Glucocorticoids upregulate decreased IL-7 receptor expression in asthmatic patients and simian immunodeficiency virus-infected non-human primates.

Jul 9, 2013Journal of biological regulators and homeostatic agents

Glucocorticoids increase low IL-7 receptor levels in people with asthma and virus-infected monkeys

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Circadian Biology on OpenScience ↗PubMed ↗

Abstract

Expression of interleukin-7 receptor (IL-7R) on peripheral blood CD4+ T-cells was significantly decreased in clinically stable glucocorticoid (GC)-naive mild and moderate asthmatic patients.

A significant drop in IL-7R levels on circulating CD4+ T-cells was observed following bronchial allergen challenge in sensitized asthmatic subjects.
Inhaled GC treatment restored IL-7R levels in CD4+ T-cells of mild and moderate asthmatics to levels similar to healthy controls.
No significant differences in serum or sputum interleukin-7 levels were found among healthy controls and GC-naive or GC-treated asthmatic patients.
In vitro GC treatment and short-term oral GC administration significantly enhanced IL-7R expression in asthmatic patients.
GC-stimulated T-cells from SIV-infected non-human primates also exhibited increased IL-7R expression.

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Signaling through interleukin-7 receptor (IL-7R) is essential for regulation of T-cell homeostasis and survival. Previously, we and others have found diminished IL-7R levels in simian immunodeficiency virus (SIV) - infected non-human primates and human immunodeficiency virus (HIV) - infected patients. To date, it remains unknown whether changes in IL-7R expression could also be linked to non-infectious inflammatory diseases such as asthma or anti-inflammatory drug use. Here, we investigated through flow cytometry the levels of IL-7R expression on CD4+ and CD4- T-cells in asthmatic patients in relation to disease severity, immune status and glucocorticoid (GC) use. In addition, we sought to evaluate the effects of in vivo and in vitro GC treatment on IL-7R expression in both asthmatic patients and SIV-infected non-human primates. We demonstrated that expression of IL-7R on peripheral blood CD4+ T-cells was significantly decreased in clinically stable GC-naive mild and moderate asthmatic patients. Accordingly, the development of asthmatic reaction following bronchial allergen challenge performed in sensitized subjects was associated with a significant drop in levels of IL-7R on circulating CD4+ T-cells. In contrast, CD4+ T-cells from both, mild and moderate, but not severe asthmatics, treated with inhaled GC displayed levels of IL-7R similar to that seen in healthy controls. We did not find significant differences with serum or sputum interleukin-7 levels among healthy controls and GC-naïve and GC-treated asthmatic patients. Furthermore, both in vitro GC treatment and short-term oral GC administration to asthmatic patients resulted in a significant enhancement of IL-7R. Similarly, we demonstrated that GC-stimulated T-cells from SIV-infected non-human primates up-regulated IL-7R expression. Accordingly, experimental short-term systemic in vivo administration of GC to SIV-infected macaques led to enhancement of IL-7R expression on circulating T-cells. Our data indicate that GC bear potential to recover diminished IL-7R expression, as well in asthma as in lentiviral infection.

Glucocorticoids upregulate decreased IL-7 receptor expression in asthmatic patients and simian immunodeficiency virus-infected non-human primates.

Abstract

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