There is a negative feedbakc loop between LPS-induced inflammation and glucocorticoid (cortisol). Adrenal cortex is regulated by CRH and ACTH secreted from the brain, which is the sensor of  inflammation level via the serum concentration of pro-inflammatory cytokine (i.e. TNF-alpha, IL1-beta etc.).  When the inflamation cytokines reach enough  concentration, hypothalamus and pituitary gland begin to secrete CRH and ACTH, respectively. 

Dear Rajaram, 

Check also the reference lists to the papers:

Cellular and Molecular Neurobiology

May 2010, Volume 30, Issue 4, pp 531-541

Systemic Administration of Lipopolysaccharide Induces Cyclooxygenase-2 Immunoreactivity in Endothelium and Increases Microglia in the Mouse Hippocampus

Dae Won Chung, Ki-Yeon Yoo, In Koo Hwang, Dae Won Kim, Jin Young Chung, Choong Hyun Lee, Jung Hoon Choi, Soo Young Choi, Hwa Young Youn, In Se Lee et al. 

Effect of bacterial endotoxin and interleukin-1 beta on hippocampal serotonergic neurotransmission, behavioral activity, and free corticosterone levels: an in vivo microdialysis study

AC Linthorst, C Flachskamm, P Muller-Preuss, F Holsboer, and JM Reul              The Journal of Neuroscience, 1 April 1995, 15(4): 2920-2934;

Leptin deficiency enhances sensitivity to endotoxin-induced lethality

Raffaella Faggioni  et al.  American Journal of Physiology - Regulatory, Integrative and Comparative Physiology Published 1 January 1999 Vol. 276 no. 

Please review the following:

European Journal of Immunology Volume 19, Issue 2, pages 301–305, February 1989

Differential regulation of lipopolysaccharide-induced interleukin 1 and tumor necrosis factor synthesis: effects of endogenous and exogenous glucocorticoids and the role of the pituitary-adrenal axis

Steven H. Zuckerman1,*,

James Shellhaas2 and

Larry D. Butter1

Abstract

Intraperitoneal injection of a sublethal dose of lipopolysaccharide (LPS) into mice resulted in the appearance of tumor necrosis factor (TNF) in the serum within 45 min. Maximal serum TNF was detected by 1 h, and by 3–4 h TNF levels were no longer significantly above baseline. Injection of mice with an additional dose of LPS at 4 h resulted in no further increase in serum TNF. The in vivo kinetics of TNF appearance correlated with in vitro studies in which TNF mRNA was detected in murine peritoneal macrophages 30 min after LPS stimulation. The increase in serum TNF was not detected in mice treated with dexamethasone, 3 mg/kg, prior to LPS stimulation. The decrease in TNF correlated with the appearance of significant amounts of endogenous serum corticosterone which were maximal by 3 h. Further evidence for the role of endogenous steroids in the modulation of serum TNF levels was obtained in studies with adrenalectomized or hypophysectomized mice. Compared to sham-operated animals, serum TNF levels remain elevated 5 h post LPS stimulation in adrenalectomized or hypohysectomized mice. In contrast with the transient increase in TNF, serum IL 1 was maximal 4 h post LPS injection and remained elevated at 24 h. In vitro studies with primary cultures of human peripheral blood monocytes and human umbilical cord vein endothelial cells demonstrated that LPS-induced mono-cyte IL 1 levels were reduced approximately 5-fold by 10-1 M dexamethasone while dexamethasone had only minimal effects on endothelial cell IL 1. Therefore, the in vitro data would suggest that the maintenance of elevated IL 1 levels coincident with the appearance of endogenous corticosteroids during LPS shock is related to the synthesis of IL 1 by both monocyte-macrophages and non-myeloid cell populations including endothelial cells.

thanks alot for your valuable support and explanations Dr .Go J Yoshida, Dr Béatrice Marianne Ewalds-Kvist and Dr Amar Safdar