The DOI matches its Crossref record; 208 of the 208 references it cites were found in a registry or an index.
African trypanosome infections of the nervous system: Parasite entry and effects on sleep and synaptic functions
Abstract
The extracellular parasite Trypanosoma brucei causes human African trypanosomiasis (HAT), also known as sleeping sickness. Trypanosomes are transmitted by tsetse flies and HAT occurs in foci in sub-Saharan Africa. The disease, which is invariably lethal if untreated, evolves in a first hemo-lymphatic stage, progressing to a second meningo-encephalitic stage when the parasites cross the blood-brain barrier. At first, trypanosomes are restricted to circumventricular organs and choroid plexus in the brain outside the blood-brain barrier, and to dorsal root ganglia. Later, parasites cross the blood-brain barrier at post-capillary venules, through a multi-step process similar to that of lymphocytes. Accumulation of parasites in the brain is regulated by cytokines and chemokines. Trypanosomes can alter neuronal function and the most prominent manifestation is represented by sleep alterations. These are characterized, in HAT and experimental rodent infections, by disruption of the sleep-wake 24h cycle and internal sleep structure. Trypanosome infections alter also some, but not all, other endogenous biological rhythms. A number of neural pathways and molecules may be involved in such effects. Trypanosomes secrete prostaglandins including the somnogenic PGD2, and they interact with the host's immune system to cause release of pro-inflammatory cytokines. From the sites of early localization of parasites in the brain and meninges, such molecules could affect adjacent brain areas implicated in sleep-wakefulness regulation, including the suprachiasmatic nucleus and its downstream targets, to cause the changes characteristic of the disease. This raises challenging issues on the effects of cytokines on synaptic functions potentially involved in sleep-wakefulness alterations.
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“These findings established both cytokines, IL-1 and TNF, as substances involved in the homeostatic regulation of sleep (for review, see Refs. 299, 411).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [299]
In the citing paper
“increasing the availability of those cytokines promoted NREM sleep amount and intensity and suppressed REM sleep amount.”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [299]
In the citing paper
“blocking the biological actions of the cytokines IL-1 and TNF resulted in a reduction of physiological NREM sleep amount or NREM sleep rebound after sleep deprivation.”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [299]
In the citing paper
“pathogens, including bacteria, viruses, fungi, and parasites increase the amount and intensity of NREM sleep while decreasing the amount of REM sleep (for comprehensive review, see Refs. 299, 353).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [299]
Citations
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The Sleep-Immune Crosstalk in Health and Disease
Besedovsky, L., Lange, T., & Haack, M. (2019) · Physiological Reviews · doi:10.1152/physrev.00010.2018 · Cited by 1,479
“It has been shown that the parasite trypanosoma can produce PGs, including PGD2 with known somnogenic properties, and triggers the release of pro-inflammatory cytokines (298).”
BackgroundBrun, R., Blum, J., Chappuis, F., & Burri, C. (2010) · The Lancet · doi:10.1016/s0140-6736(09)60829-1 · Cited by 926
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Harrington, M. E. (2012) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2012.07.004 · Cited by 112
“…brucei, associated in humans with human African trypanosomiasis or ‘‘sleeping sickness’’, show reduced amplitude circadian activity rhythms, mirroring effects in humans infected with this parasite who show diurnal somnolence and nocturnal insomnia (Kristensson et al., 2010; Lundkvist et al., 2010).”
Metadata
- Authors
- Kristensson, K., Nygård, M., Bertini, G., & Bentivoglio, M.
- Affiliations
- Karolinska Institutet (SE)
- University of Verona (IT)
- Corresponding author
- Kristensson, Krister
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 91
- Issue
- 2
- Pages
- 152-171
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W2024288031
- Cited by
- 140
- References
- 208
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 5 · 2023: 3 · 2022: 10 · 2021: 6 · 2020: 8 · 2019: 11 · 2018: 7 · 2017: 7 · 2016: 7 · 2015: 7 · 2014: 13 · 2013: 17 · 2012: 13
- FWCI
- 6.71
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Trypanosoma species research and implications
- Life Sciences › Neuroscience › Cognitive Neuroscience › Sleep and Wakefulness Research
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- Trypanosoma brucei, sleeping sickness, blood-brain barrier penetration, sleep-wake cycle disruption, sleep disorders, prostaglandin D2, inflammatory cytokines, chemokines, suprachiasmatic nucleus, circadian rhythm, synaptic function, dorsal root ganglia, choroid plexus, circumventricular organs
- MeSH terms
- Animals, Brain, Humans, Synaptic Transmission, Sleep, Sleep Wake Disorders, Trypanosomiasis, African, Central Nervous System Protozoal Infections
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