What is the role of leukotrienes in a type I hypersensitivity reaction?

Correct answer: A. They mediate the sustained late-phase bronchoconstriction, mucus secretion and vascular permeability

• A. CORRECT. Leukotrienes C₄, D₄ and E₄ — historically called the slow-reacting substance of anaphylaxis — are synthesised de novo from arachidonic acid via the 5-lipoxygenase pathway when a mast cell is activated. Because they must be MADE rather than released from a pre-formed granule, they appear later than histamine and their effect is far more sustained. They are enormously potent bronchoconstrictors, on the order of a thousand times more so than histamine, and they also drive mucus hypersecretion and vascular permeability. This is why they dominate the late-phase response several hours after exposure, and why an anaphylactic patient can deteriorate again after an initial improvement.
• B. Nothing here neutralises histamine. Leukotrienes amplify and prolong the reaction rather than terminating it.
• C. The immediate seconds-to-minutes response is driven by PRE-FORMED mediators released from granules — histamine, tryptase and heparin. Leukotrienes require synthesis and therefore act later.
• D. Cross-linking is performed by the ANTIGEN binding adjacent IgE molecules on the FcεRI receptor. That is the trigger for degranulation, not a function of leukotrienes.

Note: Two waves, and it matters clinically. Pre-formed mediators (histamine, tryptase) act within minutes; newly synthesised mediators (leukotrienes, prostaglandin D₂, PAF) drive the late phase at 4 to 12 hours. This biphasic pattern is exactly why a patient treated for anaphylaxis must be observed and not simply discharged after responding to epinephrine — and it is why montelukast, a leukotriene receptor antagonist, works in asthma.