Sleep Deprivation Induces Changes in Immunity in Trichinella spiralis -Infected Rats
Open accessAbstract
Sleep is considered an important predictor of immunity. A lack of sleep may reduce immunity, which increases susceptibility to any type of infection. Moreover, sleep deprivation in humans produces changes in both, the percent of circulating immune cells (T cells and NK cells) and cytokine levels (IL-1, IFNγ, TNΦ-αα, IL-6 and IL-17). The aim of our study was to investigate whether sleep deprivation produces deregulation on immune variables during the immune response generated against the helminth parasite Trichinella spiralis. Because sleep deprivation is stressful per se, we designed another experiments to compared stress alone (consisting in movement restriction and single housing) with sleep deprivation, in both control (uninfected) and experimental (infected) rats. Our results demonstrate that the sleep deprivation and stress have a differential effect in mesenteric lymph nodes (MLN) and spleen. In uninfected rats sleep deprivation alone produces an increase in natural killer cells (NK+) and B cells (CD45+), accompanied by a decrease in cytotoxic T cells (CD3+CD8+) in spleen; while, in MLN, produces only an increase in natural killer cells (NK+). Both, SD and stress, produce an increased percentage of total T cells (CD3+) in spleen. In the MLN both are also associated to an increase in cytotoxic T cells (CD3+CD8+) and B cells (CD45+). In the spleens of parasitized rats, cell populations did not change. In spleens of both, sleep-deprived and stressed infected rats, we observed an increase in B cells (CD45+). In infected rats, sleep deprivation alone produced an increase in NK cells (NK+). In mesenteric node cell populations of parasitized rats, we observed a decrease in NK cells and an increase in T helper (CD4+) cells in both SD and stressed rats. Rats that were only subjected to stress showed a decrease in B cells (CD45+). These findings suggest that the immune response generated against infection caused by T. spiralis is affected when the sleep pattern is disrupted. These results support the notion that sleep is a fundamental process for an adequate and strong immune response generated against this parasite.
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Collectively, there is ample evidence that IL-1 and TNF, in particular, and PGD2 play a critical role in the regulation of physiological, spontaneous NREM sleep in animals, and potentially in humans, while they may not be involved in physiological REM sleep regulation.
“Collectively, there is ample evidence that IL-1 and TNF, in particular, and PGD2, play a critical role in the regulation of physiological, spontaneous NREM sleep in animals, and potentially in humans, while they may not be involved in physiological REM sleep regulation (250, 551).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [250]
REM sleep suppression may promote the generation of fever that in turn boosts immunity.
“As REM sleep is incompatible with thermoregulatory effector responses like shivering, REM sleep suppression may promote the generation of fever that in turn boosts immunity (250).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [250]
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References 39 · Cited by 30
Research works printed but not linked: 1
- [34]Leger D Ogrizek P Review on sleep and awakening disorders Rev Med Interne 2012 33 525 31 22770802
- Authors
- Ibarra-Coronado, E. G., Velazquéz-Moctezuma, J., Diaz, D., Becerril-Villanueva, L. E., Pavón, L., & Morales-Montor, J.
- Affiliations
- Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz (MX)
- ORCID
- Pavón, Lenin
- Venue
- International Journal of Biological Sciences
- Publisher
- Ivyspring International Publisher
- Published
- 2015
- Volume
- 11
- Issue
- 8
- Pages
- 901-912
- ISSN
- 1449-2288 (ISSN-L)
- PMC
- PMC4495408
- OpenAlex
- W746293730
- Cited by
- 30
- References
- 39
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 4 · 2019: 5 · 2018: 4 · 2017: 2 · 2016: 2
- FWCI
- 2.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- Locations
- International Journal of Biological Sciences (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Consejo Nacional de Ciencia y Tecnología (IN208715, 176803, CVU 288056, 99158819)
- Universidad Nacional Autónoma de México (176803, 99158819, IN208715, CVU 288056)
- Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México
- Topics
- Life Sciences › Immunology and Microbiology › Parasitology › Parasites and Host Interactions
- Health Sciences › Medicine › Infectious Diseases › Parasitic Diseases Research and Treatment
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Keywords
- sleep deprivation, Trichinella spiralis, helminthiasis, immune response, stress, natural killer cells, cytotoxic T lymphocytes, B cells, T helper cells, mesenteric lymph nodes, spleen, cytokines, host-parasite interactions
- MeSH terms
- Animals, Male, Sleep Deprivation, Trichinellosis, Immunophenotyping, Lymphocyte Subsets, Cytokines, Trichinella spiralis, Rats, Wistar, Rats
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