In fever caused by bacterial infection, the set-point of the thermoregulatory mechanism is changed to a new point above 37°C.
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 IL1β 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:

Correct option is C

Explanation-

Correct options-

(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 
Endotoxins like lipopolysaccharides (LPS) from Gram-negative bacteria stimulate immune cells like macrophages and monocytes. These cells release cytokines (e.g., IL-1, IL-6, TNF-α), initiating the fever cascade. This is the first step in fever development.
(D) The cytokines produced from the macrophages by endotoxins act as endogenous pyrogens in the infected person.
These cytokines (especially IL-1 and TNF-α) are called endogenous pyrogens because they originate from within the body and trigger fever. They act on the hypothalamus to raise the set-point for body temperature.
(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.
The OVLT is one of the circumventricular organs that lacks a blood-brain barrier. Cytokines reach the OVLT, leading to prostaglandin E₂ (PGE₂) production. This activates the hypothalamic preoptic area, resetting the thermoregulatory set-point, causing fever.

Incorrect options -

(A) The infection-induced cytokines inhibit PGE₂ in the hypothalamus, and that increases the body temperature.
PGE₂ is essential for fever development. Cytokines stimulate PGE₂ synthesis (especially via COX-2), which raises the set-point. So, inhibition of PGE₂ would prevent fever — the statement is false.
(B) The increased levels of circulating TNF-α and IL-1β after infection are not able to induce fever.
Both TNF-α and IL-1β are key endogenous pyrogens. They directly or indirectly (via PGE₂) lead to fever. Saying they don’t induce fever contradicts known mechanisms.
(F) The inhibition of COX-2 gene expression by the increased level of circulating cytokines causes the rise of body temperature in the infected person.
Cytokines upregulate COX-2, not inhibit it. COX-2 catalyzes the conversion of arachidonic acid to PGE₂, which then raises the hypothalamic set-point. So, inhibiting COX-2 would block fever — the statement is false.

Final Answer:
The correct statements are C, D, and E, which matches - Option c