Regulatory, Integrative and Comparative Physiology

Systemic bacterial invasion induced by sleep deprivation

Carol A. Everson, Linda A. Toth


Profound sleep disruption in humans is generally believed to cause health impairments. Through comparative research, specific physical effects and underlying mechanisms altered by sleep deprivation are being elucidated. Studies of sleep-deprived animals previously have shown a progressive, chronic negative energy balance and gradual deterioration of health, which culminate in fatal bloodstream infection without an infectious focus. The present study investigated the conditions antecedent to advanced morbidity in sleep-deprived rats by determining the time course and distribution of live microorganisms in body tissues that are normally sterile. The tissues cultured for microbial growth included the blood, four major organs, six regional lymph nodes, the intestine, and the skin. The principal finding was early infection of the mesenteric lymph nodes by bacteria presumably translocated from the intestine and bacterial migration to and transient infection of extraintestinal sites. Presence of pathogenic microorganisms and their toxins in tissues constitutes a septic burden and chronic antigenic challenge for the host. Bacterial translocation and pathogenic sequelae provide mechanisms by which sleep deprivation appears to adversely affect health.

  • bacterial translocation
  • bacterial infections
  • immunity
  • immunocompetence
  • neuroimmunology


  • Portions of this work were presented at the 11th Annual Meeting of the Association of Professional Sleep Societies and the 14th Congress of the European Sleep Research Society.

  • The principal research support was provided by the National Heart, Lung, and Blood Institute Grant HL-59271. Additional support was provided by National Institutes of Health Grants NS-26429, NS-25378, and CA-21765, and the American Lebanese Syrian Associated Charities.

  • Present address for L. A. Toth: Dept. of Pharmacology, Southern Illinois Univ. School of Medicine, Springfield, IL 62794.

  • Present address and address for reprint requests and other correspondence: C. A. Everson, Neurology Research 151, VA Medical Center, Milwaukee, WI 53295 (E-mail: ceverson{at}

  • The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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