Prostaglandin-mediated mechanisms were shown to have important role in the mode of this action of IL-1β, since paracetamol pretreatment partially prevented the development of the above mentioned hyperthermia.
Administration of IL-1ß induced fever, lethargy and anorexia for∼two-to-three days and increased the concentration of IL-1ß in the hippocampus and hypothalamus for at least eight hours.
The role of circulating immune complexes and biocompatibility of staphylococcal protein A immunoadsorption in mitomycin C-induced hemolytic uremic syndrome.
These studies establish that the dominant pI 7 form of recombinant human IL-1 possesses immunological and inflammatory properties and acts on the central nervous system to produce fever.
The extent to which PGE<sub>2</sub> and other pro-inflammatory cytokines such as TNF-α, IL-6, or IL-1β could be involved in the induction of behavioural fever in fish remains to be clarified.
The rapid increase of IL-1β production in the supernatants of the LPS-induced cells was significantly higher at the fourth and the twenty-fourth hours in febrile and complex febrile seizures, respectively.
ETAF/IL-1 has a multiplicity of divergent biological effects: enhancement of thymocyte proliferation, stimulation of cells in the hypothalamus to mediate fever, leukocyte chemotaxis, stimulation of hepatic synthesis of acute-phase proteins, augmentation of IL-2 production and keratinocyte proliferation.
In this report, the effects of elevated temperature and dexamethasone on LPS-stimulated IL-1 beta and TNF alpha mRNA gene expression and protein synthesis were studied in human astrocytoma cell lines and primary cultures of human fetal astrocytes.
Now, in mice, we report the effect of AT2 gene disruption on the hyperthermia induced by immunological (interleukin-1 (IL-1) injection) and non-immunological (saline injection or cage switch) stress.2.
Mice lacking the Tak1 gene in brain endothelial cells showed a blunted fever response and reduced lethargy upon intravenous injection of the endogenous pyrogen IL-1β.
We conclude that IL-6 is formed in brain in response to both i.v. and i.c.v. pyrogens; however, its formation, whether requiring the prior induction of IL-1 or not, does not appear to be critical for the development of the fever.
In this study, we examined the possible effects of anti-Ly6G-mediated systemic neutrophil depletion and liposome-encapsulated clodronate (LEC)-mediated systemic macrophage depletion on the inflammatory signs (thermal hyperalgesia, mechanical allodynia, oedema and fever) and measured the levels of various inflammation markers (tumour necrosis factor-α (TNF-α), interleukins (IL)-1β, IL-4, IL-10, macrophage inflammatory protein-1 alpha (MIP-1α/CCL3) and myeloperoxidase (MPO) in paw and spinal cord tissues in carrageenan (CG)-induced hindpaw inflammation model in rats.
CAPS are associated with gain-of-function mutations in the NLRP3 inflammasome, a multiprotein complex critical for the activation of IL-1ß, and are characterized by episodes of fever, urticaria-like rash, musculoskeletal, ocular, and neurological symptoms.
CAPS are associated with GOF mutations in the NLRP3 inflammasome and activation of IL-1ß leading to episodes of fever, cutaneous, musculoskeletal, articular, ocular, and neurological symptoms.
These results support the hypothesis that elevated temperature is one of the physiologic signals for down-regulation of IL-1 beta biosynthesis through a mechanism related to the induction of hsp.
Freshly isolated leukemic cells from patients with adult T-cell leukemia (ATL) produce high levels of interleukin-1 (IL-1), which is believed to play an important role in neutrophilia, elevation of C-reactive protein, osteolytic bone lesions, hypercalcemia, and fever in ATL.