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Stress and infections

T W Klein1

  • 1Department of Medical Microbiology and Immunology, University of South Florida College of Medicine.

The Journal of the Florida Medical Association
|June 1, 1993
PubMed
Summary
This summary is machine-generated.

Stress impacts the immune system, making individuals more susceptible to infections. This connection involves complex interactions between the brain and immune cells, affecting T lymphocytes and the hypothalamic-pituitary-adrenal axis.

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Area of Science:

  • Neuroimmunology
  • Psychoneuroimmunology
  • Host-pathogen interactions

Background:

  • Bidirectional communication exists between the nervous and immune systems.
  • Stress is known to influence immune responses and susceptibility to infection.
  • Existing research indicates a correlation between stress levels and infection risk in humans and animals.

Purpose of the Study:

  • To explore the intricate relationship between stress, immune function, and infection susceptibility.
  • To elucidate the cellular and molecular mechanisms underlying stress-induced immune modulation.
  • To understand how neuroendocrine hormones and immune cytokines interact to affect host resistance.

Main Methods:

  • Review of experimental studies in human subjects and animal models.

Related Experiment Videos

  • Analysis of stressors including forced exercise, avoidance learning, restraint, isolation, and cold exposure.
  • Examination of immune cell function, particularly T lymphocytes.
  • Investigation of the hypothalamic-pituitary-adrenal axis activity.
  • Assessment of cytokine and hormone production by immune and brain cells.

    • Main Results:

    • Human subjects with high stress indices exhibit increased susceptibility to common cold viruses.
    • Experimental animal models demonstrate that various laboratory stressors enhance susceptibility to viral and bacterial infections.
    • Stress-induced alterations in T lymphocyte function and hypothalamic-pituitary-adrenal axis activity are implicated.
    • Changes in cytokine and hormone profiles from both immune and brain sources are involved in modulating host resistance.

    Conclusions:

    • Stress significantly compromises host resistance to infections through neuroimmunological pathways.
    • Altered functioning of T lymphocytes and the hypothalamic-pituitary-adrenal axis are key mechanisms.
    • Further research is needed to fully understand the complex cellular and molecular basis of stress-induced immune modulation.