Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats
| Autor: | Carol A. Everson |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Male
Physiology medicine.medical_treatment Immunoglobulins Inflammation Immunoglobulin E Rats Sprague-Dawley Leukocyte Count Physiology (medical) medicine Animals Circadian rhythm biology medicine.disease Adaptation Physiological Sleep in non-human animals Privation Rats Endotoxins Sleep deprivation medicine.anatomical_structure Cytokine Immunology biology.protein Cytokines Sleep Deprivation Bone marrow medicine.symptom |
| Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 289:R1054-R1063 |
| ISSN: | 1522-1490 0363-6119 |
| DOI: | 10.1152/ajpregu.00021.2005 |
| Popis: | The specific systems and mechanisms affected by sleep deprivation that may perpetuate disease processes in humans still are speculative. In laboratory rats, prolonged sleep deprivation induces a state marked by abnormal control over indigenous bacteria that results in transient infections of internal tissues and eventual lethal septicemia. The present studies investigated changes in blood, serum, and bone marrow parameters that may provide diagnostic clues to immunopathology. Prolonged sleep deprivation was produced in rats by the disk-over-water method, a well-established and selective means that does not interfere with normal waking behaviors. Measurements included bone and blood differential white blood cell counts, multiple serum cytokines and chemokines, several major Ig classes and subclasses, and serum endotoxin concentrations. The results indicated mild, regenerative neutrophilia in sleep-deprived rats, initially accompanied by immature neutrophils and later by monocytosis. The corresponding serum cytokine profile revealed an evolving proinflammatory state, particularly by high incidence of interleukin-1β, implicating mononuclear phagocytes and resident tissue cells as main intermediary sources. In addition, multiple serum Ig classes were increased by sleep deprivation without experimental administration of an exogenous antigen. Despite this immune activation, there was failure to eradicate invading bacteria and toxins, suggesting competing anti-inflammatory processes or interference with immune effector functions during sleep deprivation. Nearly all of the immune-related events that emerged as responses to sleep deprivation have been implicated as etiological or provocative factors in other disease processes and may provide means by which sleep deprivation as a risk factor in disease may become understood. |
| Databáze: | OpenAIRE |
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