Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery. Am J Physiol Regul Integr Comp Physiol 2008 Dec;295(6):R2067-74
Date
10/24/2008Pubmed ID
18945949Pubmed Central ID
PMC2685300DOI
10.1152/ajpregu.90623.2008Scopus ID
2-s2.0-57749108208 (requires institutional sign-in at Scopus site) 29 CitationsAbstract
Sleep is understood to possess recuperative properties and, conversely, sleep loss is associated with disease and shortened life span. Despite these critical attributes, the mechanisms and functions by which sleep and sleep loss impact health still are speculative. One of the most consistent, if largely overlooked, signs of sleep loss in both humans and laboratory rats is a progressive increase in circulating phagocytic cells, mainly neutrophils. The destination, if any, of the increased circulating populations has been unknown and, therefore, its medical significance has been uncertain. The purpose of the present experiment was to determine the content and location of neutrophils in liver and lung tissue of sleep-deprived rats. These are two principal sites affected by neutrophil migration during systemic inflammatory illness. The content of neutrophils in the intestine also was determined. Sleep deprivation in rats was produced for 5 and 10 days by the Bergmann-Rechtschaffen disk method, which has been validated for its high selectivity under freely moving conditions and which was tolerated and accompanied by a deep negative energy balance. Comparison groups included basal conditions and 48 h of sleep recovery after 10 days of sleep loss. Myeloperoxidase (MPO), an enzyme constituent of neutrophils, was extracted from liver, lung, and intestinal tissues, and its activity was determined by spectrophotometry. Leukocytes were located in vasculature and interstitial spaces in the liver and the lung by immunohistochemistry. Heme oxygenase-1, also known as heat shock protein-32 and a marker of cellular stress, and corticosterone also were measured. The results indicate neutrophil migration into extravascular liver and lung tissue concurrent with cell stress and consistent with tissue injury or infection induced by sleep loss. Plasma corticosterone was unchanged. Recovery sleep was marked by increased lung heme oxygenase-1, increased intestinal MPO activity, and abnormally low corticosterone, suggesting ongoing reactive processes as a result of prior sleep deprivation.
Author List
Everson CA, Thalacker CD, Hogg NAuthors
Carol A. Everson PhD Professor in the Medicine department at Medical College of WisconsinChrista D. Thalacker NP APP Outpatient in the Orthopaedic Surgery department at Medical College of Wisconsin
MESH terms used to index this publication - Major topics in bold
AnimalsCell Movement
Corticosterone
Disease Models, Animal
Heme Oxygenase (Decyclizing)
Immunohistochemistry
Intestines
Liver
Lung
Male
Neutrophil Infiltration
Neutrophils
Peroxidase
Rats
Rats, Sprague-Dawley
Recovery of Function
Sleep
Sleep Deprivation
Stress, Physiological
Time Factors
