The impact of acute-stressor exposure on splenic innate immunity: A gene expression analysis

Exposure to intense, acute-stressors modulates immune function. We have previously reported, for example, that exposure to a single session of inescapable tailshock suppresses acquired and potentiates innate immune responses mediated by the spleen. The mechanisms for these changes remain unknown, however, they likely involve stress-induced modulation of cytokines. Cytokines operate in coordinated networks that include other immunoregulatory factors. Broad-scoped analyses are required to gain an understanding of the net-impact of stress on these immunoregulatory factors and the immune system. The goal of this study, therefore, is to examine the impact of acute-stressor exposure on network-wide changes in splenic immunoregulatory factor expression. One hundred and sixty-one genes linked to innate immune responses were quantified in the spleen following exposure to tailshock using an RT-PCR based gene array. Expression changes in 17 of the measured genes were confirmed using individual RT-PCR reactions. Further assessment of the expression changes using Exploratory Gene Association Networks (EGAN) identified important ontologies, processes and pathways that are indicative of a broader impact of stress on the immune system. Interestingly, EGAN identified several linkages between immunoregulatory factors that may be important in explaining previous results concerning the functional consequences of stress on splenic immunity. Additional processes, some of which are novel to this study, were also uncovered that may be important in directing future studies examining the impact of stress on the immune system. In this way, these analyses provide a better understanding of how acute stressor exposure modulates splenic immunity and may function as predictive tool for future related studies.

► An EGAN analysis of stress altered, innate immune gene expression reveals cytokine and chemokine networks that help explain alterations in immunity.