- In fever caused by bacterial infection, the set-point of the thermoregulatory mechanism is changed to a new point above 37OC. The following statements were proposed by a researcher to explain the pathogenesis of this fever:
(A) The infection induced cytokines inhibit PGE2 in the hypothalamus, and that increases the body temperature.
(B) The increased levels of circulating TNFα and lL 1β after infection are not able to induce
fever.
(C) The endotoxins of bacteria act on the macrophages and monocytes of the infected person to initiate the process that results in the rise of body temperature.
(D) The cytokines produced from the macrophages by endotoxins act as endogenous pyrogens in the infected person.
(E) The infection induced circulating cytokines act on the organum vasculosum of lamina
terminalis (OVLT) which activates pre-optic area of hypothalamus resulting in the increase of body temperature.
(F) The inhibition of COX2 gene expression by the increased level of circulating cytokines causes the rise of body temperature in the infected person.
Choose the option with all correct statements:
(1) A, B and C (2) B, C and D
(3) C, D and E (4) D, E and FFever Pathogenesis in Bacterial Infection: The Cytokine and Prostaglandin Connection
Fever, a hallmark of bacterial infections, is a complex physiological response resulting from interactions between the immune system and the central nervous system (CNS). Understanding how cytokines and prostaglandins contribute to increasing the body’s thermoregulatory set-point is essential in comprehending fever’s role in host defense.
Reviewing the Proposed Statements
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(A) The infection-induced cytokines inhibit PGE2 in the hypothalamus, and that increases body temperature:
This statement is incorrect. Cytokines actually stimulate prostaglandin E2 (PGE2) production in the hypothalamus, which raises the thermostatic set point and causes fever. -
(B) The increased levels of circulating TNFα and IL-1β after infection are not able to induce fever:
This is false. TNFα and IL-1β are key endogenous pyrogens that induce fever by acting on the hypothalamus to increase PGE2 synthesis. -
(C) The endotoxins of bacteria act on macrophages and monocytes of the infected person to initiate the process that results in the rise of body temperature:
This is true. Bacterial endotoxins trigger macrophages and monocytes to release pyrogenic cytokines that start the febrile response. -
(D) The cytokines produced from macrophages by endotoxins act as endogenous pyrogens in the infected person:
This is true. These cytokines, including IL-1 and TNFα, are the endogenous pyrogens responsible for fever generation. -
(E) The infection-induced circulating cytokines act on the organum vasculosum of lamina terminalis (OVLT) which activates the pre-optic area of hypothalamus resulting in increased body temperature:
This is true. OVLT is a circumventricular organ with an incomplete blood-brain barrier, allowing cytokines to influence hypothalamic neurons and increase temperature set point. -
(F) The inhibition of COX2 gene expression by increased circulating cytokines causes the rise of body temperature:
This is false. Cytokines induce, rather than inhibit, COX-2 expression, leading to increased prostaglandin synthesis that raises body temperature.
Correct Combination of Statements
From the evaluation above, the correct statements are:
C, D, and E -
