Question

If IL-1 was blocked by a monoclonal antibody, which of the following would be true? There may be more than one true statement. (4pts)

***use the diagram attached to see the molecular pathway being referred to***

A. Less cox-2 being made

B. More LPS being made by the body

C. Taking a few days longer to fight off pathogens than if IL-1 had not been blocked from binding to its receptor

D. More frequent fever seizures in people who had previously had a fever seizure

E. Elevated set point temp. In the hypothalamus

F. Elevated core body temp.

G. Decreased symptoms in patients with periodic fever syndromes

H. FeweR prostaglandin E2 (PGE2) molecules being made

Answer 1

Xi IL-1 monocional antibody Cell membrane Phospholipid PLA2 Arachidonic acid NFKB cox-2 Prostaglandin H2 厂 inflammatory gene: COX2 PGE synthase Prostaglandin E2 (PGE2) Nucleus FEVER!! A. Less cox-2 being made H. FeweR prostaglandin E2 (PGE2) molecules being made G. Decreased symptoms in patients with periodic fever syndromes

Reason:

Interleukin-1 is the immune inflammatory mediator that binds with the cell surface membrane receptors that stimulate Nf-kB to initiate transcription of DNA (inflammatory gene) finally to synthesize cycloxygenase enzyme -2 (COX-2) through protein synthesis. This enzyme promotes arachidonic acid metabolism and trigger generation of prostaglandin HH to prostaglandin E2 metabolites result in fever due to stimulation of hypothalamic activity. Therefore, inhibition of the interleukin-1 by any monoclonal antibody is leading to inhibition of Nf-kB activation and followed by low generation of COX-2 to produce inflammatory mediators (PGE2) to trigger fever.