Reciprocal regulation of the neural and innate immune systems

Irwin, Michael R.; Cole, Steven W.

doi:10.1038/nri3042

Cited by 756 publications

(815 citation statements)

References 80 publications

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“…Although continuous perineural analgesia used in our study subjects precluded assignment of laminitis grades beyond OG2, the degree of lamellar separation evident on histologic evaluation of the samples is indicative of OG3 laminitis 15. Interestingly, perineural analgesia itself has been reported to cause a decrease in gene expression of inflammatory proteins, and a relationship between cytokines and neuro‐hormonal feedback and perineural anesthesia and suppression of inflammation has been observed in both humans and animals 18, 19, 20, 21. Although this relationship has yet to be investigated in laminitis, a recent study of inflammatory signaling in SRL was conducted without the use of perineural anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Effect of Delayed Digital Hypothermia on Lamellar Inflammatory Signaling in the Oligofructose Laminitis Model

Dern

Watts

Werle

et al. 2017

Veterinary Internal Medicne

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BackgroundIn the oligofructose (OF) model of sepsis‐related laminitis (SRL), digital hypothermia (“cryotherapy”) initiated before the onset of clinical signs is reported not only to limit lamellar injury, but also to cause marked inhibition of lamellar inflammatory signaling.Hypothesis/ObjectivesBecause hypothermia also has been reported to be protective when not initiated until the onset of lameness in the OF model of SRL, we hypothesized that the lamellar protection conferred by hypothermia is caused by local lamellar inhibition of inflammatory signaling as described when hypothermia was initiated earlier in the disease process.AnimalsEight Standardbred geldings aged 3–11 years with no lameness and no abnormalities of the feet detectable by gross or radiographic examination.MethodsUsing the OF model of SRL, lamellar mRNA concentrations of proinflammatory cytokines, chemokines, and endothelial adhesion proteins were compared between samples from treated limbs (CRYO, submerged in ice water for 36 hour starting at the onset of lameness), untreated limbs (NON‐CRYO, opposite limb from CRYO limbs maintained at ambient temperature), and untreated limbs from normal horses in which laminitis was not induced (CON).ResultsAlthough OF administration resulted in increases in lamellar mRNA concentrations of several inflammatory mediators in NON‐CRYO limbs (vs CON), digital hypothermia had no significant effect on these increases.Conclusions and Clinical ImportanceThe lack of inflammatory inhibition in lamellar tissue samples in our study indicates that the protective effects of digital hypothermia instituted at the onset of clinical signs of laminitis do not arise from inhibition of inflammatory pathways.

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Section: Discussionmentioning

confidence: 99%

Effect of Delayed Digital Hypothermia on Lamellar Inflammatory Signaling in the Oligofructose Laminitis Model

Dern

Watts

Werle

et al. 2017

Veterinary Internal Medicne

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“…A more detailed account of the specific mechanisms whereby social factors regulate immune system responses is presented elsewhere (Irwin and Cole, 2011;Slavich and Cole, 2013;Slavich and Irwin, 2014). Here, we summarize research that highlights several of the consequences of having an immune system that is sensitive to features of the social environment.…”

Section: Part Ii: Social Behavior As An Organizer Of Inflammatory Actmentioning

confidence: 97%

“…To understand why social factors can increase inflammatory activity, it is important to know that inflammation is regulated at multiple levels. First, inflammation is regulated by factors in the periphery, such as exposure to an extracellular pathogen, which then leads to the activation of inflammatory-related transcription factors and the increased production of proinflammatory cytokines (Irwin and Cole, 2011). However, inflammation is also regulated neurally, which allows inflammatory processes to be shaped by certain features of the environment that predict a greater likelihood of wounding and infection and thus a greater need for inflammatory activity.…”

Section: Part Ii: Social Behavior As An Organizer Of Inflammatory Actmentioning

confidence: 99%

“…However, inflammation is also regulated neurally, which allows inflammatory processes to be shaped by certain features of the environment that predict a greater likelihood of wounding and infection and thus a greater need for inflammatory activity. These threatening features are processed neurally, resulting in sympathetic nervous system (SNS) activation as well as activation of the hypothalamicpituitary-adrenocortical (HPA) axis, which can then influence inflammatory responding (Irwin and Cole, 2011;Eisenberger and Cole, 2012). (Specifically, under normal conditions, acute SNS activation enhances inflammatory activity, whereas acute HPA activation inhibits inflammatory responding .…”

Section: Part Ii: Social Behavior As An Organizer Of Inflammatory Actmentioning

confidence: 99%

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In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

Eisenberger

Moieni

Inagaki

et al. 2016

Neuropsychopharmacol

301

220

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Although it has commonly been assumed that the immune system and the processes that govern social behavior are separate, non-communicating entities, research over the past several decades suggests otherwise. Considerable evidence now shows that inflammatory processes and social behavior are actually powerful regulators of one another. This review first summarizes evidence that inflammatory processes regulate social behavior, leading to characteristic changes that may help an individual navigate the social environment during times of sickness. Specifically, this review shows that inflammation: (1) increases threatrelated neural sensitivity to negative social experiences (eg, rejection, negative social feedback), presumably to enhance sensitivity to threats to well-being or safety in order to avoid them and (2) enhances reward-related neural sensitivity to positive social experiences (eg, viewing close others and receiving positive social feedback), presumably to increase approach-related motivation towards others who might provide support and care during sickness. Next, this review summarizes evidence showing that social behavior also regulates aspects of inflammatory activity, preparing the body for situations in which wounding and infection may be more likely (social isolation). Here, we review research showing: (1) that exposure to social stressors increases proinflammatory activity, (2) that individuals who are more socially isolated (ie, lonely) show increased proinflammatory activity, and (3) that individuals who are more socially isolated show increased proinflammatory activity in response to an inflammatory challenge or social stressor. The implications of the co-regulation of inflammation and social behavior are discussed.

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“…For example, meditation might conserve cerebral gray matter by reducing stress levels and thus modulating the potentially harmful effects of immune response genes expression (Irwin and Cole, 2011), HPA axis hyperactivity (McEwen, 2008), down-regulation of neurogenesis (Varela-Nallar et al, 2010), activation of pro-inflammatory processes and the production of reactive oxygen species (Swaab et al, 2005). Direct or indirect effects of stress reduction might manifest, especially in regions that are known to be particularly vulnerable against stress (e.g., the hippocampus; see cluster C1) and/or directly involved in the regulation of stress (e.g., the hypothalamus; see cluster C8).…”

Section: Possible Underlying Mechanismsmentioning

confidence: 99%

Forever Young(er): potential age-defying effects of long-term meditation on gray matter atrophy

Lüders

Kurth

Lauche

2015

Deutsche Zeitschrift für Akupunktur

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While overall life expectancy has been increasing, the human brain still begins deteriorating after the first two decades of life and continues degrading further with increasing age. Thus, techniques that diminish the negative impact of aging on the brain are desirable. Existing research, although scarce, suggests meditation to be an attractive candidate in the quest for an accessible and inexpensive, efficacious remedy. Here, we examined the link between age and cerebral gray matter re-analyzing a large sample (n = 100) of long-term meditators and control subjects aged between 24 and 77 years. When correlating global and local gray matter with age, we detected negative correlations within both controls and meditators, suggesting a decline over time. However, the slopes of the regression lines were steeper and the correlation coefficients were stronger in controls than in meditators. Moreover, the age-affected brain regions were much more extended in controls than in meditators, with significant group-by-age interactions in numerous clusters throughout the brain. Altogether, these findings seem to suggest less age-related gray matter atrophy in long-term meditation practitioners.

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Reciprocal regulation of the neural and innate immune systems

Cited by 756 publications

References 80 publications

Effect of Delayed Digital Hypothermia on Lamellar Inflammatory Signaling in the Oligofructose Laminitis Model

Effect of Delayed Digital Hypothermia on Lamellar Inflammatory Signaling in the Oligofructose Laminitis Model

In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

Forever Young(er): potential age-defying effects of long-term meditation on gray matter atrophy

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