• Pearl, Dennis Keith (PI)
  • Pearl, Dennis Keith (PI)
  • Glaser, Ronald (PI)
  • Glaser, Ronald (PI)
  • Glaser, Ronald (PI)
  • Glaser, Ronald (PI)
  • Glaser, Ronald (PI)

Project: Research project

Project Details


Studies from our laboratory and others have shown that relatively
minor aversive events such as academic examinations can have a
significant impact on cellular immunity. Although it is generally
presumed that the immune system is the central mediating link
between stressful events and an increased incidence of infectious
disease, very few studies have simultaneously shown a relationship
between psychological distress, altered immunity, and health
changes. We have shown that the medical student model using exam-
ination stress is a reliable model psychological measuring changes,
particularly in the cellular immune response as it relates to
psychological stress. We now plan to use this model to study
mechanisms underlying the central nervous system (CNS)-
endocrineimmune axis. We will incorporate detailed immunological
and endocrine studies as part of the program project grant
proposal, allowing us to explore the effects of psychological
stress on the immune system and endocrine systems in humans, and
the interaction between the two systems under controlled
conditions. There are two phases in this project. Initially, we
will follow two separate groups of 20 medical students (total n =
40) over one academic year. We will use selected immunological
assays, based on our previous studies on academic stress. These
measures will include natural killer cell activity, the blastogenic
response to two mitogens, phytohemagglutinin, and concanavalin A,
the production of gamma interferon, and reactivation of latent
Epstein-Barr virus by measuring changes in antibody titers (as a
measure of cellular immunity), and endocrine assays (in
collaboration with Dr. W. Malarkey, Project No. 3) to study
mechanisms that we hypothesize underlie the changes in cellular
immunity previously observed by our laboratory and others. We
predict that medical students will show cyclical downward changes
in immune function during examination periods. When this phase is
completed, we will examine other aspects of cellular immunity that
nave not been examined to date. Using the medical student model,
we will explore the mechanisms whereby psychological stress down-
regulates the immune response. The focus of this series of studies
will be macrophage function, T-cell immunity, and gene
expression/production in lymphocytes of two "stress hormones,"
prolactin and growth hormone. We will measure the production of
interleukin-l (a monokine) by macrophages, HLA-DR, HLA-DQ, and HLA-
DP expression, and macrophage mediated cell killing. Detailed
hormonal studies performed in Project 3 will interface with these
studies, providing a means to study the CNS-endocrine-immune axis.
Effective start/end date1/1/018/31/94