Immune System Learning Objectives
1) Understanding the physiological mechanisms of an allergic reaction.
2) Recognize the symptoms of anaphylaxis and know the physiological condition necessary to induce it.
3) Identify and assess the different means of physiological exposure to antigens
4) Identify the cellular steps in the immunology of allergen (antigen) sensitization.
5) Know the process of inflammation, how it is induced, what chemical signals mediate it, and what alterations in the function of blood vessels occur.
6) Understand how local alterations in vascular function lead to general changes in the cardiovascular system/body fluid balance.
7) Understand the effects of sympathetic innervation/ catecholamine release on the cardiovascular/respiratory system.
A Bad Day in the Park: Case Study on the Immune System
A 31-year-old male is rushed from a local state park to the emergency room. The skin on his face, limbs, and torso is markedly swollen. He is having trouble swallowing and his breathing is labored and diflicult. He feels faint, and a blood pressure determination reveals a systolic/diastolic pressure of 90/60 mmHg. His friends report that he had eaten a large picnic lunch earlier in the day. Later, he had taken a walk through a wildflower garden that was fully in bloom. Wandering off a path and into the woods, he had disturbed a wasp’s nest. After being stung, he had to run through a large patch of poison ivy to escape from the wasps. Returning quickly to his friends, he rapidly developed the symptoms described above and was rushed to the hospital.
1) (1 pt) What is the name for the patient’s allergic reaction?
Answer: Anaphylaxis (Ref. 5, p. 744).
2) (1 pt) List all of the potential allergens that he encountered at the park.
Answer: Food, plant pollen, wasp venom, chemical irritants in poison ivy.
3) (0.5 pt) What must happen to an aZZergen in order for it to induce such a reaction (i.e., where must it go once it enters the body)?
Answer: To induce anaphylaxis, the allergen must circulate systemically and affect mast cells throughout the body (Ref. 5, p. 744).
4) (2 pt) On the basis of this requirement, which of the allergens that you listed is most likely to have induced the reaction? Explain briefly. What types of allergic responses would you have expected from the other allergens that you identified, and how would they have differed from the reaction observed?
Answer: Wasp venom. Because the wasp venom is injected into the capillary-rich tissue of the dermis of the skin, it is likely to be carried by the circulation (blood, lymph) to the rest of the body. Pollen in the air contacts the respiratory surfaces and is likely to induce a local type I response (hay fever; Ref. 5, p. 744 and 92). The chemical irritants in poison ivy diffuse into the skin from the surface and cause a delayed hypersensitivity in the immediate area of contact (Ref. 5, p. 92). Ingested food can be allergenic. The response is local and typically involves digestive disturbances upon contact. However, some foods have permeable antigens that can cause anaphylaxis.
5) (0.5 pt) Before this form of allergic reaction can occur what type of defensive cell has to havepreviously encountered the allergen to sensitize the individual?
Answer: Macrophages must engulf, process, and present the allergen (antigen; Ref. 5, p.745).
6) (0.5 pt) Which immune cell responds next in the process of sensitization to the aUergen?
Answer: B cells (and T cells; Ref. 5, p. 745).
7) (0.5 pt) What type of immunoglobulin does this cell produce?
Answer: Cells produce immunoglobulin E (Ref. 5, p. 744-745).
8) (0.5 pt) What types of cells will then carry this antibody on their membranes in anticipation of a second exposure to the antigen?
Answer: Mast cells and basophils (Ref. 5, p. 744-745).
9) (0.5 pt) How do these cells respond when they encounter the antigen ? What cbemica2 signals do these cells release?
Answer: When antigens encounter the antibodies carried on the surface of these inflammatory cells, this induces the release of histamine, heparin, monokines (Ref. 5, p. 744745), kinins, and prostaglandins (class notes).
IO) (1 pt) How does the release of these chemical signals lead to the pathological symptoms observed? List each of the symptoms and explain how the chemical signals would cause them.
Answer: Drop in blood pressure/faintness-caused by peripheral vasodilation (induced by inflammatory chemicals). Swelling of skin-caused by increased capillary permeability in skin (inflammatory chemicals). Difficulty swallowing (due to swelling of pharynx)- caused by increased capillary permeability in skin (inflammatory chemicals). DifCculty breathingconstriction of respiratory passageways (inflammatory chemicals; Ref. 5, p. 745).
11) (0.5 pt) Is this response an immediate or delayed hypersensitivity?
Answer: Immediate (type I; Ref. 5, p. 745 and Ref. 7a, p. 92).
12) (1.5 pt) Why would epinepbrine be a good treatment for the patient’s condition, i.e., how would epinepbriuze help to alleviate each pathological symptom? Explain briefly.
Answer: Epinephrine (like sympathetic nervous stimulation) causes vasoconstriction in skin and digestive viscera (Ref. 5, Table 16-4); reduces blood flow to skin (increases blood pressure, reduces delivery of fluids to the skin, reduces swelling); reduces blood flow to digestive viscera (Ref. 5, Table 16-4; reduces fluid delivery to tissues of pharynx, increase blood pressure); causes increased cardiac output (increased blood pressure); causes dilation of respiratory passageways (Ref. 5, Table 16-4; restores normal breathing); and causes inhibition of the release of inflammatory chemicals (3).
We thank Clyde Herreid and Nancy Cliff for critical reading of the manuscript and Connie Odrzywolski for secretarial assistance. This material was presented at the Case Studies in Science Workshop sponsored by the Office of Teaching Effectiveness, State University of New York at Buffalo, May 3 I-June 2, 1995. Address for reprint requests: W. H. Cliff, Dept. of Biology, Niagara University, Niagara, NY 14 109 (E-mail: [email protected]). Received 26 June 1995; accepted in final form 7 February 1996.