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Mycoplasma fermentans activates the hypothalamo-pituitary adrenal axis in the rat

J Weidenfeld1, A Wohlman, R Gallily

  • 1Department of Neurology, Hadassah University Hospital, Jerusalem, Israel.

Neuroreport
|April 19, 1995
PubMed

Insights

Heat-inactivated Mycoplasma fermentans activates the hypothalamo-pituitary-adrenal axis in rats, increasing adrenocorticotrophin (ACTH) and corticosterone (CS). This response involves central mechanisms and is sensitive to glucocorticoid feedback.

Area of Science:

  • Neuroendocrinology
  • Immunology
  • Microbiology

Background:

  • Mycoplasma fermentans infections are associated with various diseases.
  • The activation of the hypothalamo-pituitary-adrenal (HPA) axis by microbial components is a known phenomenon.
  • Understanding the specific pathways involved in Mycoplasma-induced immune responses is crucial.

Purpose of the Study:

  • To investigate the effect of Mycoplasma fermentans on the HPA axis in rats.
  • To elucidate the central mechanisms underlying the HPA axis activation by M. fermentans.
  • To determine the role of glucocorticoid feedback in this response.

Main Methods:

  • Intracerebroventricular administration of heat-inactivated Mycoplasma fermentans in rats.
  • Assessment of serum adrenocorticotrophin (ACTH) and corticosterone (CS) levels.
  • Studies in rats with hypothalamic deafferentation.
  • Administration of dexamethasone to assess glucocorticoid feedback.
  • Experiments in lipopolysaccharide (LPS) unresponsive mice.

Main Results:

  • M. fermentans administration caused a dose- and time-dependent increase in ACTH and CS.
  • Hypothalamic deafferentation completely inhibited the ACTH and CS responses to M. fermentans.
  • Dexamethasone pretreatment abolished the adrenocortical response.
  • M. fermentans elicited a normal corticosterone response in LPS-unresponsive mice.

Conclusions:

  • Mycoplasma fermentans activates the HPA axis through a central mechanism involving hypothalamic ACTH secretagogues.
  • The activation pathway is sensitive to negative glucocorticoid feedback.
  • Elevated glucocorticoid levels during mycoplasma infection may contribute to disease pathogenesis.

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