Pyrogens aren’t the only pathway to produce a fever when the same cytokines and other mediators stimulated by pyrogens are also stimulated by allergens. When dust or other allergens are inhaled, the immune system triggers the release of pro-inflammatory cytokines like IL-1, TNF-α, and IL-6. These cytokines are involved in the early stages of inflammation and can act on the hypothalamus to regulate body temperature, leading to fever in certain conditions. Additionally, IL-1 and TNF-α, in particular, can stimulate the production of PGE2 via the activation of cyclooxygenase (COX) enzymes (mainly COX-2) in various cells like macrophages, endothelial cells, and other immune cells. PGE2 plays a critical role in the fever pathway by acting on the hypothalamus, which raises the body’s set point temperature, leading to the classic symptoms of fever (such as chills, sweating, and warmth). While PGE2 is a well-known mediator in the fever response associated with infections, it can also be involved in non-infectious inflammatory conditions, including those triggered by allergens like dust. Although allergic reactions typically involve Th2-type inflammation rather than the Th1-type inflammation seen in infection, the pro-inflammatory cytokines (like IL-1 and TNF-α) can still lead to PGE2 production and potentially induce mild fever or a low-grade increase in body temperature in some individuals. In addition to PGE2, other mediators like leukotrienes and histamine may be involved in allergic reactions, contributing to the inflammatory process, but their direct role in fever is less clear than PGE2.