Activation of the hypothalamic-pituitary-adrenal axis differentially affects the anti-mycobacterial activity of macrophages from BCG-resistant and susceptible mice
There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
The effect of hypothalamic-pituitary-adrenal (HPA) axis activation and exogenous glucocorticoids
on the ability of splenic macrophages to control the growth of Mycobacterium avium
was evaluated. We found that activation of the HPA axis by restraint stress or the
addition of corticosterone increased the susceptibility of macrophages from mice that
are innately susceptible to the in vivo growth of M. avium. In contrast, the ability
of macrophages from innately resistant, congenic mice to control the growth of M.
avium was not affected by HPA activation or the addition of corticosterone. The effect
of restraint and of corticosterone on macrophage function was abrogated by either
treating mice with the glucocorticoid receptor antagonist RU486 or the addition of
the drug to cultures of macrophages. Activation of the HPA axis as well as the addition
of corticosterone to cultures of macrophages resulted in a suppression of the production
of tumor necrosis factor (TNF)-alpha and of reactive nitrogen intermediates by macrophages
from both strains of mice. The lack of effect of HPA activation and of corticosterone
on the mycobacterial resistance of macrophages from BCG-resistant mice, while at the
same time suppressing the production of reactive nitrogen intermediates, appears to
rule out a role for this antimicrobial pathway in innate resistance to mycobacterial
growth.