The concept regarding the pathogenesis of pyrexia is almost exclusively concentrated on humoral mediatory mechanism. As per these views, exogenous pyrogens first persuade the formation of pyrogenic cytokines and these endogenous pyrogens order to increase the synthesis of prostaglandin E in different structures of the central nervous system (CNS). The subsequent alterations of CNS functions are reflected in the modifications of peripheral thermoregulatory effector functions, which hoist body temperature during the development of fever and maintain it during the whole fever course. Brewer's yeast-induced pyrexia model has been furnished in the chapter.
关于发热发病机制的概念几乎完全集中在体液介导机制上。根据这些观点，外源性致热原首先促使致热细胞因子的形成，这些内源性致热原会促使中枢神经系统（CNS）不同结构中前列腺素E的合成增加。随后中枢神经系统功能的改变反映在外周体温调节效应器功能的改变上，在发热过程中体温升高，并在整个发热过程中维持该体温。本章提供了啤酒酵母诱导的发热模型。
