Stress and immunological phagocytosis: possible nongenomic action of corticosterone

Life Sciences
Gyselle C BaccanBernardo Mantovani

Abstract

Some immunological responses triggered by stress can be mediated by corticosterone activity through cytosolic receptors regulating gene expression. There are, however some reports on the possibility of a nongenomic effect of this hormone to explain phenomena observed in a few minutes. We have found that macrophages from mice subjected to 10 min of cold stress (at -15 degrees C) showed a lower phagocytic capacity mediated by Fcgamma-receptors than cells from control animals. Treating mice with glucocorticoid antagonist RU 486 did not block the decrease in phagocytic capacity. This inhibitory effect on phagocytosis was also observed by experiments in vitro with corticosterone in the concentration found in serum after stress, and could not be prevented by RU 486, actinomicyn D or cycloheximide. These results indicate that corticosterone could affect phagocytosis by macrophages through a nongenomic mechanism, and may have physiological implications.

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Citations

Mar 15, 2008·Respirology : Official Journal of the Asian Pacific Society of Respirology·Fei LongXian-Qiao Jin
Jul 23, 2013·Lasers in Medical Science·Anuska Aparecida Marques LimaAlena Peixoto Medrado
Mar 30, 2011·Stress : the International Journal on the Biology of Stress·M D C IgnacchitiB Mantovani
Jun 13, 2006·Pulmonary Pharmacology & Therapeutics·Gabor HorvathAdam Wanner
Jun 5, 2016·Comparative Immunology, Microbiology and Infectious Diseases·Stephanie HingStephanie S Godfrey
Feb 19, 2016·Experimental and Therapeutic Medicine·Guo-Zhu HuQing-Xian Zhu
Sep 12, 2019·Frontiers in Immunology·Jan M EhrchenKatarzyna Barczyk-Kahlert

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