Hydrocortisone treatment of BCG-infected mice impairs the activation and enhancement of antimicrobial activity of peritoneal macrophages.
The present study concerns the effect of hydrocortisone (HC) on the effector functions of Bacillus Calmette Guerin-purified protein derivative (BCG-PPD)-activated macrophages. Such activated macrophages release greater amounts of H2O2 and NO2-, inhibit the intracellular proliferation of T. gondii and kill L. monocytogenes more efficiently than resident macrophages. This activation was not fully expressed by macrophages from BCG-activated mice that had received a subcutaneous injection of HC 2 days before intraperitoneal injection of PPD, since the inhibition of the intracellular proliferation of T. gondii, the release of NO2- and the rate of intracellular killing of L. monocytogenes were lower than in macrophages from BCG-PPD-activated mice. However, treatment with HC did not impair the release of H2O2 by BCG-PPD-activated macrophages. The results show that the treatment of infected mice with HC inhibits their ability to develop adequate intracellular microbicidal mechanisms.
Stokvis
H
H
Department of Infectious Diseases, University Hospital, Leiden, The Netherlands.
Langermans
J A
JA
de Backer-Vledder
E
E
van der Hulst
M E
ME
van Furth
R
R
D000818:Animals; D006854:Hydrocortisone / Q000494:pharmacology*; D006861:Hydrogen Peroxide / Q000378:metabolism; D008089:Listeria monocytogenes / Q000276:immunology; D008262:Macrophage Activation / Q000187:drug effects*; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA; D009163:Mycobacterium bovis; D009585:Nitrogen Dioxide / Q000378:metabolism; D014122:Toxoplasma / Q000254:growth & development; D014376:Tuberculosis / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D014409:Tumor Necrosis Factor-alpha; D006861:Hydrogen Peroxide; D009585:Nitrogen Dioxide; D006854:Hydrocortisone