In vitro activity: Hydrocortisone prevents endothelial barrier breakdown in response to pro-inflammatory stimuli (TNFalpha administration) in the human brain microvascular endothelial cell line hCMEC/D3, which could be demonstrated to be partly based on maintenance of occludin levels. Hydrocortisone-treated dendritic cells (DCs) show a decreased expression of MHC II molecules, the costimulatory molecule CD86, and the DC-specific marker CD83, as well as a strongly reduced IL-12 secretion. Hydrocortisone-treated DCs inhibits production of IFN-gamma but induces an increased release of IL-4 and no change in IL-5. Hydrocortisone reduces T-cell proliferation in dendritic cells. Hydrocortisone prevents TNF-alpha induced severe degradation of the glycocalyx, increased coronary resistance, heightened vascular leak and permeability to hydroxyethyl starch and caused mast-cell degranulation in isolated guinea pig hearts. Hydrocortisone reduces postischemic oxidative stress, perfusion pressure, and transudate formation in isolated guinea pig hearts. Hydrocortisone inhibits postischemic shedding of syndecan-1, heparan sulfate, and hyaluronan, as well as release of histamine from resident mast cells. Hydrocortisone increases the levels of IL-4-induced germ line C epsilon transcripts by twofold and delivers the signal required for transcription of mature C epsilon mRNA. Hydrocortisone induces S mu-S epsilon deletional switch recombination in IL-4-treated B cells, and support a model of sequential isotype switching from IgM to IgE via IgG4.

J Physiol. 2008 Apr 1;586(7):1937-49; J Allergy Clin Immunol. 2001 Aug;108(2):242-9.