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Related Experiment Videos

Hypothalamic-pituitary cytokine network.

Anastasia Kariagina1, Dmitry Romanenko, Song-Guang Ren

  • 1Cedars-Sinai Medical Center-University of California, Los Angeles School of Medicine, California 90048, USA.

Endocrinology
|September 27, 2003
PubMed
Summary

Leukemia inhibitory factor (LIF) and corticotropin-releasing hormone (CRH) play roles in the stress response. Proinflammatory cytokines can compensate for deficiencies in CRH and LIF, activating the HPA axis.

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Area of Science:

  • Neuroendocrinology
  • Immunology
  • Molecular Biology

Background:

  • Cytokines in the brain regulate the hypothalamus-pituitary-adrenal (HPA) axis.
  • Leukemia inhibitory factor (LIF) and its receptors are present in the pituitary and hypothalamus.
  • LIF influences proopiomelanocortin (POMC) gene transcription and ACTH secretion, potentiating CRH effects.

Purpose of the Study:

  • To investigate the specific roles of CRH and LIF in the inflammatory HPA response.
  • To generate and analyze double-knockout mice deficient in both CRH and LIF.

Main Methods:

  • Generation of double-knockout mice (CRH/LIFKO) by breeding single gene null mutants.
  • Induction of inflammation via intraperitoneal injection of lipopolysaccharide (LPS).
  • Measurement of pituitary POMC induction, ACTH secretion, and corticosterone response.

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Main Results:

  • CRH/LIF-deficient mice showed pituitary POMC induction comparable to wild-type mice and significantly higher than single null animals following LPS injection.
  • Double-knockout mice exhibited a robust corticosterone response to inflammation.
  • Elevated POMC mRNA levels correlated with increased TNF-alpha, IL-1beta, and IL-6 in the hypothalamus and pituitary.

Conclusions:

  • Increased central proinflammatory cytokine expression can compensate for impaired HPA axis function.
  • The HPA axis can be activated by inflammatory cytokines even in the absence of CRH and LIF.
  • This study highlights the compensatory mechanisms within the neuroendocrine-immune interface during inflammatory stress.