We propose the term deficiency of the interleukin-1-receptor antagonist, or DIRA, to denote this autosomal recessive autoinflammatory disease caused by mutations affecting IL1RN.
One hundred femtomoles of ET-1 increased body temperature when injected in the POA of conscious Wistar rats; this effect was significantly counteracted by the coinjection of 600 pmol IL-1 receptor antagonist (IL-1ra).
Interleukin-1beta mediates the memory impairment associated with a delayed type hypersensitivity response to bacillus Calmette-Guérin in the rat hippocampus.
We observed that: (1) intracerebral ventricular injection of (ICV) IL-1beta induced pressor responses; (2) hypertension induced by IL-1beta was blocked by ICV an IL-1 antagonist, IL-1ra; (3) ICV IL-1ra attenuated the pressor response induced by FS but intravenous injection of IL-1ra did not significantly reduce this response; (4) the hypertensive response to conditioned fear stimuli was reversed by ICV IL-1ra; (5) FS-induced-analgesia was attenuated by ICV IL-1ra and this effect disappeared 15 min after ICV IL-1ra.
Endotoxin-induced cytokine gene expression in vivo. IV. Expression of interleukin-1 alpha/beta and interleukin-1 receptor antagonist mRNA during endotoxemia and during endotoxin-initiated local acute inflammation.
Influence of the course of brain inflammation on the endogenous IL-1beta/IL-1Ra balance in the model of brain delayed-type hypersensitivity response to bacillus Calmette-Guérin in Lewis rats.
Endotoxin-induced cytokine gene expression in vivo. IV. Expression of interleukin-1 alpha/beta and interleukin-1 receptor antagonist mRNA during endotoxemia and during endotoxin-initiated local acute inflammation.