The consequences of parasitic infection for the behavior of the mammalian host.

Donovick, Peter J.; Burright, Richard G.

doi:10.1289/ehp.8773247

Cited by 17 publications

(8 citation statements)

References 51 publications

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“…A similar situation could be proposed for the relationship between T. canis larvae, rodents and dogs and some authors have actually verified the occurrence of behavioral alterations in mice infected by larvae of this ascarid 2,6,7,8,9,10 , though not as clearly as has been demonstrated for the interaction between Toxoplasma gondii and rodents. Moreover, the great majority of papers on this issue used mice and not Rattus norvegicus.…”

Section: Discussionsupporting

confidence: 56%

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Behavioral changes in Rattus norvegicus experimentally infected by Toxocara canis larvae

Chieffi

Aquino²,

Pasqualotti³

et al. 2010

Rev. Inst. Med. trop. S. Paulo

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SUMMARYToxocara canis is a common canine nematode parasite and one of its possible transmission mechanisms is the predation of infected rodents by canids. Fifty Rattus norvegicus were used to study behavioral alterations in rodents infected by T. canis larvae. The rats were divided into three groups: G1, 20 rats infected with 300 T. canis eggs; G2, 20 rats infected with 2,000 T. canis eggs; and G3, 10 non-infected rats. Thirty and 60 days post-infection, rats from all the groups were submitted to an open-field apparatus for five min and subsequently, to an elevated plus-maze apparatus, again for five min. The data obtained indicated improvement in mobility (total locomotion time and rearing frequency) and exploratory behavior in infected rats, principally in G2, which provides some support for the hypothesis that behavioral alterations in rodents infected by Toxocara canis larvae enhance the transmission rate of this ascarid to dogs.

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Section: Discussionsupporting

confidence: 56%

“…Some authors have reported behavioral alterations and learning impairment in mice infected by T. canis larvae 2,6,7,8,9,10 . Recently, one study reported diminished muscular strength in R. norvegicus experimentally infected by T. canis larvae, suggesting some enhancement of the preypredation mechanisms of infection 3 .…”

Section: Introductionmentioning

confidence: 99%

Behavioral changes in Rattus norvegicus experimentally infected by Toxocara canis larvae

Chieffi

Aquino²,

Pasqualotti³

et al. 2010

Rev. Inst. Med. trop. S. Paulo

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“…Parasitic infections can also alter sleep patterns, due to the resulting immune response or through direct effects. Because parasites are multicellular organisms, they can modify certain behaviors to facilitate infection and complete their life cycle [ 89 ]. It is possible that sleep is a state in which they can exploit the infected host, because the responsiveness to external stimuli declines, rendering the host more susceptible to infection.…”

Section: Parasitic Infections and Sleepmentioning

confidence: 99%

The Bidirectional Relationship between Sleep and Immunity against Infections

Ibarra-Coronado

Pantaleón-Martínez

Velázquez‐Moctezuma

et al. 2015

Journal of Immunology Research

173

158

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Sleep is considered an important modulator of the immune response. Thus, a lack of sleep can weaken immunity, increasing organism susceptibility to infection. For instance, shorter sleep durations are associated with a rise in suffering from the common cold. The function of sleep in altering immune responses must be determined to understand how sleep deprivation increases the susceptibility to viral, bacterial, and parasitic infections. There are several explanations for greater susceptibility to infections after reduced sleep, such as impaired mitogenic proliferation of lymphocytes, decreased HLA-DR expression, the upregulation of CD14+, and variations in CD4+ and CD8+ T lymphocytes, which have been observed during partial sleep deprivation. Also, steroid hormones, in addition to regulating sexual behavior, influence sleep. Thus, we hypothesize that sleep and the immune-endocrine system have a bidirectional relationship in governing various physiological processes, including immunity to infections. This review discusses the evidence on the bidirectional effects of the immune response against viral, bacterial, and parasitic infections on sleep patterns and how the lack of sleep affects the immune response against such agents. Because sleep is essential in the maintenance of homeostasis, these situations must be adapted to elicit changes in sleep patterns and other physiological parameters during the immune response to infections to which the organism is continuously exposed.

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“…Acute and chronic sleep deprivation modifies the immune response, and conversely, immunological challenges modify the normal sleep pattern. They may be able to modify certain behaviours to facilitate infection and complete their life cycles 38 . However, this field still remains poorly studied, and consequently the function of sleep in the immune response to pathogens beginning to be understood.…”

Section: Discussionmentioning

confidence: 99%

Sleep Deprivation Induces Changes in Immunity in Trichinella spiralis-Infected Rats

et al. 2015

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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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The consequences of parasitic infection for the behavior of the mammalian host.

Cited by 17 publications

References 51 publications

Behavioral changes in Rattus norvegicus experimentally infected by Toxocara canis larvae

Behavioral changes in Rattus norvegicus experimentally infected by Toxocara canis larvae

The Bidirectional Relationship between Sleep and Immunity against Infections

Sleep Deprivation Induces Changes in Immunity in Trichinella spiralis-Infected Rats

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