The Role of the Vagus Nerve in Cytokine-to-Brain Communication
ABSTRACT Peripheral interleukin-1 beta (IL-beta) and inflammatory stimuli that induce the synthesis and release of IL-1 beta produce a variety of central nervous system responses. Most proposals designed to explain how peripheral IL-1 beta influences the CNS have focused on blood-borne routes of communication. We will review data that indicate that at least some of the CNS response to peripheral IL-1 beta are instead mediated by a neural route of communication between the periphery and the CNS. IL-1 beta activates afferent vagal fibers that terminate in the nucleus tractus solitarius, and communication via the vagus is responsible for much of the hyperalgesia, fever, anorexia, taste aversions, increased levels of plasma corticosteroid, and brain norepinephrine changes produced by intraperitoneal injections of IL-1 beta and LPS. Data extending this analysis to TNF-alpha and intravenous routes will be described.
SourceAvailable from: Kuldeep Dhama[Show abstract] [Hide abstract]
ABSTRACT: Neuroimmunomodulation involves interactions among nervous, endocrine and immune systems. An integrated function is performed by nervous and immune systems that is responsible for preservation of integrity and homeostasis of the organism. Though central nervous system (CNS) has a limited repertoire for its own protection, it has the blood brain barrier (BBB) and the capacity to engage peripheral immune system to eliminate infections and xenobiotics. Neural cells involved in the process of providing neural immunity include: glial cells, astrocytes and oligodendrocytes. Besides working as sentinels to get rid of pathogens in the process of neurodevelopment, both central as well as peripheral immune cells actively participate helping in cognitive brain functions. Neurogenesis process may also be regulated by adaptive immune cells peripherally. Recently there is a discovery of cholinergic anti-inflammatory pathway wherein vagal nerve has shown anti-inflammatory role in endotoxemia and shock. Hormones viz., nor-epinephrine, epinephrine and glucocorticoids prepare immune system to combat infections and enhance distribution and trafficking of immune cells by several ways. This review focuses on neurobiology, neuro-immune cross talk, neuroimmunoregulation, stress and neuroimmunomodulation which will be beneficial for researchers, professionals and academicians. Topics like neurotoxic and neuroprotective roles of immune reactions (which are innate in nature) in the process of aging are highly debated among researchers. In this review, topics like neuroinflammation and neurodegeneration, role of vitamins, minerals, herbs and drugs, and volatile oils in the process of neuroimmunomodulation and particularly countering various diseases, disorders, infections, stress and aging have been discussed vividly to enhance and update the knowledge of the scientific community regarding this particular topic ‘Neuroimmunomodulation’.International Journal of Pharmacology 02/2015; 11(2):76-94. DOI:10.3923/ijp.2015.76.94 · 0.98 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Sickness behavior, a coordinated set of behavioral changes in response to infection, lies at the intersection of immunology, endocrinology, and evolutionary biology. Sickness behavior is elicited by pro-inflammatory cytokines, is thought to be an adaptive means of redirecting energy away from disadvantageous behaviors and toward mounting an effective immune response, and may be modulated by hormones, including testosterone and oxytocin. Research on sickness behavior in humans has lagged behind non-human animal research due to methodological complexities. Here we review what is known about sickness behavior in humans, the effects of various hormones on sickness behavior, the possible role of cytokine gene variation in influencing sickness behavior responses, and the ways in which culture and gender norms could similarly influence these behavioral changes. We also propose methodologies for advancing further studies of sickness behavior in humans.American Journal of Physical Anthropology 01/2015; DOI:10.1002/ajpa.22698 · 2.51 Impact Factor
[Show abstract] [Hide abstract]
ABSTRACT: Study design:Review article.Objectives:The objective of this study is to provide an overview of the many factors that contribute to the chronic inflammatory state typically observed following spinal cord injury (SCI).Methods:Literature review.Results:Not applicable.Conclusion:SCI is typically characterized by a low-grade inflammatory state due to a number of factors. As bidirectional communication exists between the nervous, endocrine and immune systems, damage to the spinal cord may translate into both endocrinal and immune impairment. Damage to the autonomic nervous system may induce immune dysfunction directly, through the loss of neural innervation of lymphoid organs, or indirectly by inducing endocrinal impairment. In addition, damage to the somatic nervous system and the corresponding loss of motor and sensory function increases the likelihood of developing a number of secondary health complications and metabolic disorders associated with a state of inflammation. Lastly, numerous related disorders associated with a state of chronic inflammation have been found to be at a substantially higher prevalence following SCI. Together, such factors help explain the chronic inflammatory state and immune impairment typically observed following SCI. An understanding of the interactions between systems, both in health and disease, and the many causes of chronic inflammation may aid in the effective future treatment of immune dysfunction and related disorders following SCI.Spinal Cord advance online publication, 4 November 2014; doi:10.1038/sc.2014.184.Spinal Cord 11/2014; 53(1). DOI:10.1038/sc.2014.184 · 1.70 Impact Factor