scholarly journals The Legacy of Sickness Behaviors

2020 ◽  
Vol 11 ◽  
Author(s):  
Keith W. Kelley ◽  
Stephen Kent
Keyword(s):  
Immune System ◽  
Body Temperature ◽  
Communication Systems ◽  
Memory Deficits ◽  
Sleep Disruption ◽  
Sickness Behaviors ◽  
Systemic Infections ◽  
The Brain ◽  
Conceptual Advance

Systemic infections of all types lead to a syndrome known as sickness behaviors. Changes in the behavior of febrile humans and animals formed the original basis for this concept. Body temperature is behaviorally regulated in both endotherms and ectotherms. However, infections cause other changes in body functions, including sleep disruption, anorexia, cognitive and memory deficits and disorientation. The brain mediates this entire cluster of symptoms, even though most major infections occur outside the brain. The true importance of sickness behaviors is not the numerous discoveries of symptoms that affect all of us when we get sick. Instead, the legacy of 30 years of research in sickness behaviors is that it established the physiologic importance of reciprocal communication systems between the immune system and the brain. This conceptual advance remains in its infancy.

Sickness and the social brain: How the immune system regulates behavior across species

2021 ◽  
Author(s):  
Benjamin A. Devlin ◽  
Caroline J. Smith ◽  
Staci D. Bilbo
Keyword(s):  
Immune System ◽  
Social Behavior ◽  
Brain Regions ◽  
Behavior Changes ◽  
Social Brain ◽  
Evolutionary Origins ◽  
Immune Mediators ◽  
The Social ◽  
Sickness Behaviors ◽  
The Brain

Many instances of sickness critically involve the immune system. The immune system talks to the brain in a bi-directional loop. This discourse affords the immune system immense control, such that it can influence behavior and optimize recovery from illness. These behavioral responses to infection are called sickness behaviors and can manifest in many ways, including changes in mood, motivation, or energy. Fascinatingly, most of these changes are conserved across species, and most organisms demonstrate some form of sickness behaviors. One of the most interesting sickness behaviors, and not immediately obvious, is altered sociability. Here, we discuss how the immune system impacts social behavior, by examining the brain regions and immune mediators involved in this process. We first outline how social behavior changes in response to infection in various species. Next, we explore which brain regions control social behavior and their evolutionary origins. Finally, we describe which immune mediators establish the link between illness and social behavior, in the context of both normal development and infection. Overall, we hope to make clear the striking similarities between the mechanisms that facilitate changes in sociability in derived and ancestral vertebrate, as well as invertebrate, species.

Evaluation of Temperature Transients at Various Body Temperature Measuring Sites Using a Fast Response Thermistor Bead Sensor

2013 ◽  
Author(s):  
Oleg Vesnovsky ◽  
L. D. Timmie Topoleski ◽  
Laurence W. Grossman ◽  
Jon P. Casamento ◽  
Liang Zhu
Keyword(s):  
Immune System ◽  
Body Temperature ◽  
Pulmonary Artery ◽  
Temperature Control ◽  
Surgical Procedures ◽  
Fast Response ◽  
The Body ◽  
Control Center ◽  
Post Surgery ◽  
The Brain

Body temperature monitoring of humans has been an important tool for helping clinicians diagnose infections, detect fever, monitor thermoregulation functions during surgical procedures, and assess post-surgery recovery.1–3 Fever itself is typically not considered a disease. It is a response of the body to a disease, which is often inflammatory in nature. Elevation of the set point at the body temperature control center, the brain hypothalamus, is caused by circulating pyrogens produced by the immune system responding to diseases. Since the brain hypothalamus is not easily accessed by thermometers, other body locations have been identified as alternative measuring sites. Those sites include the pulmonary artery, rectum, bladder, distal esophagus and nasopharynx, sublingual surface of the tongue, under the armpit, tympanic membrane, and forehead.

Potential immunotherapy for Alzheimer disease and age-related dementia

2019 ◽  
Vol 21 (1) ◽  
pp. 21-25 ◽  
Keyword(s):  
Immune System ◽  
Alzheimer Disease ◽  
Cross Talk ◽  
Immune Checkpoint ◽  
Short Review ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
New Approach ◽  
Age Related ◽  
The Brain

Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain's pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain's disease hallmarks. Here, we provide a short review of the mechanisms orchestrating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD.

Potential immunotherapy for Alzheimer disease and age-related dementia

2019 ◽  
Vol 21 (1) ◽  
pp. 21-25 ◽  
Keyword(s):  
Immune System ◽  
Alzheimer Disease ◽  
Cross Talk ◽  
Immune Checkpoint ◽  
Short Review ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
New Approach ◽  
Age Related ◽  
The Brain

Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain’s pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain’s disease hallmarks. Here, we provide a short review of the mechanisms orchestrating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD.

025 Sleep Disruption on an Orbital Shaker alters Glutamate in Prairie Vole Prefrontal Cortex

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A11-A12
Author(s):  
Carolyn Jones ◽  
Randall Olson ◽  
Alex Chau ◽  
Peyton Wickham ◽  
Ryan Leriche ◽  
...  
Keyword(s):  
Autism Spectrum Disorder ◽  
Prefrontal Cortex ◽  
Early Life ◽  
Autism Spectrum ◽  
Prairie Vole ◽  
Sleep Disruption ◽  
Glutamatergic Synapses ◽  
The Brain ◽  
Orbital Shaker

Abstract Introduction Glutamate concentrations in the cortex fluctuate with the sleep wake cycle in both rodents and humans. Altered glutamatergic signaling, as well as the early life onset of sleep disturbances have been implicated in neurodevelopmental disorders such as autism spectrum disorder. In order to study how sleep modulates glutamate activity in brain regions relevant to social behavior and development, we disrupted sleep in the socially monogamous prairie vole (Microtus ochrogaster) rodent species and quantified markers of glutamate neurotransmission within the prefrontal cortex, an area of the brain responsible for advanced cognition and complex social behaviors. Methods Male and female prairie voles were sleep disrupted using an orbital shaker to deliver automated gentle cage agitation at continuous intervals. Sleep was measured using EEG/EMG signals and paired with real time glutamate concentrations in the prefrontal cortex using an amperometric glutamate biosensor. This same method of sleep disruption was applied early in development (postnatal days 14–21) and the long term effects on brain development were quantified by examining glutamatergic synapses in adulthood. Results Consistent with previous research in rats, glutamate concentration in the prefrontal cortex increased during periods of wake in the prairie vole. Sleep disruption using the orbital shaker method resulted in brief cortical arousals and reduced time in REM sleep. When applied during development, early life sleep disruption resulted in long-term changes in both pre- and post-synaptic components of glutamatergic synapses in the prairie vole prefrontal cortex including increased density of immature spines. Conclusion In the prairie vole rodent model, sleep disruption on an orbital shaker produces a sleep, behavioral, and neurological phenotype that mirrors aspects of autism spectrum disorder including altered features of excitatory neurotransmission within the prefrontal cortex. Studies using this method of sleep disruption combined with real time biosensors for excitatory neurotransmitters will enhance our understanding of modifiable risk factors, such as sleep, that contribute to the altered development of glutamatergic synapses in the brain and their relationship to social behavior. Support (if any) NSF #1926818, VA CDA #IK2 BX002712, Portland VA Research Foundation, NIH NHLBI 5T32HL083808-10, VA Merit Review #I01BX001643

scholarly journals Loss of Ftsj1 perturbs codon-specific translation efficiency in the brain and is associated with X-linked intellectual disability

2021 ◽  
Vol 7 (13) ◽  
pp. eabf3072
Author(s):  
Y. Nagayoshi ◽  
T. Chujo ◽  
S. Hirata ◽  
H. Nakatsuka ◽  
C.-W. Chen ◽  
...  
Keyword(s):  
Intellectual Disability ◽  
State Level ◽  
Memory Deficits ◽  
Ribosome Profiling ◽  
Translation Efficiency ◽  
Trna Modification ◽  
Synaptic Organization ◽  
Transfer Rnas ◽  
The Brain

FtsJ RNA 2′-O-methyltransferase 1 (FTSJ1) gene has been implicated in X-linked intellectual disability (XLID), but the molecular pathogenesis is unknown. We show that Ftsj1 is responsible for 2′-O-methylation of 11 species of cytosolic transfer RNAs (tRNAs) at the anticodon region, and these modifications are abolished in Ftsj1 knockout (KO) mice and XLID patient–derived cells. Loss of 2′-O-methylation in Ftsj1 KO mouse selectively reduced the steady-state level of tRNAPhe in the brain, resulting in a slow decoding at Phe codons. Ribosome profiling showed that translation efficiency is significantly reduced in a subset of genes that need to be efficiently translated to support synaptic organization and functions. Ftsj1 KO mice display immature synaptic morphology and aberrant synaptic plasticity, which are associated with anxiety-like and memory deficits. The data illuminate a fundamental role of tRNA modification in the brain through regulation of translation efficiency and provide mechanistic insights into FTSJ1-related XLID.

Assessing the Use of Biometric Ear Tags as Body Temperature Monitoring Devices in Swine

2021 ◽  
Vol 99 (Supplement_2) ◽  
pp. 45-46
Author(s):  
Ellie A Amerson ◽  
Harrison Moss ◽  
Suresh Kumar ◽  
Terry D Brandebourg
Keyword(s):  
Body Temperature ◽  
Pearson Correlation ◽  
Disease Outbreaks ◽  
Correlation Coefficients ◽  
Raspberry Pi ◽  
Herd Health ◽  
Swine Industry ◽  
Sickness Behaviors ◽  
Large Production ◽  
Monitoring Devices

Abstract It is difficult to detect the subtle changes associated with sickness behaviors in individual pigs early enough to prevent disease outbreaks in group housing settings within large production facilities. This failure results in significant losses to the swine industry. Strategies that allow early detection of parameters such as febrile responses could therefore significantly improve herd health and producer profitability. Our objective was to determine if the use of a biometric ear tag capable of measuring temperature could be used to accurately monitor body temperature in swine. To accomplish this, 42-d-old pigs (n = 21) were fitted with biometric ear tags for 35 d. These devices continuously measured auricular skin temperature and allowed data collection via a paired raspberry pi aggregator. During this period, repeated epidermal temperatures were also taken daily on the rump, shoulder, and ear using a clinical grade infrared thermometer. Correlation analysis using the PROC CORR procedure of SAS was then conducted to determine the ability of the biometric device to estimate body temperature relative to estimates from the clinical device. Infrared temperature readings for the ear significantly correlated with those taken at the shoulder (P < 0.0001) and rump (P < 0.0001). Importantly, temperature readings measured by the biometric ear tags also significantly correlated with infrared readings at the ear (P < 0.0001), shoulder (P < 0.0001) and rump (P < 0.0001) with Pearson Correlation coefficients of 0.51, 0.21, and 0.23, respectively. Collectively, these data support the hypothesis that the biometric ear tag device tested during this trial can be used to continuously monitor body temperature in young swine. These results indicate that further efforts to develop these devices as novel herd health monitoring devices is indeed warranted with the next step involving the assessment of their ability to detect physiological changes in body temperature.

Physiology and pathophysiology of the RANKL/RANK system

2010 ◽  
Vol 391 (12) ◽  
Author(s):  
Reiko Hanada ◽  
Toshikatsu Hanada ◽  
Josef M. Penninger
Keyword(s):  
Body Temperature ◽  
Mammary Gland Development ◽  
Basal Body Temperature ◽  
Central Nervous Systems ◽  
Rank System ◽  
Functional Relevance ◽  
Rank Signaling ◽  
Gland Development ◽  
The Brain ◽  
Node Formation

Abstract The TNF family molecule RANKL and its receptor RANK are key regulators of bone remodeling, lymph node formation, and mammary gland development during pregnancy. RANKL and RANK are also expressed in the central nervous systems (CNS). However, the functional relevance of RANKL/RANK in the brain was entirely unknown. Recently, our group reported that the RANKL/RANK signaling pathway has an essential role in the central regulation of body temperature via the prostaglandin axis. This review discusses novel aspects of the RANKL/RANK system as key regulators of fever and female basal body temperature in the CNS.

The T4 gene encodes the AIDS virus receptor and is expressed in the immune system and the brain

Cell ◽  
1986 ◽  
Vol 47 (3) ◽  
pp. 333-348 ◽  
Author(s):  
Paul Jay Maddon ◽  
Angus G. Dalgleish ◽  
J.Steven McDougal ◽  
Paul R. Clapham ◽  
Robin A. Weiss ◽  
...  
Keyword(s):  
Immune System ◽  
Virus Receptor ◽  
Aids Virus ◽  
The Brain
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