagocytes have receptors that help in identifying antigens and subsequently adhering to them, which is accomplished through opsonization. The plasma membrane of the phagocyte extends to surround the antigen and then pinches off followed by internalizing the antigen to form a phagosome. Phagosome fuses with lysosome from phagocytes to create an acidic environment called phagolysosome that participates in the killing of the internalized pathogen.
Nutrition and Its Impact on Wound Healing
Wound healing phases comprise the inflammatory stage, proliferative stage, and wound reduction and repair phase. The inflammatory phase starts with the commencement of the wound with the key objective of preparing the injured site for healing as well as eradicating any debris. It also assists in the activating growth of epithelial cells, formation of blood vessels, as well as attraction of fibroblast to make collagen and extracellular matrix. Similarly, the proliferative stage helps in creating new tissue. To attain this, fibroblast produces growth factors and collagen and the stage ends with epithelialization, which seeks to encourage the creation of scar tissues (Barchitta et al., 2019). The last phase is remodeling and repair of the wound. In this phase, the scar tissue gets reoriented to enhance the strength of the new tensile tissue, and the process is accomplished through the utilization of collagen synthesis as well as lysis using collagen enzymes.
Vitamin C plays a critical role in the synthesis and lysis of collagen, hence becoming an essential part of the wound-healing process. Vitamin C is not only needed in completing the three stages but also for the synthesis of collagen. Vitamin C serves as an antioxidant to impact phagocytes, lymphocytes, and leukocytes (Barchitta et al., 2019). The body does not naturally synthesize vitamin C so it can be obtained from various foods and fruits such as guava, broccoli, brussels sprouts, citrus fruits, and cauliflower. Another important nutritional element is vitamin A, which is an integral part of the wound-healing process. Vitamin A contributes to wound synthesis, epithelialization, and capillary formation. Sources of vitamin A in the diet include eggs, milk, liver, fish, leafy green vegetables, tomatoes, and oranges.
Conclusion
In conclusion, the process of inflammation, tissue remodeling, and wound healing is a convoluted, stepwise process that encompasses several factors at play. The acute inflammatory response begins when the tissue is damaged just as seen in the case involving Carlton’s foot. Visceral inflammation is different from local inflammation as seen in the lack of generation of heat. Immunological events that follow inflammation encompass margination and grip to the endothelial tissue, migration across the endothelial tissue, chemotaxis, and activation coupled with phagocytosis. The importance of proper nutrition remains key in the management of the wound healing process. Therefore, humans should consume foods rich in Vitamins A and C to furnish the body with the appropriate elements that play key roles in the phases of wound healing.
References
Abdulkhaleq, L. A., Assi, M. A., Abdullah, R., Zamri-Saad, M., Taufiq-Yap, Y. H., & Hezmee, M. N. M. (2018). The crucial roles of inflammatory mediators in inflammation: a review. Veterinary World, 11(5), 11-627. Web.
Barchitta, M., Maugeri, A., Favara, G., Magnano San Lio, R., Evola, G., Agodi, A., & Basile, G. (2019). Nutrition and wound healing: an overview focusing on the beneficial effects of curcumin. International journal of molecular sciences, 20(5), 2-14. Web.
Hannoodee, S., & Nasuruddin, D. N. (2021). Acute inflammatory response. In StatPearls [Internet]. StatPearls Publishing. Web.