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A role for intestinal TLR4-driven inflammatory response during activity-based anorexia.

Liliana Belmonte1,2,3,4, Najate Achamrah1,2,3,4, Séverine Nobis1,2,3

  • 1Normandie Univ, UR, Rouen, France.

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Anorexia nervosa is linked to inflammation and gut changes. Toll-like receptor 4 (TLR4) activation in the gut precedes brain changes, but TLR4 deficiency worsens anorexia nervosa symptoms and mortality.

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Area of Science:

  • Immunology
  • Neuroscience
  • Gastroenterology

Background:

  • Anorexia nervosa (AN) is characterized by low-grade systemic inflammation and gut microbiota alterations.
  • The precise molecular drivers of inflammation in AN remain unidentified.
  • Toll-like receptors (TLRs) regulate innate immunity and may influence food intake.

Purpose of the Study:

  • To investigate the role of Toll-like receptor 4 (TLR4) in anorexia-associated inflammation using an activity-based anorexia (ABA) model.
  • To elucidate the contribution of TLR4 to the inflammatory and neuroendocrine responses during ABA.

Main Methods:

  • Utilized the activity-based anorexia (ABA) mouse model.
  • Assessed intestinal inflammatory status, including TLR4 expression on colonic epithelial cells and macrophages.
  • Measured downstream mucosal cytokine production, hypothalamic changes, and plasma corticosterone levels.
  • Compared ABA outcomes in wild-type and TLR4-deficient mice.

Main Results:

  • ABA rapidly induced intestinal inflammation, with early upregulation of TLR4 in the colon.
  • Increased mucosal cytokine production preceded hypothalamic alterations and elevated IL-1β, IL-1R1, and corticosterone.
  • TLR4-deficient mice showed increased vulnerability and mortality during ABA, indicating a protective role of TLR4.

Conclusions:

  • TLR4-mediated immune responses in the gut play a significant early role in the pathophysiology of anorexia nervosa.
  • Gut inflammation and TLR4 activation precede central neuroendocrine changes in ABA.
  • Despite contributing to inflammation, TLR4 signaling appears crucial for mitigating the severity and mortality associated with ABA-induced weight loss.