|Kehrli jr, Marcus|
Submitted to: Journal of Leukocyte Biology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 5/3/1997
Publication Date: N/A
Citation: Interpretive Summary: An anti-inflammatory steroid was tested in vivo for its effects on a family of receptors important to regulation of immune responses. This compound, dexamethasone, was given to several groups of dairy cattle and was found to increase the number of Type II receptors for an important compound that initiates immune responses. These Type II receptors are believed to be "decoys," which then would serve to block the immune response and may thus define an important mechanism of action of steroid hormones as anti-inflammatory compounds. Future experiments will evaluate whether a similar effect is seen during natural periods of stress in dairy cows. This type of experimentation should be useful in better understanding immune function, and may ultimately reduce the use of antibiotics in cattle.
Technical Abstract: The effects of glucocorticoids on in vivo regulation of type I IL-1 receptor (IL-1RI) and type II IL-1 receptor (IL-1RII) mRNA levels were investigated using Holstein cattle injected with dexamethasone (0.04 mg/kg). Using semi-quantitative RT-PCR and Northern analysis, we observed that IL-1RI and IL-1RII mRNAs were up-regulated in bovine peripheral blood mononuclear cells (PBMCs) and neutrophils (PMNs) as a result of dexamethasone treatment in vivo. IL-1RII mRNA was strongly induced in both bovine PBMCs and PMNs at 24 hours after dexamethasone administration, and had returned to baseline levels by 72 hours after dexamethasone injection. IL-1RI mRNA was increased in PBMCs and PMNs at 24 and 72 hours after dexamethasone injection, with the greatest increase detected at 72 hours. These data provide evidence for differential in vivo regulation of IL-1RI and IL-1RII mRNA by dexamethasone, and describe a large animal model for investigating the modulation of IL-1 receptors as part of the anti-inflammatory mechanisms of glucocorticoids.