Systemic immune challenge activates an intrinsically regulated local inflammatory circuit in the adrenal gland.
Endocrinology. 2008-04-01; 149(4): 1436-1450
Lire sur PubMed
1. Endocrinology. 2008 Apr;149(4):1436-50. doi: 10.1210/en.2007-1456. Epub 2008 Jan
Systemic immune challenge activates an intrinsically regulated local inflammatory
circuit in the adrenal gland.
Engström L(1), Rosén K, Angel A, Fyrberg A, Mackerlova L, Konsman JP, Engblom D,
(1)Department of Clinical and Experimental Medicine, Faculty of Health Sciences,
Linköping University, Linköping, Sweden.
Endocrinology. 2008 Apr;149(4):1433-5.
There is evidence from in vitro studies that inflammatory messengers influence
the release of stress hormone via direct effects on the adrenal gland; however,
the mechanisms underlying these effects in the intact organism are unknown. Here
we demonstrate that systemic inflammation in rats elicited by iv injection of
lipopolysaccharide results in dynamic changes in the adrenal immune cell
population, implying a rapid depletion of dendritic cells in the inner cortical
layer and the recruitment of immature cells to the outer layers. These changes
are accompanied by an induced production of IL-1beta and IL-1 receptor type 1 as
well as cyclooxygenase-2 and microsomal prostaglandin E synthase-1 in these
cells, implying local cytokine-mediated prostaglandin E(2) production in the
adrenals, which also displayed prostaglandin E(2) receptors of subtypes 1 and 3
in the cortex and medulla. The IL-1beta expression was also induced by
systemically administrated IL-1beta and was in both cases attenuated by IL-1
receptor antagonist, consistent with an autocrine signaling loop. IL-1beta
similarly induced expression of cyclooxygenase-2, but the cyclooxygenase-2
expression was, in contrast, further enhanced by IL-1 receptor antagonist. These
data demonstrate a mechanism by which systemic inflammatory agents activate an
intrinsically regulated local signaling circuit that may influence the adrenals’
response to immune stress and may help explain the dissociation between plasma
levels of ACTH and corticosteroids during chronic immune perturbations.
PMID: 18174279 [Indexed for MEDLINE]