American Journal of Immunology

Effects of Short Term in vitro Stress Hormone Exposure on Regulatory T Cell Number and Function in Asthma

Kristina E. Rehm and Gailen D. Marshall, Jr.

DOI : 10.3844/ajisp.2015.1.9

American Journal of Immunology

Volume 11, Issue 1

Pages 1-9

Abstract

Asthma is characterized by alterations in the immune system, including regulatory T cells (Treg). Further alterations in Treg numbers and/or function caused by stress hormones may be a contributing factor in asthma pathogenesis. We compared Treg populations and the effects of Dexamethasone (DEX, a laboratory analog of cortisol) on Treg cell number and function in patients with asthma and a control group. We isolated Peripheral Blood Mononuclear Cells (PBMC) from asthma patients (n = 7) and normal controls (n = 8) and quantified CD4+, CD4+CD25hi and CD4+CD25hiFoxP3+ T cells by flow cytometry. To determine the effects of in vitro stress hormones on Treg number and function, we incubated PBMC with 10-9 M, 10-8 M and 10-7 M DEX for 24 h and then CD4+CD25hiFoxP3+ Treg were quantified by flow cytometry. To assess function, CD4+CD25+ were separated and added to cultures of bead-stimulated CD4+CD25- cells and proliferation was measured and compared to the CD4+CD25- cultures incubated with beads alone. The asthma group had significantly fewer CD4+CD25hi and CD4+CD25hiFoxP3+ cells than the control group. DEX significantly decreased Treg number in the control group but not in the asthma group. DEX had no effect on CD4+CD25+ function in either group and the suppressive capacity of the CD4+CD25+ cells was no different between the asthma group and the normal control group. These data suggest that while asthmatics have fewer Treg than normal controls, their function does not differ. These data also suggest that Treg from asthmatics may be less susceptible to the effects of stress hormones.

Copyright

© 2015 Kristina E. Rehm and Gailen D. Marshall, Jr.. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.